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This function searchs [GDS](https://www.ncbi.nlm.nih.gov/gds) database, and return a data.frame for all the search results.

Usage

searchGEO(query, step = 500L)

Arguments

query

character, the search term. The NCBI uses a search term syntax which can be associated with a specific search field with square brackets. So, for instance "Homo sapiens\[ORGN\]" denotes a search for `Homo sapiens` in the “Organism” field. Details see <https://www.ncbi.nlm.nih.gov/geo/info/qqtutorial.html>. The names and definitions of these fields can be identified using [entrez_db_searchable][rentrez::entrez_db_searchable].

step

the number of records to fetch from the database each time. You may choose a smaller value if failed.

Value

a data.frame contains the search results

Details

The NCBI allows users to access more records (10 per second) if they register for and use an API key. [set_entrez_key][rentrez::set_entrez_key] function allows users to set this key for all calls to rentrez functions during a particular R session. You can also set an environment variable `ENTREZ_KEY` by [Sys.setenv][base::Sys.setenv]. Once this value is set to your key rentrez will use it for all requests to the NCBI. Details see <https://docs.ropensci.org/rentrez/articles/rentrez_tutorial.html#rate-limiting-and-api-keys>

Examples

GEOquery::searchGEO("diabetes[ALL] AND Homo sapiens[ORGN] AND GSE[ETYP]")
#>                                                                                                                                                                                                                                                         Title
#> 1                                                                              Shifts in the Immunoepigenomic Landscape of Monocytes in Response to a Diabetes-Specific Social Support Intervention: A Pilot Study Among Native Hawaiian Adults with Diabetes
#> 2                                                                                                                                                                                                     Vitreous of proliferative diabetic retinopathy patients
#> 3                                                                                                                                 Circulating small non-coding RNA profiling as potential biomarkers of atherosclerotic plaque composition in Type 1 diabetes
#> 4                                                                                                                                                    Independent phenotypic plasticity axes define mammalian metabolic and obesity sub-types [RNA-seq, human]
#> 5                                                                                                                                                                 Transcriptional regulation of liver lipotoxicity in non-alcoholic steatohepatitis [RNA-seq]
#> 6                                                                                                                                                                Transcriptional regulation of liver lipotoxicity in non-alcoholic steatohepatitis [ATAC-seq]
#> 7                                                                                                                                 Distinctive exercise-induced inflammatory response and exerkine induction in skeletal muscle of people with type 2 diabetes
#> 8                                                                                                                         Bioinformatic analysis of the mechanism by which metformin enhances chemosensitivity of head and neck squamous cell carcinoma cells
#> 9                                                                                                                                                    Glucagon-like Peptide-1 (GLP-1) Rescue Diabetic Cardiac Dysfuntions in Human iPSC-Derived Cardiomyocytes
#> 10                                                                                                                                                          DNA Methylation Profiling Reveals Novel Pathway Implicated in Cardiovascular Diseases of Diabetes
#> 11                                                                                                                                     Transcriptome analysis of Newly Diagnosed Type 2 Diabetes Subjects identifies genes to predict Metformin drug Response
#> 12                                                                                                                Hepatic senescence is associated with clinical progression of NAFLD/NASH: Role of BMP4 and its antagonist Gremlin1 (Visceral adipose cells)
#> 13                                                                                                                                                                                             Single-cell Transcriptome Atlas of the Human Corpus Cavernosum
#> 14                                                                                                                       Genome-wide placental gene methylations in gestational diabetes mellitus, fetal growth and metabolic health biomarkers in cord blood
#> 15                                                                                                                                                              Development of a physiological insulin resistance model in human stem cell-derived adipocytes
#> 16                                                                                                                                                                  Bulk RNA-seq on mouse model of diabetic nephropathy and in vitro model of SRSF7 knockdown
#> 17                                                                                                                         Altered expressions of transfer RNA-derived small RNAs and microRNAs in the vitreous humour of proliferative diabetic retinopathy.
#> 18                                                                                                                                                              Synovial inflammatory pathways characterize anti-TNF-responsive rheumatoid arthritis patients
#> 19                                                                                      Self-amplifying Loop of NF-κB and Periostin Initiated by PIEZO1 Accelerates Mechano-induced Senescence of Nucleus Pulposus Cells and Intervertebral Disc Degeneration
#> 20                                                                                                                                                                                        Patient iPSCs with NEUROG3 mutation reveal pancreatic insufficiency
#> 21                                                                                                                                                                                                     Gene expression data from human omental adipose tissue
#> 22                                                                                                                                               Expression profiles of placenta and umbilical cord blood with or without gestational diabetes mellitus (GDM)
#> 23                                                                                           Reduced representation bisulfite sequencing (RRBS) methylation profiles of placenta and umbilical cord blood with or without gestational diabetes mellitus (GDM)
#> 24                                                                                                              Methylation profiling (RRBS) and expression profiling (RNA-seq) of placenta and umbilical cord blood with gestational diabetes mellitus (GDM)
#> 25                                                                                                                                                     Deciphering protective mechanism against human type 2 diabetes through in vitro β cell differentiation
#> 26                                                                                                                                                                              High-throughput analysis of ANRIL circRNA isoforms in human pancreatic islets
#> 27                                                        LncRNA LYPLAL1-DT screening from type 2 diabetes with macrovascular complication contributes protective effects on human umbilical vein endothelial cells via regulating the miR-204-5p/SIRT1 axis.
#> 28                                                                                                                                                                                     DNA Methylation-Based Prediction of Post-Operative Atrial Fibrillation
#> 29                                                                                                                                                                                  DNA Methylation-Based Prediction of Post-Operative Atrial Fibrillation II
#> 30                                                                                                                                                                                   DNA Methylation-Based Prediction of Post-Operative Atrial Fibrillation I
#> 31                                                                                                                          RNA-seq profiling of tubulointerstitial tissue reveals a potential therapeutic role of dual anti-phosphatase 1 in kidney diseases
#> 32                                                                                                                                              Bone metabolism-related serum miRNAs to diagnose postmenopausal osteoporosis in middle-aged and elderly women
#> 33                                                                                                                                                           Transcription Factor Binding Analysis of Wild Type and HHEX-/- ES-derived Pancreatic Progentiors
#> 34                                                                                                                                                                    Chromatin Landscape Analysis of Wild Type and HHEX-/- ES-derived Pancreatic Progentiors
#> 35                                                                                                                                                                Transcription Landscape Analysis of Wild Type and HHEX-/- ES-derived Pancreatic Progentiors
#> 36                                                                                                                                                                                     Effect of O-GlcNAc Transferase (OGT) siRNA in trophoblastic BeWo cells
#> 37                                                                                                                                                        Polysome profiling quantified by RNA sequencing in PANC1 cells treated with MNK2 inhibitors or DMSO
#> 38                                                                                                                                       Circulating extracellular vesicles exhibit a differential miRNA profile in gestational diabetes mellitus pregnancies
#> 39                                                                                                                                          Serum miRNA profile in diabetic patients with ischemic heart disease (IHD) as a promising non-invasive biomarker.
#> 40                                                                                                                                                        Identification of significant immune-related genes for diabetic foot ulcers: validated by scRNA-seq
#> 41                                                                                                                              Spatial Environment Affects HNF4A Mutation-Specific Proteome Signatures and Cellular Morphology in hiPSC-Derived β-Like Cells
#> 42                                                                                                                                                            Genome-wide Analysis Reflects Novel 5-Hydroxymethylcytosines Implicated in Diabetic Nephropathy
#> 43                                  Transcriptome analysis and weighted gene co-expression network reveal candidate genes and pathways responses to lactate dehydrogenase inhibition (oxamate) in hyperglycemic human renal proximal epithelial tubular cells
#> 44                                                                                                                                                   Fourteen-weeks combined exercise epigenetically modulated 118 genes of menopausal women with prediabetes
#> 45                                                                                                                                                                       Human placental tissues:control group vs non-diabetic fetal macrosomia (NDFMS) group
#> 46                                                                                                             Multi-dimensional modeling disrupted synapse formation underlying psychiatric disorders of Wolfram syndrome reveals essentiality of astrocytes
#> 47                                                                                                                           Transcriptional and chromatin accessibility changes underlying progression from islet autoantibody positivity to type 1 diabetes
#> 48                                                                                                                                                       Transcriptional changes underlying progression from islet autoantibody positivity to type 1 diabetes
#> 49                                                                                                                                               Chromatin accessibility changes underlying progression from islet autoantibody positivity to type 1 diabetes
#> 50                                                                                                                                                                                    In-depth molecular profiling specifies human retinal microglia identity
#> 51                                                                                                                                                                   Probiotic normalization of systemic inflammation in siblings of Type 1 diabetes patients
#> 52                                                                                                                                          Characterization of peripheral blood TCR in patients with Type 1 Diabetes Mellitus by BD Rhapsody™ VDJ CDR3 Assay
#> 53                                                                                         Diverging metabolic effects of two energy restricted diets differing in nutrient quality: a 12-week randomized controlled trial in subjects with abdominal obesity
#> 54                                                                                         RNA aptamers specific for transmembrane p24 trafficking protein 6 and Clusterin for the targeted delivery of imaging reagents and RNA therapeutic to human β cells
#> 55                                                                                                                                             Bariatric surgery mediated weight loss reduces breast cancer risk by reducing estrogen receptor alpha activity
#> 56                                                                                                                                              RNA-seq profiles between human parental and 5-FU drug resistant HCT116 and SW480 colorectal cancer cell lines
#> 57                                                                             Identification of Key LncRNAs and Pathways in Prediabetes and Type 2 Diabetes Mellitus for Hypertriglyceridemia Patients Based on Weighted Gene Co-Expression Network Analysis
#> 58                                                                                                                                                                                    Increased insulin secretion in ZNT8 mutant stem-cell derived beta cells
#> 59                                                                                                                         Differentially-expressed mRNAs, microRNAs and long noncoding RNAs in intervertebral disc degeneration identified by RNA-sequencing
#> 60                                                                                                                                                Human Tubular Epithelial Cells Activate a Coordinated Stress Response after Serum Exposure [RNAseq-pid2019]
#> 61                                                                                                                                                Human Tubular Epithelial Cells Activate a Coordinated Stress Response after Serum Exposure [RNAseq-pid1830]
#> 62                                                                                                                            VPA-treatment of Panc-1-cells to study epigenetic impact mediated by histone acetylation on epithelial-mesenchymal transmission
#> 63                                                                                                                                                                        Human Pluripotent Stem Cell-derived Islets Ameliorate Diabetes in Nonhuman Primates
#> 64                                                                                                                                                     Human Pluripotent Stem Cell-derived Islets Ameliorate Diabetes in Nonhuman Primates [human_singlecell]
#> 65                                                                                                                                                           Human Pluripotent Stem Cell-derived Islets Ameliorate Diabetes in Nonhuman Primates [human_bulk]
#> 66                                                                                                                                                                                             RNA-seq of human adipose tissue macrophage subtypes in obesity
#> 67                                                                                                                                                                       Genome-wide DNA methylation profiling in anorexia nervosa discordant identical twins
#> 68                                                                                        Loci-specific differences in blood DNA methylation in HBV-negative populations at risk for hepatocellular carcinoma development - post-diagnostic HCC blood samples
#> 69                                                                                         Loci-specific differences in blood DNA methylation in HBV-negative populations at risk for hepatocellular carcinoma development - pre-diagnostic HCC blood samples
#> 70                                                                                                                                                         MYCL-mediated in vivo reprogramming expands pancreatic insulin-producing cells to reverse diabetes
#> 71                                                                                  Single-cell RNA-sequencing reveals the heterogeneity of microglia in fibrous membrane derived from proliferative diabetic retinopathy and proliferative vitreoretinopathy
#> 72                                                                                                                                             HAMSAB supplement enhances SCFA production associated with microbiota and immune modulation in type 1 diabetes
#> 73                                                                                                      An HNF1A truncation associated with maturity-onset diabetes of the young impairs pancreatic progenitor differentiation by antagonising HNF1B function
#> 74                                                                                                                                                                                         Limited extent and consequences of pancreatic SARS-CoV-2 infection
#> 75                                                                                                                                Exosomal RNA expression profiles and their prediction performance in gestational diabetes mellitus patients with macrosomia
#> 76                                                                                                                                                                                                                   circRNA profiles of diabetic retinopathy
#> 77                                                                                                                    A global analysis on the differential regulation of RNA binding proteins (RBPs) by TNF–α as potential modulators of metabolic syndromes
#> 78                                                                                                          RNA sequencing of control and PTPN2 knocked down transcriptomes in EndoC-    H1 cells with or without the treatment of pro-inflammatory cytokines
#> 79                                                                                                                                         Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes
#> 80                                                                                                                                                  A miR-125 / Sirtuin-7 pathway drives pro-calcific potential of myeloid cells in diabetic vascular disease
#> 81                                                                                                                     Exploring the mechanism of Jiangtang Tiaozhi Recipe in the treatment of obese T2DM patients with dyslipidemia based on transcriptomics
#> 82                                                                                                                                                                                                                A single cell atlas of human adipose tissue
#> 83                                                                                                                                                         Characterization of the stromal vascular fraction (SVF) of human subcutaneous adipose tissue (SAT)
#> 84                                                                                                                                                                                           Epigenomic and Transcriptional Basis of Human Insulin Resistance
#> 85                                                                                                                            Prevalence of inflammatory pathways over immuno-tolerance in peripheral blood mononuclear cells of recent-onset type 1 diabetes
#> 86                                                                                                                                                               Inflammatory pathways in peripheral blood expression profile of recent-onset type 1 diabetes
#> 87                                                                                                                                 Integrated analysis of the transcriptome-wide m6A methylome in gestational diabetes mellitus and healthy control placentas
#> 88                                                                                                                                                                          RNA sequence of gestational diabetes mellitus (GDM) and healthy control placentas
#> 89                                                                                                                     Integrated analysis of the transcriptome-wide m6A methylome in gestational diabetes mellitus and healthy control placentas [meRIP-seq]
#> 90                                                                                                                                                                                        HO1 activates autophagy to protect intervertebral disc degeneration
#> 91                                                                                                                                                             Heterogeneous Gene Expression Patterns of Tuberculosis-Diabetes Interaction in Diverse Cohorts
#> 92                                                                                                                                                              Epigenetic alterations are associated with gastric emptying disturbances in Diabetes Mellitus
#> 93                                                                              Integratome analysis of adipose tissues reveals abnormal epigenetic regulation of adipogenesis, inflammation, and insulin signaling in obese individuals with type 2 diabetes
#> 94                                                                         Whole Transcriptomic analysis of placenta and its released extracellular vesicles in normal and preeclampsia pregnancies: insigths into novel biomarkers and mechanisms of disease
#> 95                                                                                     SmallRNA analysis of placenta and its released extracellular vesicles in normal and preeclampsia pregnancies: insigths into novel biomarkers and mechanisms of disease
#> 96                                                                               Transcriptomic analysis of placenta and its released extracellular vesicles in normal and preeclampsia pregnancies: insigths into novel biomarkers and mechanisms of disease
#> 97                                                                                                                                         Persistent Coxsackievirus B1 infection results in extensive changes in the transcriptome of a pancreatic cell line
#> 98                                                                                                                                                           Germline-like TCR alpha chains dominate shared self-reactive T cell receptors in type 1 diabetes
#> 99                                                                                            Human Tongue Fungiform Papilla Transcriptome and Proteome Reveal Sex Differences in Long Intergenic Noncoding RNA, Immune Response and Metabolism Genes [array]
#> 100                                                                                                                                                  DNA methylation profiling of cord blood progenitor endothelial cells from overweight and GDM pregnancies
#> 101                                                                                                                                                       Single cell trajectory modeling identifies a primitive trophoblast state defined by BCAM enrichment
#> 102                                                                                                                     TGF-β-induced miR143/145 influences differentiation, insulin signaling and exercise response in human skeletal muscle [small RNA-seq]
#> 103                                                                                                                           TGF-β-induced miR143/145 influences differentiation, insulin signaling and exercise response in human skeletal muscle [RNA-seq]
#> 104                                                                                                                                 LncRNA expression profile and target gene prediction of calcification in human aortic smooth muscle cells induced by DPP4
#> 105                                                                                                                                                                  Abnormal exocrine-endocrine cell crosstalk promotes β-cell dysfunction and loss in MODY8
#> 106                                                                                                                              Exploratory study reveals far reaching systemic and cellular effects of verapamil treatment in subjects with type 1 diabetes
#> 107                                                                                                                                                    Changes in CIDEA expression associate with adipocytes size and functionality in adolescent obese girls
#> 108                                                                                                                                                 A validated single-cell-based strategy to identify diagnostic and therapeutic targets in complex diseases
#> 109                                                                                                                          A validated single-cell-based strategy to identify diagnostic and therapeutic targets in complex diseases [study of 13 diseases]
#> 110                                                                                                                                                                            Effect of salivary exosomal miR-25-3p on periodontitis with insulin resistance
#> 111                                                                                                                                               Alterations of 5-Hydroxymethylcytosines in Circulating Cell-free DNA Reflect Retinopathy in Type 2 Diabetes
#> 112                                                                   Adipocyte Precursor Cells from First Degree Relatives of type 2 diabetic patients feature changes of hsa-mir-23a-5p, -193a-5p, and -193b-5p and Insulin-Like Growth Factor 2 expression
#> 113                                                    Adipocyte Precursor Cells from First Degree Relatives of type 2 diabetic patients feature changes of hsa-mir-23a-5p, -193a-5p, and -193b-5p and Insulin-Like Growth Factor 2 expression [smallRNA-seq]
#> 114                                                         Adipocyte Precursor Cells from First Degree Relatives of type 2 diabetic patients feature changes of hsa-mir-23a-5p, -193a-5p, and -193b-5p and Insulin-Like Growth Factor 2 expression [RNA-Seq]
#> 115                                                                                                                                                                  Transcriptome dataset of two different adipose tissues in gestational diabetes patients.
#> 116                                                                              Gene-expression profiles of whole blood cells from a Han Chinese population with or without Type-2 Diabetes Mellitus or/and its complications in nephropathy and retinopathy
#> 117                                                                                                                                                                              RNAsequencing of control and STAT3 knocked down transriptomes of EndoC cells
#> 118                                                                                                                                                                                                                              Perturb-Seq using T2D islets
#> 119                                                                                                                                                                                                                                 scGOF-Seq using ND islets
#> 120                                                                                                                                                                                        BACH2 inhibition reverses β-cell failure in type 2 diabetes models
#> 121                                                                                                                                                       Isoforms of SEMA3E-containing supernatant treated gene expression in human aortic endothelial cells
#> 122                                                                                                                                                                                              Single Cell Transcriptomic Landscape of Diabetic Foot Ulcers
#> 123                                                                                  In-depth molecular characterization of neovascular membranes suggests a role for hyalocytes-to-myofibroblasts transdifferentiation in proliferative diabetic retinopathy
#> 124                                                                                                                                                                     Impaired Skeletal Muscle Repair in Healthy Young Adults with Type 1 Diabetes Mellitus
#> 125                                                                                                                                                                                   Spatial transcriptomics of healing and non-healing diabetic foot ulcers
#> 126                                                                                                                                                             Adipocyte-derived extracellular vesicles promote breast cancer progression in type 2 diabetes
#> 127                                                                                 Dysregulated lncRNA and mRNA may promote the progression of ischemic stroke via immune and inflammatory pathways: results from RNA sequencing and bioinformatics analysis
#> 128                                                                                                                                                   Lnc-SLC15A1-1 Up-regulates CXCL10/CXCL8 Expression in Endothelial Cells by Sponging MicroRNAs (RNA-Seq)
#> 129                                                                                                                                                                       Distinct hepatic gene expression patterns characterize progressive disease in NAFLD
#> 130                                                                                                                                           Transcriptome-wide N6-methyladenine profiling in low input multiplex samples by a kit-free multi-barcode method
#> 131                                                                                                                                                                      ENTPD3 Marks Mature Stem Cell Derived Beta Cells Formed by Self-Aggregation in Vitro
#> 132                                                                                                                                                        RNA-seq analysis for wild-type fibroblasts and patient fibroblasts bearing the m.3243A>G mutatioin
#> 133                                                                                            Progressive ER stress over time due to human insulin gene mutation contributes to pancreatic β-cell dysfunction, islet inflammation and compensatory responses
#> 134                                                                                                                                                                                            Altered Human Alveolar Bone Gene Expression in Type 2 Diabetes
#> 135                                                                                                                                           Impaired bone fracture healing in type 2 diabetes is caused by defective functions of skeletal progenitor cells
#> 136                                                                                                                                    Increased adipose tissue fibrogenesis, not impaired expandability, is associated with nonalcoholic fatty liver disease
#> 137                                                                                                                                                                                   Role of microRNA-143, -150 and 126 in pathological retinal angiogenesis
#> 138                                                                                                            10X genomics single cell GEX and VDJ 5' sequencing of PBMC from Type 1 Diabetes patients treated with Treg therapy alone or plus low dose IL-2
#> 139                                                                                                                         Early developmental alteration of neurite outgrowth occurs besides late-appearing neurodegenerative processes in Wolfram syndrome
#> 140                                                                                                                                                           Transcriptome analysis of human pancreatic preadipocytes and in vitro differentiated adipocytes
#> 141                                                                                                                     Novel diabetes gene discovery through comprehensive characterization and integrative analysis of longitudinal gene expression changes
#> 142                                                                                                                                                              Lipid droplets protect human β-cells from lipotoxic-induced stress and cell identity changes
#> 143                                                                                                                                                                          Acetylation State of Histone Core Defines Macrophage Dynamics in Diabetic Wounds
#> 144                                                                                                                                     Permutational immune analysis reveals architectural similarities between inflammaging, Down syndrome and autoimmunity
#> 145                                                                                                                                                       Combinatorial transcription factor profiles predict mature and functional human islet α and β cells
#> 146                                                                                                                                              Heme-Oxygenase 1 is a Master Regulator of Cell Fate Following Oxidative Stress Response in Endothelial Cells
#> 147                                                                           ATAC-seq and multi-omics analysis of human liver highlight a hepatocyte-specific enhancer for ACOT1 regulating the balance of acyl-CoA and free fatty acids in type 2 diabetes.
#> 148                                                                                                                             Microvessels support engraftment and functionality of human islets and hESC-derived pancreatic progenitors in diabetes models
#> 149                                                                                                             Epigenetic impairment and blunted transcriptional response to Mycobacterium tuberculosis of alveolar macrophages from persons living with HIV
#> 150                                                                                                   Epigenetic impairment and blunted transcriptional response to Mycobacterium tuberculosis of alveolar macrophages from persons living with HIV (RNA-Seq)
#> 151                                                                                                  Epigenetic impairment and blunted transcriptional response to Mycobacterium tuberculosis of alveolar macrophages from persons living with HIV (ATAC-Seq)
#> 152                                                                                                                                                                           Circulating circRNA signature in pregnancies with gestational diabetes mellitus
#> 153                                                                                                                      High-throughput mediation analysis of human proteome and metabolome identifies mediators of post-bariatric surgical diabetes control
#> 154                                                                                                      mRNA-seq read counts of peripheral blood mononuclear cells from congenital generalized lipodystrophy patients and their gender/aged-matched controls
#> 155                                                                                                                            Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle
#> 156                                                                                                               Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle [Affymetrix]
#> 157                                                                                                                  Disrupted Circadian Oscillations in Type 2 Diabetes are Linked to Altered Rhythmic Mitochondrial Metabolism in Skeletal Muscle [RNA-seq]
#> 158                                                                                                                                                       Identification of circulating miRNA molecular signature for erectile dysfunction in type 2 diabetes
#> 159                                                                                                                                                High resolution chromosome conformation capture from gene promoters at COVID-19, T1D, AS and RBC GWAS loci
#> 160                                                                                                                                          Angiogenin Released from ABCB5+ Stromal Precursors Improves Healing of Diabetic Wounds by Promoting Angiogenesis
#> 161                                                                                                                                                                   A Critical Role of Hepatic GABA in The Metabolic Dysfunction and Hyperphagia of Obesity
#> 162                                                                                                                                                                   Islet Sympathetic Innervation and Islet Neuropathology in Patients with Type 1 Diabetes
#> 163                                                                                                                                          Gene expression signatures for human non-diabetic (hND) islets and human type 2 diabetes mellitus (hT2DM) islets
#> 164                                                                                                                                      RNA-seq analysis with isolated human pancreatic islets treated with human breast cancer cell secreted Evs or control
#> 165                                                                                                                 Modelling HNF1B-associated monogenic diabetes using human iPSCs reveals an early stage impairment of the pancreatic developmental program
#> 166                                                                                                                                             TCF7L2 lncRNA: A Link between Bipolar Disorder and Body Mass Index through Glucocorticoid Signaling [RNA-Seq]
#> 167                                                                                                                                            TCF7L2 lncRNA: A Link between Bipolar Disorder and Body Mass Index through Glucocorticoid Signaling [ChIP-Seq]
#> 168                                                                                                                                                                       Serum miRNA profiling for early PDAC diagnosis and prognosis: a retrospective study
#> 169                                                                                                                                                                                                     Transcriptomic phenotyping of human labor myometrium.
#> 170                                                                                                                                                            RNA Sequencing of Blood in Coronary Artery Disease; Involvement of Regulatory T Cell Imbalance
#> 171                                                                                                                                         RNA Sequencing of Blood in Coronary Artery Disease; Involvement of Regulatory T Cell Imbalance [Discovery Cohort]
#> 172                                                                                                                                            Using single-nucleus RNA-sequencing to interrogate transcriptomic profiles of archived human pancreatic islets
#> 173                                                                                                                                           Effects of oral-glucose load on the gene expression of peripheral blood mono-nuclear cells in Asian-Indian men.
#> 174                                                                                                                   Genetic variants associated with development of colorectal cancer, type 1 diabetes, Hodgkin lymphoma and  Diffuse large B-cell lymphoma
#> 175                                                                                                                                                                            Self-Renewing Tri-Potent Stem/Progenitor-like Cells from Adult Human Pancreas 
#> 176                                                                                                Areca catechu-(Betel-nut)-induced whole transcriptome changes in a human monocyte cell line that may have relevance to diabetes and obesity; a pilot study
#> 177                                                                                                                                                                                            Generation of Human Islet Cell-Type-Specific Identity Genesets
#> 178                                                                                                                                                                 Identification of potential genomic alterations in primary and recurrent synovial sarcoma
#> 179                                                                                                                                                                  Transcriptome sequencing in serum exosomes from proliferative diabetic retinopathy (PDR)
#> 180                                                                                                                                   RECK isoforms are differentially expressed in patients with stable and unstable coronary artery disease: A pilot study.
#> 181                                                                                      Human and rat skeletal muscle single-nuclei multi-omic integrative analyses nominate causal cell types, regulatory elements, and SNPs for complex traits [snRNA-seq]
#> 182                                                                                     Human and rat skeletal muscle single-nuclei multi-omic integrative analyses nominate causal cell types, regulatory elements, and SNPs for complex traits [snATAC-seq]
#> 183                                                                                                                                                                          Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes
#> 184                                                                                                                                                              Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes [CHIRP-seq]
#> 185                                                                                                                                                                Profiling of CD14+ monocytes from humans with Type diabetes and without diabetes [RNA-Seq]
#> 186                                                                                                                                                                                  Genome wide methylation of cord blood from gestational diabetes mellitus
#> 187                                                                                                                                                                         Modeling pancreatic beta cell senescence by induction of DNA double-strand breaks
#> 188                                                                                                                                                                                                            RNA-seq of HUVECs stimulated with HG and oxLDL
#> 189                                                                                                                                                     Pancreatic Differentiation of stem cells reveals pathogenesis of a syndrome of Ketosis-Prone Diabetes
#> 190                                                                                                                                                                                      The effect of homocysteine on Human Aortic Endothelial Cells [miRNA]
#> 191                                                                                                                                                                                        The effect of homocysteine on Human Aortic Endothelial Cells [RNA]
#> 192                                                                                                                                                   Circulating exosomal miRNA signature in pregnancies with gestational diabetes mellitus across gestation
#> 193                                                                                                                            RNA Sequencing Facilitates Quantitative Analysis of Transcriptomes of adipose stem cells from diabetic, old and young patients
#> 194                                                                                                                          DNA methylation in skeletal muscle of patients with hypertension and diabetes undergoing coronary artery bypass grafting surgery
#> 195                                                                                                                                                                      Muscle transcriptomic profiling of chronological aging and metabolic syndrome in men
#> 196                                                                                                                                                                   Single cell RNA-sequencing reveals placenta cellular heterogeneity in adverse pregnancy
#> 197                                                                                                                                                                Nicotinamide mononucleotide increases muscle insulin sensitivity in women with prediabetes
#> 198                                                                                                                                                                                                    scRNA-seq analysis of SARS-CoV-2 infected human islets
#> 199                                                                                                                                                       In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy
#> 200                                                                                                                                            In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy (smallRNA)
#> 201                                                                                                                                            In-depth transcriptomic analyses investigating molecular mechanisms underlying diabetic retinopathy (totalRNA)
#> 202                                                                                                                                                                                         An inter-dependent network of enhancers regulates INK4a/ARF locus
#> 203                                                                                                                         Multi-omics profiling of living human pancreatic islet donors reveals heterogeneous beta cell trajectories toward type 2 diabetes
#> 204                                                                                                                                              Temporal evolution of cellular heterogeneity during the progression to advanced, AR-negative prostate cancer
#> 205                                                                                                             Obese Insulin Resistant Humans with Compensatory Hyperinsulinemia Dissociate Lipolysis from Glycemia as Possible Adaptive Response to Fatness
#> 206                                      The effects of a novel oral nutritional supplement as compared to standard care on body composition, physical function and skeletal muscle mRNA expression in Dutch older adults with (or at risk of) undernutrition
#> 207                                                                                                                                                 Neonatal diabetes mutations disrupt a chromatin pioneering function that activates the human insulin gene
#> 208                                                                                                   Single-cell transcriptomic resolution of human pancreatic islets reveals cellular states and intercellular interactions associated with type 1 diabetes
#> 209                                                                                                                                                              Identification of human glucocorticoid response markers using integrated multi-omic analysis
#> 210                                                                                                                                             Identification of human glucocorticoid response markers using integrated multi-omic analysis [Adipose Tissue]
#> 211                                                                                                                         Identification of human glucocorticoid response markers using integrated multi-omic analysis [Peripheral blood mononuclear cells]
#> 212                                                                                                                                                        Expression data from peripheral blood mononuclear cells(PBMCs) in newly diagnosed type 2 diabetes
#> 213                                                                                                                   Unravelling the Biological Functions of Type 1 Diabetes Associated Noncoding Single-Nucleotide Polymorphism in Human Pancreatic β Cells
#> 214                                                                                                                                      Glucocorticoid signaling in pancreatic islets modulates gene regulatory programs and genetic risk of type 2 diabetes
#> 215                                                                                                              Human Placental Exosomes in Gestational Diabetes Mellitus Carry a Specific Set of miRNAs Associated with Skeletal Muscle Insulin Sensitivity
#> 216                                                                                                                     Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors
#> 217                                                                                                                                                                               Interpreting type 1 diabetes risk with genetics and single cell epigenomics
#> 218                                                                               Transcriptional deregulation in subcutaneous adipose tissue from severely obese patients is associated with cancer: focus on gender differences and role of type 2 diabetes
#> 219                                                                                                                          ALTERED DUODENAL MUCOSAL MITOCHONDRIAL GENE EXPRESSION IS ASSOCIATED WITH DELAYED GASTRIC EMPTYING IN DIABETIC GASTROENTEROPATHY
#> 220                                                                                                              ALTERED DUODENAL MUCOSAL MITOCHONDRIAL GENE EXPRESSION IS ASSOCIATED WITH DELAYED GASTRIC EMPTYING IN DIABETIC GASTROENTEROPATHY [miRNA-Seq]
#> 221                                                                                                               ALTERED DUODENAL MUCOSAL MITOCHONDRIAL GENE EXPRESSION IS ASSOCIATED WITH DELAYED GASTRIC EMPTYING IN DIABETIC GASTROENTEROPATHY [mRNA-Seq]
#> 222                                                                                                                                              Population and single cell RNAseq analysis of CD4+ T cells in FOXP3 mutant mice ( scurfy") and IPEX patients
#> 223                                                                                                                                 Gene expression analysis of human mortal renal tubular epithelial cells chronically exposed to elevated levels of glucose
#> 224                                                                                                                                                                                         miRNA expression during BMSCs from human jaw in Type 2 diabetics.
#> 225                                                                                                                       Single-cell RNAseq (10x Genomics) analysis of human CD4+ T cells in IPEX patients, healthy donors and heterozygous mothers (blood).
#> 226                                                                                                                                                                  Impaired peripheral mononuclear cell metabolism in patients at risk of developing sepsis
#> 227                                                                                                                                                    A histological and transcriptional characterization of the pancreatic acinar tissue in type 1 diabetes
#> 228                                                                                                                                                                      Transcriptional analysis of islets of Langerhans from organ donors of different ages
#> 229                                                                                                                      Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes (RNA-Seq)
#> 230                                                                                                                     Analysis of the transcriptome and DNA methylome in response to acute and recurrent low glucose in human primary astrocytes (BeadChip)
#> 231                                                                                                                                        DNA methylation data throughout human muscle cell differentiation in individuals with type 2 diabetes and controls
#> 232                                                                                                                                                            DNA methylation data for human muscle cells from individuals with type 2 diabetes and controls
#> 233                                                                                                                                        mRNA expression data throughout human muscle cell differentiation in individuals with type 2 diabetes and controls
#> 234                                                                                                                                                            mRNA expression data for human muscle cells from individuals with type 2 diabetes and controls
#> 235                                                                                                           Integrative analysis of DNA methylation and gene expression data among preterm and/or small for gestational age infants during perinatal period
#> 236                                                                                             Integrative analysis of DNA methylation and gene expression data among preterm and/or small for gestational age infants during perinatal period [methylation]
#> 237                                                                                                                                                             Large-scale single-cell analysis reveals critical immune characteristics of COVID-19 patients
#> 238                                                                                                                                                                                   Urinary single cell profiling captures cellular diversity of the kidney
#> 239                                                                                                                                                                                                           SARS-CoV-2 infection of human pancreatic islets
#> 240                                                                                                                                             Transcriptomic characterization of the delayed wound healing response in a diabetic skin humanized mice model
#> 241                                                                                                                                                Exposure to Gestational Diabetes Mellitus In Utero Alters DNA Methylation in Placenta and Fetal Cord Blood
#> 242                                                                                                                                     Exposure to Gestational Diabetes Mellitus In Utero Alters DNA Methylation in Placenta and Fetal Cord Blood [Placenta]
#> 243                                                                                                                                        Exposure to Gestational Diabetes Mellitus In Utero Alters DNA Methylation in Placenta and Fetal Cord Blood  [Cord]
#> 244                                                                                                                                                      Pancreatic progenitor epigenome maps prioritize type 2 diabetes risk genes with roles in development
#> 245                                                                            Ayurvedic herbal preparation supplementation does not improve metabolic health in impaired glucose tolerance subjects; observations from a randomised placebo controlled trial
#> 246                                                                                                                 Single cell chromatin accessibility identifies pancreatic islet cell type- and state-specific regulatory programs of diabetes risk [Hi-C]
#> 247                                                                                                                        Single-cell chromatin accessibility identifies pancreatic islet cell type- and state-specific regulatory programs of diabetes risk
#> 248                                                                                                              Single-cell chromatin accessibility identifies pancreatic islet cell type- and state-specific regulatory programs of diabetes risk [RNA-seq]
#> 249                                                                                                           Single-cell chromatin accessibility identifies pancreatic islet cell type– and state-specific regulatory programs of diabetes risk [snATAC-seq]
#> 250                                                                                                    Type 2 Diabetes Mellitus is Associated with Transcriptome Alterations in Cortical Neurones and Associated Neurovascular Unit Cells in the Ageing Brain
#> 251                                                                                                                         Hyperglycemic memory of innate immune cells promotes in vitro proinflammatory responses of human monocytes and murine macrophages
#> 252                                                                                                                                        Expression profiles of human adipose tissue, adipocytes and stromal-vascular pellet cells from multiple body sites
#> 253                                                                                                                                                       miRNA sequencing profile of human plasma samples from healthy, diabetic, and gastroparesis patients
#> 254                                                                                                                                                                                                                 Pericardial fluid exosome miRNA profiling
#> 255                                                                                                                                                                                                         Long non-coding RNA screening for type 2 diabetes
#> 256                                                                                                                                                                      GLP-1 receptor signaling increases PCSK1 and beta-cell features in human alpha-cells
#> 257                                                                                                                       Distinct exhausted-like CD8 T cell populations are linked to C-peptide preservation in alefacept-treated, recent onset T1D subjects
#> 258                                                                                                                                                Identification of SRSF6 splicing regulatory map and its impact on diabetes susceptibility genes regulation
#> 259                                                                                                                                                                                Transcriptomic Signatures of Kidney Injury in Human Renal Biopsy Specimens
#> 260                                                                                                                                              The human aortic endothelium undergoes dose-dependent DNA methylation in response to transient hyperglycemia
#> 261                                                                                                                            Distinct exhausted CD8 T cell populations are linked to C-peptide preservation in alefacept-treated, recent onset T1D subjects
#> 262                                                                                                                                         Clinical, histopathologic and molecular features of idiopathic and diabetic nodular mesangial sclerosis in humans
#> 263                                                                                                                                                                                Array comparative genomic hybridization analysis of metastatic lung tumors
#> 264                                                                                                                                           Drug-drug interaction between metformin and sorafenib alters antitumor effect in hepatocellular carcinoma cells
#> 265                                                                                                  Estrogen-driven control of diabetogenic gene networks is associated with reduced levels of miR-224/452 circulating in extracellular vesicles [miRNA-Seq]
#> 266                                                                                                                                   The postprandial transcriptomic response of adipose tissue to high fat meals in middle-aged men with metabolic syndrome
#> 267                                                                                                                                                                                                      Human PBMCs: Healthy vs Diabetic nephropathy vs ESRD
#> 268                                                                                                                                                                              Multi-locus imprinting disturbances in a family harboring a ZFP57 truncation
#> 269                                                                                                                                                          Whole transcriptome sequencing of peripheral blood mononuclear cells from patients with COVID-19
#> 270                                                                                                                              Gene cascade analysis in human granulosa tumor cells (KGN) following exposure to high levels of free fatty acids and insulin
#> 271                                                                                                                                                                     Relationship between insulin sensitivity and gene expression in human skeletal muscle
#> 272                                                                                                                                                           Relationship between insulin sensitivity and gene expression in human skeletal muscle (Study B)
#> 273                                                                                                                                                           Relationship between insulin sensitivity and gene expression in human skeletal muscle (Study A)
#> 274                                                                                                                                                                     Identification of a human gut-derived LEAP2 fragment as a novel insulin secretagogue 
#> 275                                                                                                                                                                          RNA-seq of human dendritic cells cultured with PSAB-liposomes and/or Liraglutide
#> 276                                                                                                                                                                              Epigenome analysis of cord blood DNA from infants born into the UPBEAT study
#> 277                                                                                                                                Integrative omics analyses reveal epigenetic memory in diabetic cells regulating genes associated with kidney dysfunction.
#> 278                                                                                                                   Integrative omics analyses reveal epigenetic memory in diabetic cells regulating genes associated with kidney dysfunction. [sequencing]
#> 279                                                                                                                   Integrative omics analyses reveal epigenetic memory in diabetic cells regulating genes associated with kidney dysfunction. [microarray]
#> 280                                                                                                                                                                          Phospho-antibody microarray anayses for control and DG-LRG1 treated HUVEC cells.
#> 281                                                                                            Persistent or Transient Human β-cell Dysfunction Induced by Metabolic Stress Associated with Specific Signatures and Shared Gene Expression of Type 2 Diabetes
#> 282                                                                    Single-cell  analysis  of  adipose tissue  T cells in diabetic persons with HIV  reveals high proportions of clonally expanded CMV-like CD4+ T cells with cytotoxic RNA transcriptomes
#> 283                                                                                                                                                    Cell-free DNA Methylation and Transcriptomic Signature Prediction of Pregnancies with Adverse Outcomes
#> 284                                                                                                                                          Cell-free DNA Methylation and Transcriptomic Signature Prediction of Pregnancies with Adverse Outcomes [RNA-seq]
#> 285                                                                                                                                             Cell-free DNA Methylation and Transcriptomic Signature Prediction of Pregnancies with Adverse Outcomes [WGBS]
#> 286                                                                                                                Type 2 Diabetes reduces the enteroendocrine GLP-1 cell lineage in human obesity:  characterization in enriched human enteroendocrine cells
#> 287                                                                                                                                                                     A whole-genome CRISPRa screening metformin resistance related gene in prostate cancer
#> 288                                                                                                                                    A high glycemic burden drives functional and metabolic alterations of human monocytes in patients with type 1 diabetes
#> 289                                                                                                                                     Single cell transcriptomics of human islet ontogeny defines the molecular basis of beta cell dedifferentiation in T2D
#> 290                                                                                                                                                Single cell lineage analysis reveals cell fate determination events during directed β-cell differentiation
#> 291                                                                                                                                                                              RNAseq from human islets treated with brefeldin A as a model of Golgi stress
#> 292                                                                                                                                                                   Deregulated immune signature orchestrated by FOXM1 impairs human diabetic wound healing
#> 293                                                                                                                                                                                      Two distinct immunopathological profiles in lungs of lethal COVID-19
#> 294                                                                                                                               Baseline assessment of circulating microRNAs near diagnosis of type 1 diabetes predicts future stimulated insulin secretion
#> 295                                                                                                                      Liver-specific knockdown of class IIa HDACs has limited efficacy on glucose metabolism but entails severe organ side effects in mice
#> 296                                                                                                                                                                                                        Immune Gene Expression Profile of Tr1 Skewed Tregs
#> 297                                                                                             Transcriptomic analysis of peripheral blood mononuclear cells (PBMC) of patients with type 2 Diabetes Melittus(T2DM), Dyslipidemia (DL) and Periodontitis (P)
#> 298                                                                                                                                                                             Genomewide transcriptional analysis of growth hormone-treated human podocytes
#> 299                                                                                                                                                                 Differential effects of voclosporin and tacrolimus on insulin secretion from human islets
#> 300                                                                                                                                     Genome-Wide Profiling of DNA Methylation and Gene Expression Identifies Candidate Genes for Human Diabetic Neuropathy
#> 301                                                                                                                              Genome-Wide Profiling of DNA Methylation and Gene Expression Identifies Candidate Genes for Human Diabetic Neuropathy (RRBS)
#> 302                                                                                                                           Genome-Wide Profiling of DNA Methylation and Gene Expression Identifies Candidate Genes for Human Diabetic Neuropathy (RNA-Seq)
#> 303                                                                                                                                                              Comparison of Regulatory Type of Macrophages and PCMO Cells from perspective of RNAseq data.
#> 304                                                                                                                    Comparative transcriptome analysis of human skeletal muscle in response to cold acclimation and exercise training in human volunteers.
#> 305                                                                                                             Comparative transcriptome analysis of human skeletal muscle in response to cold acclimation and exercise training in human volunteers. [A391]
#> 306                                                                                                             Comparative transcriptome analysis of human skeletal muscle in response to cold acclimation and exercise training in human volunteers. [A294]
#> 307                                                                                                                                                      Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq human vascular)
#> 308                                                                                                                                                                       Stress-induced RNA–chromatin interactions promote endothelial dysfunction (RNA-seq)
#> 309                                                                                                                                                            Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI replicate 2)
#> 310                                                                                                                                                                                 Stress-induced RNA–chromatin interactions promote endothelial dysfunction
#> 311                                                                                                                                                                     Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq)
#> 312                                                                                                                                                                        Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI)
#> 313                                                                                                                                                                          Stress-induced RNA–chromatin interactions promote endothelial dysfunction (Hi-C)
#> 314                                                                                                                  Combined transcriptome and proteome profiling of the pancreatic β-cell response to palmitate unveils key pathways of β-cell lipotoxicity
#> 315                                                                                                                                                                                                                 Human pancreatic islets methylation array
#> 316                                                                                                                  Induced Expression of VEGFC, ANGPT, and EFNB2 and Their Receptors Characterizes Neovascularization in Proliferative Diabetic Retinopathy
#> 317                                                                                     DNA microarray analysis of blood before and after ingesting carotenoid-rich vegitable beverage for 8 weeks, a randomized and double-blinded controlled clinical trial
#> 318                                                                                                                                                                                                      Modeling human T-cell mediated beta cell destruction
#> 319                                                                                                                                                                                               The role of long noncoding RNAs during pancreas development
#> 320                                                                                                                                                             RNA-sequencing analysis of forearm skin in diabetic patients with or without foot ulcerations
#> 321                                                                                                                             Transcriptomic and Chromatin accessibility profiling of functional brown adipocytes derived from human pluripotent stem cells
#> 322                                                                                                                                The role of TCF7L2 rs290487 variant in hepatic glucose metabolism: an integrated analysis of clinical and multi-omics data
#> 323                                                                                               Increased long noncoding RNA maternally expressed gene 3 contributes to podocyte injury induced by high glucose through regulation of mitochondrial fission
#> 324                                                                                                                                   Identification of an Anti-diabetic, Orally Available Small Molecule that Regulates TXNIP Expression and Glucagon Action
#> 325                                                                                                                                                                                     Derivation and Characterization of a UCP1 Reporter Human ES Cell Line
#> 326                                                                                                                                                          A common genetic trait through multistep hepatocarcinogenesis in a case with chronic hepatitis C
#> 327                                                                                                             Circulating miRNAs as a predictive biomarkers of progression from prediabetes to diabetes: outcomes of 5-year prospective observational study
#> 328                                                                                                                                        Vitamin C supplementation reduces expression of circulating miR-451a in poorly controlled type 2 diabetes mellitus
#> 329                                                                                                                               Expression data from of FACS separated acinar and duct cell at day 4 of suspension cultured human pancreatic exocrine cells
#> 330                                                                                                                                                       Expression data from day of isolation and day 4 suspension cultured human pancreatic exocrine cells
#> 331                                                                                                                                                                   Immune dysfunction in intermediate hyperglycaemia and diabetes patients in tuberculosis
#> 332                                                                                                                                                          Whole-blood transcriptome profiling reveals signatures of metformin and its therapeutic response
#> 333                                                                                                                                                                        Transcriptional Profiling of Normal, Stenotic, and Regurgitant Human Aortic Valves
#> 334                                                                                                                                                                                   Identified differentially expressed lncRNAs in type 2 diabetes patients
#> 335                                                                                                                                                              Unique molecular signatures of microRNAs in ocular fluids and plasma in diabetic retinopathy
#> 336                                                                                                                                            Differenatiation of ceRNA (circRNA, lncRNA and mRNA) expression  in PBMCs (peripheral blood mononuclear cells)
#> 337                                                                                                                                                                       Differenatiation of miRNA expression  in PBMCs (peripheral blood mononuclear cells)
#> 338                                                                                                                                         Discovery of CD80 and CD86 as recent activation markers on regulatory T cells by protein-RNA single-cell analysis
#> 339                                                                                                         RIPK1 gene variants associate with increased obesity in humans and can be therapeutically silenced to improve metabolic dysfunction in obese mice
#> 340                                                                                                                                                                                            MicroRNA arrays for early diagnosis of diabetic kidney disease
#> 341                                                                                                                                                   Epithelial membrane protein 2 (EMP2) regulates hypoxia induced angiogenesis in retinal epithelial cells
#> 342                                                                                                                                                                Successful Preclinical Islet Transplantation in the Subcutaneous Space for Type 1 Diabetes
#> 343                                                                                                                                                               Transimmunom whole blood RNA-seq data  from type 1 diabetic patients and healthy volunteers
#> 344                                                                                                                      The PPAR agonist Rosiglitazone induces paracrine signaling in melanoma cells that activate stromal cells and enhances tumor growth.
#> 345                                                                                                                                                            Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes
#> 346                                                                                          Gene expression profiles of human retinal microvascular pericytes (HRMVPC) and human lipoaspirate derived mesenchymal stromal cells (adipose stromal cells, ASC)
#> 347                                                                                                                                                        DNA methylation analysis of human peripheral blood mononuclear cell collected in the AIRWAVE study
#> 348                                                                                                                                                                               The omentum of obese girls harbors small adipocytes and browning transcrips
#> 349                                                                                                                                                                 Patient iPSCs identify vascular smooth muscle AADAC as protective against atherosclerosis
#> 350                                                                                                               Next generation sequencing identifies differentially expressed genes between breast cancer with diabetes and breast cancer without diabetes
#> 351                                                                                                                                                                                                                 Gestational diabetes and human amniocytes
#> 352                                                                                                                                                                         Transcriptomic changes in response to modulation of long-non-coding RNA LINC00473
#> 353                                                                                                                                            Single Cell Sequencing Analysis for Wolfram Syndrome (WS4) Unedited and Corrected Stem Cell-Derived Beta Cells
#> 354                                                                                                                                                                        Transcriptomic changes in response to modulation of long-non-coding RNA, LINC00473
#> 355                                                                                                                   An Exome-Wide Association Study Identifies New Susceptibility Loci for the Risk of Nicotine Dependence in European-American Populations
#> 356                                                                                                                 An integrated multi-omics approach identifies the landscape of interferon-a-mediated responses of human pancreatic beta cells [RNA-seq 2]
#> 357                                                                                                                  An integrated multi-omics approach identifies the landscape of interferon-a-mediated responses of human pancreatic beta cells [ATAC-seq]
#> 358                                                                                                                   An integrated multi-omics approach identifies the landscape of interferon-a-mediated responses of human pancreatic beta cells [RNA-seq]
#> 359                                                                                                                         Inhibition of Grb14, a negative modulator of insulin signaling,  improves glucose homeostasis without causing cardiac dysfunction
#> 360                                                                                                                    An Exome-Wide Association Study Identifies New Susceptibility Loci for the Risk of Nicotine Dependence in African-American Populations
#> 361                                                                                                                                           Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes
#> 362                                                                                                                              Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes (scATAC-seq)
#> 363                                                                                                                                    Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes (WGBS)
#> 364                                                                                                                          VEGF-B Signaling Impairs Endothelial Glucose Transcytosis via an LDLR-dependent Decrease in Membrane Cholesterol Loading [HBMEC]
#> 365                                                                                                              A long noncoding RNA, LOC157273, is the effector transcript at the chromosome 8p23.1-PPP1R3B metabolic traits and type 2 diabetes risk locus
#> 366                                                                                                                                                                                  Analysis of association between LPHN3 markers and substance use disorder
#> 367                                                                                                                          BET bromodomain containing epigenetic reader proteins regulate vascular smooth muscle cell proliferation and neointima formation
#> 368                                                                                                                                                Skeletal muscle enhancer interactions identify genes controlling whole body metabolism in humans [RNA-seq]
#> 369                                                                                                                                               Skeletal muscle enhancer interactions identify genes controlling whole body metabolism in humans [cHiC-seq]
#> 370                                                                                                                                               Skeletal muscle enhancer interactions identify genes controlling whole body metabolism in humans [ChIP-seq]
#> 371                                                                                                                                                    Single Cell RNA sequencing of MAFB +/+ and -/- cells at the pancreatic progenitor and beta-like stages
#> 372                                                                                                                                Differential DNA methylation encodes proliferation and senescence programs in human adipose-derived mesenchymal stem cells
#> 373                                                                                                                                                                                        A method for the generation of human stem cell-derived alpha cells
#> 374                                                                                                                                                                  Mendelian randomization identifies FLCN expression as a mediator of diabetic retinopathy
#> 375                                                                                                                                                                                          Longitudinal DNA methylation differences precede type 1 diabetes
#> 376                                                                                                                                      Interfering with DNA replication improves beta cell differentiation and maturation from human pluripotent stem cells
#> 377                                                                                                                                                                                 Transcriptional responses to TNF-alpha in germline A20 haploinsufficiency
#> 378                                                                                                                                                     Pancreas single cell patch-seq links physiologic dysfunction in diabetes to transcriptomic phenotypes
#> 379                                                                                                                                                                                            Molecular characterization of clonal human renal forming cells
#> 380                                                                                                     Sexually dimorphic methylation of CD3+ T-lymphocyte DNA in offspring of overweight and obese mothers in a high risk, minority population in the Bronx
#> 381                                                                                                                           Whole genome bisulfite sequencing of human spermatozoa reveals differentially methylated patterns from type 2 diabetic patients
#> 382                                                                                                                                                                            A composite immune signature parallels disease progression across T1D subjects
#> 383                                                                                                                                                      A composite immune signature parallels disease progression across T1D subjects (RNA-Seq Cohort 0 WB)
#> 384                                                                                                                                                    5-Hydroxymethylcytosines in Circulating Cell-free DNA Reveal Vascular Complications of Type 2 Diabetes
#> 385                                                                                                                                                                Genome Wide Analysis of Gene Expression Changes in Skin from Patients with Type 2 Diabetes
#> 386                                                                 Whole genome transcriptomics of pre-access veins and hemodialysis arteriovenous fistula (AVF) samples from two-stage AVF patients with different maturation outcomes (matured vs. failed)
#> 387                                                                                                                                                  Angiogenin derived from ABCB5+ mesenchymal stem cells improves diabetic wound via enhancing angiogenesis
#> 388                                                                                                     Vascular Progenitors Generated from Tankyrase Inhibitor-Regulated Naive Diabetic Human iPSC Potentiate Efficient Revascularization of Ischemic Retina
#> 389                                                                                                     In vivo hyperglycemia exposure elicits distinct period-dependent effects on human pancreatic progenitor differentiation, conveyed by oxidative stress
#> 390                                                                                                                                                                    Skeletal muscle regeneration is compromised in advanced diabetic peripheral neuropathy
#> 391                                                                                                                                                                               Adipocyte serine uptake curbs ROS generation and visceral adiposity [Human]
#> 392                                                                                                                                                                                                  Knockdown PTPRN expression inhibits U87 cell line growth
#> 393                                                                                                                                              Neutrophil extracellular trap induced dendritic cell activation leads to Th1 polarization in type 1 diabetes
#> 394                                                                                                                                               Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]
#> 395                                                                                                                               DNA methylation profiles in Taiwanese patients of Type-2 Diabetes (T2D) associated to Nephropathy (DN) and Retinopathy (DR)
#> 396                                                                                                                                                                                                                                       Fat_challenge_tests
#> 397                                                                                                                                                                         Profiling of RNAs from human islet-derived exosomes in a model of type 1 diabetes
#> 398                                                                                     Loss of ER and nuclear envelope-associated neutral sphingomyelinase SMPD4 causes a severe neurodevelopmental disorder with microcephaly and congenital arthrogryposis
#> 399                                                                                                                                                                                          bulk RNA-seq of human nucleusus pulposus from scoliosis patients
#> 400                                                                                                                                                                                  Identified  differentially expressed lncRNAs in Type 1 Diabetes Patients
#> 401                                                                                                                                                        bulk RNA-seq of human nucleusus pulposus cell differentiations from embryonic stem cells and iPSCs
#> 402                                                                                                  Transient PAX8 Expression in Islets During Pregnancy Correlates With β-Cell Survival, Revealing a Novel Candidate Gene in Gestational Diabetes Mellitus.
#> 403                                                                                                                                                                CD31 positive-extracellular vesicles from patients with type 2 diabetes: a miRNA signature
#> 404                                                                                                                   Transcriptome analysis-identified long noncoding RNA CRNDE in maintaining endothelial cell proliferation, migration, and tube formation
#> 405                                                                                                                                                                       A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.
#> 406                                                                         A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism: Liver RNA profiles of lean non-diabetic, obese non-diabetic as well as obese diabetic humans.
#> 407                                                                                                          Comparison of Kidney Transcriptomic Profiles of Early and Advanced Diabetic Nephropathy Reveals Potential New Mechanisms for Disease Progression
#> 408                                                                                                                                                                          Expression data for patients with myocardial infarction (MI) vs healthy patients
#> 409                                                                                     Transcriptome analysis between primary and iPS-derived monocytes and macrophages and comparison of iPS-derived macrophages between CCR5 patients and healthy controls
#> 410                                                                                                                                              Transcriptome signatures reveal candidate key genes in the whole blood of patients with lumbar disc prolapse
#> 411                                                                                                                                        Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity
#> 412                                                                                                                                            Urinary sediment transcriptomic and longitudinal data to investigate renal function decline in type 1 diabetes
#> 413                                                                                                                    Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [Islet ATAC-Seq]
#> 414                                                                                                                     Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [Islet RNA-Seq]
#> 415                                                                                                                                                      miRNA142-3p targets Tet2 and impairs Treg differentiation and stability in models of type 1 diabetes
#> 416                                                                                                                                                      miRNA142-3p targets Tet2 and impairs Treg differentiation and stability in models of type 1 diabetes
#> 417                                                                                           Combined use of astragalus polysaccharide and berberine attenuates insulin resistance in IR-HepG2 cells via regulation of the gluconeogenesis signaling pathway
#> 418                                                                                                                       Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [RNA-Seq III]
#> 419                                                                                                                                                      miRNA142-3p targets Tet2 and impairs Treg differentiation and stability in models of type 1 diabetes
#> 420                                                                                                                          Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [ATAC-seq]
#> 421                                                                                                                        Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [H1 RNA-seq]
#> 422                                                                                                                     Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [small RNA-seq]
#> 423                                                                                                                                                                                                                     6mer seed toxicity in viral microRNAs
#> 424                                                                                                                                                                Transcriptome profiling of subcutaneous and visceral adipose tissue from obese individuals
#> 425                                                                                                                                                   Single Cell RNASeq profiling of stromal vascular fraction from Subcutaneous and visceral adipose tissue
#> 426                                                                                 Multi-Parameter Analysis of Biobanked Human Bone Marrow Stromal Cells Shows Little Influence for Donor Age and Mild Comorbidities on Phenotypic and Functional Properties
#> 427                                                                                                                                                     Signaling protein antibody microarray analyses for islets of control and IFT88 knockout mice [SET100]
#> 428                                                                                                                                                               Phospho-antibody microarray analyses for islets of control and IFT88 knockout mice [PEX100]
#> 429                                                                                                                                                                                      Human Islet Response to Selected Type 1 Diabetes Associated Bacteria
#> 430                                                                                                                                                                            Edematous Severe Acute Malnutrition is Characterized by Hypomethylation of DNA
#> 431                                                                                                                                                      Cellular recruitment by podocyte-derived pro-migratory factors in assembly of the human renal filter
#> 432                                                                                                                                                                   Circular RNA expression profiling in diabetic foot ulcers and human normal acute wounds
#> 433                                                                                                                                                       A global transcriptome analysis of human epidermal keratinocytes upon knockdown of hsa_circ_0084443
#> 434                                                                                                                                                                                         Large-scale gene expression profiling  of hepatocellular adenomas
#> 435                                                                                                                                                                Placental Accreta Spectrum: Upregulated Cytotrophoblast DOCK4 Contributes to Over Invasion
#> 436                                                    Genome-wide analysis of hepatic gene expression in patients with non-alcoholic steatohepatitis (NASH) before and after 1 year supplementation with n-3 polyunsaturated fatty acids (PUFA) from fishoil
#> 437                                                                                                                                                                           Effect of high glucose on transcriptomic expression of cholangiocarcinoma cells
#> 438                                                                                                                                                Comparative Analysis of the Transcriptome of Latent Autoimmune Diabetes (LADA) Patients from Eastern China
#> 439                                                                                                                        The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes
#> 440                                                                                                                The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [UMI-4C]
#> 441                                                                                                      The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [H3K27ac ChIP-seq]
#> 442                                                                                                              The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [ATAC-seq]
#> 443                                                        Differential messenger RNA expression in Granulosa Cells from polycystic ovary syndrome with Normoandrogen and Hyperandrogen: Identification of gene sets through bioinformatic Filtering analysis
#> 444                                                                                                                                           Proteomics in gastroparesis: Unique and overlapping protein signatures in diabetic and idiopathic gastroparesis
#> 445                                                                                                                                                                Metformin-induced alterations in peripheral blood cell trancriptome of healthy individuals
#> 446                                                                                                                                                                              The Single Cell Transcriptomic Landscape of Early Human Diabetic Nephropathy
#> 447                                                                                                                                   Systematic assessment of blood-borne microRNAs highlights molecular profiles of endurance sport and carbohydrate uptake
#> 448                                                                                                                                                  Single-cell sequencing reveals the relationship between phenotypes and genotypes of Klinefelter syndrome
#> 449                                                                                                                                                                                     Hyperglycemia promotes an aggressive phenotype in breast cancer cells
#> 450                                                                                                                                               Environmental Factors Influence the Epigenetic Signature of Newborns from Mothers with Gestational Diabetes
#> 451                                                                                                                                                  miRNA-27b-3p and miRNA-1228-3p correlate with the progression of Kidney Fibrosis in Diabetic Nephropathy
#> 452                                                                                                                                                                                                                           SC-beta Cell in vivo Maturation
#> 453                                                                                                                                                                                                                            RNA sequencing human monocytes
#> 454                                                                                                                                                  N6-methyladenosine (m6A) profiling of EndoC-bH1 cell line and RNA seq of Mettl14 knockout mice beta cell
#> 455                                                                                                                                                                    Phospho-antibody microarray analyses for islets of control and  Mettl14 knock-out mice
#> 456                                                                                                                                                                                             N6-methyladenosine (m6A) profiling of type II diabetes islets
#> 457                                                                                                                                                      Hyperglycemia acts in synergy with hypoxia to maintain the pro-inflammatory phenotype of macrophages
#> 458                                                                                                      Transcriptome as marker for nutrition-related health: added value of time course analyses during challenge tests before and after energy restriction
#> 459                                                                                                                   A transcriptomic analysis of primary mature adipocytes from lean, obese, and type 2 diabetic subjects: role of the extracellular matrix
#> 460                                                                                                                                                 Point mutations in the PDX1 transactivation domain impair human β-cell development and function (RNA-Seq)
#> 461                                                                                                                                                Point mutations in the PDX1 transactivation domain impair human β-cell development and function (ChIP-Seq)
#> 462                                                                                                                                         Point mutations in the PDX1 transactivation domain impair human β-cell development and function (mRNA microarray)
#> 463                                                                                                                                 Metformin alters human host responses to Mycobacterium tuberculosis in-vitro and in healthy human subjects [PBMC RNA-Seq]
#> 464                                                                                                                        Metformin alters human host responses to Mycobacterium tuberculosis in-vitro and in healthy human subjects [Ex vivo Blood RNA-Seq]
#> 465                                                                                                                                                                      scRNA-seq analysis of the dual expressors, B cells and T cells of a diabetes patient
#> 466                                                                                                                                           A single-nucleus RNA-sequencing pipeline to decipher the molecular anatomy and pathophysiology of human kidneys
#> 467                                                                                   Phenotypic cooperation of a KCNQ2 exon 7 partial duplication and compound copy number variations in genes associated to a severe epileptic and neurodevelopmental delay
#> 468                                                                                                                                                                                                            Liver transcriptome of statin-treated patients
#> 469                                                                                                                                                                                 Charting in vitro beta cell differentiation by single cell RNA sequencing
#> 470                                                                                                                                                              Identification of metabolically distinct adipocyte progenitor cells in human adipose tissues
#> 471                                                                                                                                                           Association of cord blood methylation with neonatal leptin: an epigenome wide association study
#> 472                                                                                                                                                                                                                                  MAIT cell RNA sequencing
#> 473                                                                                                                                                                                                         Host response to IAV infections in human patients
#> 474                                                                                                                                                                                RNA sequence data in whole cell extracts of differentiated human podocytes
#> 475                                                                                                                       HNF1A deficiency impairs β-cell fate, granule maturation and function (scRNA-seq of 309 hESC-derived cells: Differentiation day 25)
#> 476                                                                                                                                                 Acute Effects of Single Doses of Bonito Fish Peptides and Vitamin D on Whole Blood Gene Expression Levels
#> 477                                                                                                                                                                Quantitative variation in m.3243A>G mutation produce discrete changes in energy metabolism
#> 478                                                                                                                                                                                                                       ATAC-seq on human pancreatic islets
#> 479                                                                                                                                       Culture of mature adipocytes under a permeable membrane and comparative analysis with different cell culture models
#> 480                                                                                                                                                           Plasma circulating extracellular RNAs in left ventricular remodeling post-myocardial infarction
#> 481                                                                                                                                                                          Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes
#> 482                                                                                                                                                                Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [RNA-seq]
#> 483                                                                                                                                                               Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [ChIP-seq]
#> 484                                                                                                                           A co-expression analysis of the placental transcriptome in association with maternal pre-pregnancy BMI and newborn birth weight
#> 485                                                                                                                                                                                     HNF1A deficiency impairs β-cell fate, granule maturation and function
#> 486                                                                                                                                                     Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes
#> 487                                                                                                                                           Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes [RNA-seq]
#> 488                                                                                                                                 Epigenetic modulation of β-cells by interferon-α via PNPT11-miR-26a-TET2 triggers autoimmune diabetes [methylation array]
#> 489                                                                                                                                                                                 Serological autoantibody profiling of type 1 diabetes  by protein arrays.
#> 490                                                                                                                                                                                                                         ChIA-PET from MSiPS (ENCSR778FXH)
#> 491                                                                                                                                                                                                                    ChIA-PET from fibroblast (ENCSR732QOH)
#> 492                                                                                                                                                                                                                         ChIA-PET from MSLCL (ENCSR452NHL)
#> 493                                                                                                                                                       Cell type-specific immune phenotypes predict loss of insulin secretion in new-onset type 1 diabetes
#> 494                                                                                                                                                                      B lymphocyte alterations accompany abatacept resistance in new-onset type 1 diabetes
#> 495                                                                                                                                                                            Transcriptomic Profiling of Trophoblast Fusion Using BeWo and JEG-3 Cell Lines
#> 496                                                                                                              Integrated analysis of genetic variants regulating retinal transcriptome (GREx) identifies genes underlying age-related macular degeneration
#> 497                                                                                                                                                                                       Preeclamptic placentae release factors that damage neurons in vitro
#> 498                                                                                                                                          Short-term low calorie diet remodels skeletal muscle lipid profile and metabolic gene expression in obese adults
#> 499                                                                                                                                                                        Metformin reverses gene expression signautres in hyperglycaemics endothelial cells
#> 500                                                                                                    DNA Hypermethylation at Loci Associated with Diabetes, Obesity and Cardiac Abnormalities in CD3+ Lymphocytes of Intrauterine Growth Restricted Newbors
#> 501                                                                                                                                                    The diurnal rhythm of adipose tissue gene expression is reduced in obese patients with type 2 diabetes
#> 502                                                                                                                                                           Transcriptomics analysis of Colon tumor xenograft model in streptozotocin-induced diabetic mice
#> 503                                                                                                                      Transcriptomics analysis of paired tumor and normal mucosa samples in a cohort of patients with colon cancer, with and without T2DM.
#> 504                                                                                                                                           Patient adipose stem cell-derived adipocytes reveal genetic variation that predicts anti-diabetic drug response
#> 505                                                                                                                                  Circulating Exosomal miR-20b-5p is Elevated in Type 2 Diabetes and Could Impair Insulin Action in Human Skeletal Muscle.
#> 506                                                                                                                                            EndoC-βH1 multiomic profiling defines gene regulatory programs intrinsic to human β cell identity and function
#> 507                                                                                                                                                  Genome-Wide Analyses Identify Filamin-A (FLNA) as a Novel Downstream Target for Insulin and IGF1 Action.
#> 508                                                                                                               miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)
#> 509                                                                                                                                           Identification of molecular signatures of cystic fibrosis disease status using plasma-based functional genomics
#> 510                                                   High-resolution map of copy number variations in motor cortex of Control and Sporadic Amyotrphic Lateral Sclerosis patients by using a customized exon-centric comparative genomic hybridization array.
#> 511                  Genome–wide gene expression profile of adipocytes and infiltration macrophages obtained from abdominal (visceral and subcutaneous) and peripheral (thigh) adipose depots from Normal Glucose Tolerant and Type 2 Diabetics Asian Indians
#> 512                                                                                                                                                                          Affymetrix microarray analysis of the effects of isonicotinamide on HEK293 cells
#> 513                                                                                                                                                                             Affymetrix microarray analysis of the effects of nicotinamide on HEK293 cells
#> 514                                                                                                                                Primate fetal hepatic response to maternal obesity: epigenetic signaling pathways and lipid accumulation [gene expression]
#> 515                                                                                                                                                                                                         ENPP6 as a neural regulator of visceral adiposity
#> 516                                                                                                                                                                      Single cell transcriptome profiling of mouse and hESC-derived pancreatic progenitors
#> 517                                                                                                                                                                           Diabetes Remission Using Glucose-Responsive Insulin-Producing Human alpha-Cells
#> 518                                                                                                                                                                                                      Expression analysis of λH1-hESC derived β-like cells
#> 519                                                                                                                                                                               Diabetes Remission Using Glucose-Responsive Insulin-Producing Human α-Cells
#> 520                                                                                                                                             Therapeutic potential of targeting miR-141 in intervertebral disc degeneration: first steps toward the clinic
#> 521                                                                                                                      Elevated T cell levels in peripheral blood predict poor clinical response following rituximab treatment in new-onset type 1 diabetes
#> 522                                                                                                                             Effects of Cadmium Exposure on DNA Methylation at Imprinting Control Regions and Genome-Wide in Mothers and Newborn Children.
#> 523                                                                                                        Single-cell RNA sequencing enables transcriptomic analysis of iPSC-derived beta-cells in a model of neonatal diabetes caused by insulin mutations.
#> 524                                                                                                                                         Integrative molecular and clinical analysis of intrahepatic cholangiocarcinoma reveals two prognostic subclassees
#> 525                                                                                                                                                Abnormal neutrophil signature in the blood and pancreas of pre-symptomatic and symptomatic type 1 diabetes
#> 526                                                                                                                                           Pan-senescence transcriptome analysis identified RRAD as a marker and negative regulator of cellular senescence
#> 527                                                                                                                                                                             Profiling of vascular organoid endothelial cells and pericytes from iPS cells
#> 528                                                                                                   Stable oxidative cytosine modifications accumulate in cardiac mesenchymal cells from Type2 diabetes patients: rescue by alpha-ketoglutarate and TET-TDG
#> 529                                                     Stable oxidative cytosine modifications accumulate in cardiac mesenchymal cells from Type2 diabetes patients: rescue by alpha-ketoglutarate and TET-TDG functional reactivation [human cells RNA-seq]
#> 530                                                                                                                                 Diabetes Mellitus Drives Extracellular Vesicle Secretion and Promotes Increased Internalization by Circulating Leukocytes
#> 531                                                                                                         Specific targeting of the common gamma chain blocks cooperative reprogramming of human tissue-resident cytotoxic T lymphocytes by IL-15 and IL-21
#> 532                                                                                                                                                Human Pancreatic Islets Expressing HNF1A Variant Have Defective β cell Transcriptional Regulatory Networks
#> 533                                                                                                                                           High-throughput single cell transcriptome analysis and CRISPR screen identify key β cell-specific disease genes
#> 534                                                                                                                                                                NTPDase3 antibody targets adult human pancreatic β-cells for in vitro and in vivo analysis
#> 535                                                                                                                                                                     Identification of early biological changes in palmitate-treated isolated human islets
#> 536                                                                                                                                                           Gene array of laser capture microdissectioned human diabetic vs non-diabetic plaque macrophages
#> 537                                                                                                                               Circadian misalignment induces fatty acid metabolism gene profiles and induces insulin resistance in human skeletal muscle.
#> 538                                                                                                                                                          JCAD/KIAA1462, a coronary artery disease-associated gene product, regulates endothelial function
#> 539                                                                              Conventional and neo-antigenic peptides naturally processed and presented by beta cells are targeted by circulating naïve CD8+ T cells in type 1 diabetic and healthy donors
#> 540                                                                                     Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function
#> 541                                                                             Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function Changes
#> 542                                                                                                                                                                                        Endothelial cells derived from iPSC in response to diabetic medium
#> 543                                                                                                                                                                                                   Exon Level Expression Profiling of Diabetic Nephropathy
#> 544                                                                                                                               Functional Genomics Analysis of Islets from Recent and Longstanding T1D Reveals the Need for Distinct Approaches to Therapy
#> 545                                                              Innate immune activity differentiate subtypes in new onset Type 1 diabetes that predict duration of the post-onset partial remission and correlate with responsiveness to CTLA4-Ig treatment
#> 546                                                                                                                                                      A new axis linking diabetes to cancer: Glucose regulates tumor suppressor TET2 and 5hmC through AMPK
#> 547                                                                                                                                                            Expression data of A2058-TET2WT, A2058-TET2M, and Mock cells treated under high-g and normal-g
#> 548                                                                                                                                                                                         Dysregulated circRNAs in plasma from active tuberculosis patients
#> 549                                                                                                                                      Fine-mapping and functional studies highlight potential causal variants for rheumatoid arthritis and type 1 diabetes
#> 550                                                                                                                                                                                                  RNA Expression data for early diabetic nephropathy (EDN)
#> 551                                                                                                                                                                      Discovering human diabetes-risk gene function with genetics and physiological assays
#> 552                                                                                                                              Propargite, an environmental chemical, interacts with GWAS identified diabetes genes to impact human pancreatic β-cell death
#> 553                                                                                                             Propargite, an environmental chemical, interacts with GWAS identified diabetes genes to impact human pancreatic β-cell death [PTPN2 knockout]
#> 554                                                                                                       Propargite, an environmental chemical, interacts with GWAS identified diabetes genes to impact human pancreatic β-cell death [propargite treatment]
#> 555                                                                                                                                                                    CRISPR/Cas9-targeted removal of unwanted sequences from small-RNA sequencing libraries
#> 556                                                                                                                                                                 Association of Elevated Urinary miR-126, miR-155 and miR-29b with Diabetic Kidney Disease
#> 557                                                                                                                                                                                                                    Expression data from childhood obesity
#> 558                                                                                                                                              Integrated transcriptomics network analysis of miRNA and mRNA in human myometrium in term and preterm labor.
#> 559                                                                                                                                                                                      Effect of TDNC1 ectopic expression on global gene expression pattern
#> 560                                                                                                                                                        A global transcriptome analysis of human epidermal keratinocytes upon inhibition of lncRNA WAKMAR1
#> 561                                                                                                                                                                                               Discovery of a Drug Candidate for GLIS3-Associated Diabetes
#> 562                                                                                                                                                                                                                        The role of CFTR in islet function
#> 563                                                                       Pure epicatechin and inflammatory gene expression profiles in circulating immune cells in (pre) hypertensive adults; a randomized double-blind, placebo-controlled, crossover trial
#> 564                                                                                                                                                             Differential metabolic effects of insulin detemir versus NPH in patients with type 2 diabetes
#> 565                                                                                                                                                      Effect of rosiglitazone treatment on insulin sensitivity in type 2 diabetic patients skeletal muscle
#> 566                                                                                                                                                     De novo reconstruction of human adipose reveals conserved lncRNAs as regulators of brown adipogenesis
#> 567                                                                                                                                                         Altered adipose lipid mobilization predicts long-term weight gain and impaired glucose metabolism
#> 568                                                                                                                                                       Bioinformatics analysis of microRNAs related to blood stasis syndrome in diabetes mellitus patients
#> 569                                                                                                                                                   Bioinformatics analysis of transcriptome related to blood stasis syndrome in diabetes mellitus patients
#> 570                                                                                                     GABA regulates release of inflammatory cytokines from peripheral blood mononuclear cells and CD4+ T cells and is immunosuppressive in type 1 diabetes
#> 571                                                                                                                                Placental methylation arrays for the assessment of epigenetic regulation in transcriptional subtypes of human preeclampsia
#> 572                                                                                                                                                          Genome-wide analysis of PDX1 target genes in human pancreatic progenitors [expression profiling]
#> 573                                                                                                                                                         Transcriptomes of iPSC-derived and post-mortum Hypothalamus Neurons from obese and control donors
#> 574                                                                                                       The lipodystrophic hotspot lamin A p.R482W mutation deregulates the mesodermal inducer T/Brachyury and early vascular differentiation gene networks
#> 575                                                                                                                                                                                                     Unique Circulating MicroRNA profiles in HIV Infection
#> 576                                                                                                                                  Heart failure patients' peripheral blood mononuclear cell gene expression profiles before mechanical circulatory support
#> 577                                                                                                                                                        A SRp55-regulated alternative splicing network controls pancreatic beta cell survival and function
#> 578                                                                                                                                                                                                  Expression data from SOX9 overexpressing EndoC-ßH1 cells
#> 579                                                                                                                                                                                                       Expression data from PolyIC treated EndoC-ßH1 cells
#> 580                                                                                                                                                                                              Expression profiling of circular RNAs in human islet samples
#> 581                                                                                                                           FABP4 overexpressed in intratumoral hepatic stellate cells within hepatocellular carcinoma with metabolic risk factors (part 2)
#> 582                                                                                                                           FABP4 overexpressed in intratumoral hepatic stellate cells within hepatocellular carcinoma with metabolic risk factors (part 1)
#> 583                                                                                                                                                Tubulointerstitial transcriptome from ERCB subjects with chronic kidney disease and living donor biopsies.
#> 584                                                                                                                                                                         Glomerular Transcriptome from European Renal cDNA Bank subjects and living donors
#> 585                                                                                                                                                                                  Transcription factors operate across disease loci: EBNA2 in autoimmunity
#> 586                                                                                                                                                                 Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy
#> 587                                                                                                                                                         Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression
#> 588                                                                                                                                                                                                      Dermal endothelial cells of type 2 diabetic patients
#> 589                                                                                                                                   RNA sequencing data of whole blood cells of normal glucose tolerant (NGT) and gestational diabetes (GDM) pregnant women
#> 590                                                                                  Genomic Profiling of Diabetic Foot Ulcers Identifies miR-15b-5p as a Major Regulator that Leads to Suboptimal Inflammatory Response and Diminished DNA Repair Mechanisms
#> 591                                                                                                                                                                                    α Cell Function and Gene Expression Are Compromised in Type 1 Diabetes
#> 592                                                                                                                                                 Affymetrix profiling of IMIDIA biobank samples from organ donors and partially pancreatectomized patients
#> 593                                                                                                    Affymetrix profiling of IMIDIA biobank samples from organ donors and partially pancreatectomized patients [partially pancreatectomized patient cohort]
#> 594                                                                                                                            Affymetrix profiling of IMIDIA biobank samples from organ donors and partially pancreatectomized patients [organ donor cohort]
#> 595                                                                                                                                                                   HDAC inhibitor SAHA reverses inflammatory gene expression in diabetic endothelial cells
#> 596                                                                                                                                                                                          RNA-seq in neutrophils from patients with intracranial aneurysms
#> 597                                                                                                                                                                                       Glucose inhibits cardiac maturation through nucleotide biosynthesis
#> 598                                                                                                                    Altered intestinal functions and increased local inflammation in insulin-resistant obese subjects: a gene-expression profile analysis.
#> 599                                                                                                                                              Clinical Evidence Supports a Protective Role for CXCL5 in Coronary Artery Disease Progression in the Elderly
#> 600                                                                                                                           Gene expression data from Phase 2 of the SAMARA study (Supporting a Multi-disciplinary Approach to Researching Atherosclerosis)
#> 601                                                                                                                                Genotyping data from Phase 2 of the SAMARA study (Supporting a Multi-disciplinary Approach to Researching Atherosclerosis)
#> 602                                                                                                                                           Small RNA-seq analysis of circulating miRNAs to identify phenotypic variability in Friedreich's ataxia patients
#> 603                                                                                                                           Single cell transcriptome analysis of human pancreas reveals transcriptional signatures of aging and somatic mutation patterns.
#> 604                                                                                                                                                                                Real-time quantitative PCR analysis of 232 microRNAs in human oral tissues
#> 605                                                                                                                                      Small RNA-seq during acute maximal exercise reveal RNAs involved in vascular inflammation and cardiometabolic health
#> 606                                                                                                                                              Discovery and validation of a gene expression profile for human islet integrity and transplant functionality
#> 607                                                                                                                            DNA methylation in blood from neonatal screening cards and the association with BMI and insulin sensitivity in early childhood
#> 608                                                                                                                                            Plasma-derived exosome characterization reveals a distinct microRNA signature in long duration Type 1 diabetes
#> 609                                                                                                                                                         Preclinical evaluation of the BET bromodomain inhibitor BAY 1238097 for the treatment of lymphoma
#> 610                                                                                                                                            lncRNA Expression Signatures in Response to Jiangtang Tiaozhi Formular in T2DM with Obesity and Hyperlipidemia
#> 611                                                                                                                         Global gene expression profiling and senescence biomarker analysis of hESC exposed to H2O2 induced non-cytotoxic oxidative stress
#> 612                                                                                                                                                                                             Effects of isoxazole (ISX) on long-term cultured human islets
#> 613                                                                                                                    Transcriptomic profile in lymphomonocytes of healthy subjects identifies an early signature of insulin resistance and related diseases
#> 614                                                                                                                                     Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts
#> 615                                                                                                                         Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts [glomeruli]
#> 616                                                                                                                            Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts [Tub-FE]
#> 617                                                                                                                                                     Dysregulation of a miR-23b/27b-p53 axis impairs muscle differentiation in humans with type 2 diabetes
#> 618                                                                                                                                                                                         Single-cell transcriptomics of East-Asian pancreatic islets cells
#> 619                                                                                                                                           DNA methylation profiles in sibling pairs discordant for intrauterine exposure to maternal gestational diabetes
#> 620                                                                                                                                                                    Proteomic Comparison of Acute Myocardial Infarction and Stress Cardiomyopathy in Women
#> 621                                                                                                                                                                   Acute Exercise Bout Effects on GH and IGF1 in Prediabetic and Healthy African Americans
#> 622                                                                                                              Human monocyte subsets are transcriptionally and functionally altered in aging in response to pattern recognition receptor agonists [ExVivo]
#> 623                                                                                                             Human monocyte subsets are transcriptionally and functionally altered in aging in response to pattern recognition receptor agonists [InVitro]
#> 624                                                                                                                                                                            Entrainment of Breast Cell Lines Results in Rhythmic Fluctuations of MicroRNAs
#> 625                                                                                                                                                                       Effect of hyperglycemia on the transcriptional profile of primary human macrophages
#> 626                                                                                                                                                                                                              Expression data from liver of obese patients
#> 627                                                                                                                           IL-6/Stat3-Dependent Induction of Distinct, Obesity-Associated Natural Killer Cells Deteriorates Energy and Glucose Homeostasis
#> 628                                                                                                                                                                              Glucose impairs tamoxifen sensitivity modulating CTGF in breast cancer cells
#> 629                                                                                                                                                    Using hESCs to Probe the Interaction of CDKAL1 and MT1E, Two GWAS identified Diabetes Associated Genes
#> 630                                                                                                                                                                                                                         Rader HHDL and BioBank genotyping
#> 631                                                                                                                                                            Sirt6 Deficiency Exacerbates Podocyte Injury and Proteinuria through Targeting Notch Signaling
#> 632                                                                                                                                                    Serum miRNAs from Drug-induced liver injury, Hepatitis B, Liver cirrhosis and Type 2 Diabetes patients
#> 633                                                                                                                                                       Single cell RNA-seq reveals expansion of IGRP-reactive CD4+ T cells in recent onset type I diabetes
#> 634                                                                                   Single cell RNA-seq reveals expansion of IGRP-reactive CD4+ T cells in recent onset type I diabetes (single-cell RNA-seq of CD4+ pooled islet antigen-reactive T cells)
#> 635                                                                                              Single cell RNA-seq reveals expansion of IGRP-reactive CD4+ T cells in recent onset type I diabetes (single-cell RNA-seq of CD8+ influenza-reactive T cells)
#> 636                                                                                                                        Single cell RNA-seq reveals expansion of IGRP-reactive CD4+ T cells in recent onset type I diabetes (bulk RNA-seq of T-cell clone)
#> 637                                                                                                                 Single cell RNA-seq reveals expansion of IGRP-reactive CD4+ T cells in recent onset type I diabetes (single-cell RNA-seq of T-cell clone)
#> 638                                                                                                                                                                                        Glucose upregulates a limited number of genes in human beta cells.
#> 639                                                                                                                          Acute and chronic treatment of trametinib plus lapatinib in patient-derived xenografts (PDX) of pancreatic adenocarcinoma (PDAC)
#> 640                                                                                                                                                                                                 A DNA methylation atlas of the human eye and its diseases
#> 641                                                                                                                                                                 Aberrantly Expressed Long Non-coding RNAs In CD8+ T Cells Response to Active Tuberculosis
#> 642                                                                                                                                      Prenatal Pesticide Exposure Interacts with a Common Polymorphism in the PON1 Gene Leading to DNA Methylation Changes
#> 643                                                                                                                                     Characterizing the global changes in miRNA expression in human atrial appendages with persistent atrial fibrillation.
#> 644                                                                                                                                                                                                      Circulating miRNAs for gestational diabetes mellitus
#> 645                                                                                                                                                               RNA-sequencing of human skeletal myocytes from healthy, obese, and type 2 diabetic subjects
#> 646                                                                                                                                           Transcriptomic Analysis of Endothelial Cells from Fibrovascular Membranes in Proliferative Diabetic Retinopathy
#> 647                                                                                                                                         Epigenetic signatures of gestational diabetes mellitus on ATP5A1, PRKCH, SLC17A4 and HIF3A cord blood methylation
#> 648                                                                                                           Enhanced Protein Translation Underlies Improved Metabolic and Physical Adaptations to Different Exercise Training Modes in Young and Old Humans
#> 649                                                                                                                                                                        Microarray analysis of CD9high and CD9low progenitors isolated from adipose tissue
#> 650                                                                                                                                    Microarray analysis of CD9high and CD9low progenitors isolated from omental adipose tissue of morbid obese individuals
#> 651                                                                                                                                                                                                    Interaction between mitoNEET and NAF-1 in cancer cells
#> 652                                                                                                                                              Open chromatin profiling of human postmortem brain infers functional roles for non-coding schizophrenia loci
#> 653                                                                                                                                                               Differential expression analysis between Microadenoma and Macroadenoma in Cushing's Disease
#> 654                                                                                                                                         Transcriptional profiling of diabetic peripheral neuropathy patients, diabetic patients, and healthy participants
#> 655                                                                                                                               Tissue-Specific and Genetic Regulation of Insulin Sensitivity-Associated Transcripts in African Americans [skeletal muscle]
#> 656                                                                                                                          Tissue-Specific and Genetic Regulation of Insulin Sensitivity-Associated Transcripts in African Americans [subcutaneous adipose]
#> 657                                                                                         Characterization of molecular functions, pathways and protein classes affected by aging-related changes of miRNA expression in peripheral blood mononuclear cells
#> 658                                                                                                                                        Pathogenic Implications for Autoimmune Mechanisms Derived by Comparative eQTL Analysis of CD4+ Versus CD8+ T cells
#> 659                                                                                                                                                                                                  Serum microRNA profile of human type 1 diabetes mellitus
#> 660                                                                                                                                                                     Impact of Visceral Fat Adiposity on Gene Expression Profile in Peripheral Blood Cells
#> 661                                                                                                                             Adipose tissue gene expression is differentially regulated with different rates of weight loss in overweight and obese humans
#> 662                                                                                                                                                              Transcriptional Profiling of Dysregulated lncRNAs in B cells Response to Active Tuberculosis
#> 663                                                                                                                                                             Artemisinins target GABA receptor signaling to induce alpha to beta cell transdifferentiation
#> 664                                                                                                                                       Epigenome-wide association in the METSIM cohort identifies 22 novel loci for diabetes and metabolic syndrome traits
#> 665                                                              Serum microRNA signatures are indicative of skeletal fractures in post-menopausal women with and without type 2 diabetes and influence osteo-genic differentiation of mesenchymal stem cells
#> 666                                                                                                                                                                             Sequential global gene expression analysis of glucose stimulated human islets
#> 667                                                                                                                                                         Transcriptome profiles of differentiated hepatoma cells infected with oncogenic hepatitis C virus
#> 668                                                                                                                                                                                 Healthy glucocorticoid receptor N363S SNP carriers and metabolic syndrome
#> 669                                                                               Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes (single-cell RNA-seq of sorted CD8+ T-cells)
#> 670                                                                                                               Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes (microarray)
#> 671                                                                                                                      Conserved recurrent gene mutations correlate with pathway deregulation and clinical outcomes of lung adenocarcinoma in never-smokers
#> 672                                                                                                                            Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes
#> 673                                                                                                      Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes (whole blood RNA-seq)
#> 674                                                                                      Partially exhausted CD8+ T cells are associated with clinically beneficial response to Teplizumab in new onset type I diabetes (bulk RNA-seq of sorted CD8+ T-cells)
#> 675                                                                                                                                                                     Gene expression in the peripheral whole blood of established Type 1 diabetes patients
#> 676                                                                                                                      Single cell transcriptomics defines human islet cell signatures and reveals cell-type-specific expression changes in type 2 diabetes
#> 677                                                                                                        Single cell transcriptomics defines human islet cell signatures and reveals cell-type-specific expression changes in type 2 diabetes [single cell]
#> 678                                                                                                               Single cell transcriptomics defines human islet cell signatures and reveals cell-type-specific expression changes in type 2 diabetes [bulk]
#> 679                                                     Genome-wide analysis of hepatic gene expression in patients with non-alcoholic fatty liver disease  and in healthy donors in relation to hepatic fatty acid composition and other nutritional factors
#> 680                                                                                                                                                                                               Pleiotropic Analysis of Lung Cancer and Blood Triglycerides
#> 681  Transcriptome comparison of PAX6 ablated mouse beta cells to WT beta cells, ChIP-seq analysis of PAX6 bound sites both in mouse and human beta cell lines (Min6 and EndoC), and ChIP-seq analysis fo histone mark H3K9ac on mouse pancreatic beta cells.
#> 682                                                                                                                                           Differences in genome-wide gene expression response in PBMCs between young and old men upon caloric restriction
#> 683                                                                                                                                                                 Hepatocyte Nuclear Factor 1 coordinates multiple functions of intestinal epithelial cells
#> 684                                                                                                                                                                                 Continuous Aging of the Human DNA Methylome Throughout the Human Lifespan
#> 685                                                                                                                                                                                        A single-cell transcriptome atlas of the human pancreas [CEL-seq2]
#> 686                                                                                                                                                                Potential Epigenetic Biomarkers of Obesity Related Insulin Resistance in Human Whole Blood
#> 687                                                                                   Integrative Analysis of miRNA and mRNA Paired Expression Profiling of Primary Fibroblast Derived from Diabetic Foot Ulcers Reveals Multiple Impaired Cellular Functions
#> 688                                                                                                                                       A single-cell transcriptomic map of the human and mouse pancreas reveals inter- and intra-cell population structure
#> 689                                                                                                                                            Comparative study of the transcriptome of HUVECs from infants born to mothers diagnosed with GDM and controls.
#> 690                                                                                                                    Enhanced T cell responses to IL-6 in type 1 diabetes are associated with early clinical disease and increased IL-6 receptor expression
#> 691                                                                                                                             Differentially Expressed Gene Transcripts Using RNA Sequencing from the Blood of Immunosuppressed Kidney Allograft Recipients
#> 692                                                                                                      Genome-wide RNA-sequencing of human islets 48 hour after transduction with adenoviruses expressing either GFP (control), or histone chaperone ASF1B.
#> 693                                                                                                                              Expression profiling of cutaneous squamous cell carcinoma with perineural invasion implicates the p53 pathway in the process
#> 694                                                                                                                                                                                  RNA Sequencing of Single Human Islet Cells Reveals Type 2 Diabetes Genes
#> 695                                                                        Response of peripheral blood mononuclear cells from  20 healthy donor and 15 patients with type 1 diabetes to type 1 diabetogenic protein (IGRP, PPI) derived peptide stimulation.
#> 696                                     Response of peripheral blood mononuclear cells from  15 healthy donor and 15 patients with type 1 diabetes to type 1 diabetogenic protein (GAD65, IGRP, PPI, ZnT8) and influenza virus M derived peptide stimulation.
#> 697                                                                                                                                                       The expression profiling of circular RNAs (circRNA) in human intervertebral disc degeneration (IDD)
#> 698                                                                                                                                                                                                                        Tacrolimus in diabetic nephropathy
#> 699                                                                                                                                                                               The epigenetic signature of systemic insulin resistance in obese women [SC]
#> 700                                                                                                                                                                               The epigenetic signature of systemic insulin resistance in obese women [OM]
#> 701                                                                                                                                                                               The epigenetic signature of systemic insulin resistance in obese women [BL]
#> 702                                                                                                                                  Conversion of Human Gastric Epithelial Cells to Multipotent Endodermal Progenitors using Defined Small Molecules [array]
#> 703                                                                                                                        Conversion of Human Gastric Epithelial Cells to Multipotent Endodermal Progenitors using Defined Small Molecules [DNA methylation]
#> 704                                                                                                                        Conversion of Human Gastric Epithelial Cells to Multipotent Endodermal Progenitors using Defined Small Molecules [gene expression]
#> 705                                                                                High-throughput sequencing reveals key genes and immune homeostatic pathways activated in myeloid dendritic cells by Porphyromonas gingivalis 381 and its fimbrial mutants
#> 706                                                                                                                                                                                       Discovery of a Drug that Targets a Diabetes Gene identified by GWAS
#> 707                                                                                                                                          Single cell RNA-seq of human pancreatic endocrine cells from Juvenile, adult control and type 2 diabetic donors.
#> 708                                                                                                                                                       DNA methylation anaylsis of placenta samples exposed to variable levels of arsenic during pregnancy
#> 709                                                                                                                                                              Revisiting the microRNA expression profiling of human intervertebral disc degeneration (IDD)
#> 710                                                                                                                                          TGFβ contributes to impaired exercise response by suppression of mitochondrial key regulators in skeletal muscle
#> 711                                                                                                                                                                                                   A single-cell transcriptome atlas of the human pancreas
#> 712                                                                                                   RNA sequencing of pancreatic adenocarcinoma tumors yields novel expression patterns associated with long-term survival and reveals a role for *ANGPTL4*
#> 713                                                                                                                                                                                          RNA-sequencing of human pancreatic adenocarcinoma cancer tissues
#> 714                                                                                                                                                Novel Regions of Variable DNA Methylation in Human Placenta associated with Newborn Neurobehavioral Traits
#> 715                                                                                                                                                                                                Hyperglycemia induced microRNAs in endothelial dysfunction
#> 716                                                                                                                                                                                                             Comparsion of IGRP reactive CD8 T cell clones
#> 717                                                                                               DNA-methylation profiling of Whole blood genomic DNAs collected at EDIC baseline and monocytes at EDIC years 16/17 yrs from participants of DCCT/EDIC study
#> 718                                                    DNA-methylation profiling of monocyte genomic DNAs collected from participants of  Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study
#> 719                                                 DNA-methylation profiling of Whole blood genomic DNAs collected from participants of  Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study
#> 720                                                                                                                                                                         Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility
#> 721                                                                                                                                                              Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility [ATAC-seq]
#> 722                                                                                                                                                           5-hydroxymethylcytosine-mediated alteration of transposon activity associated with Preeclampsia
#> 723                                                                                                                                  Embryonic atrazine exposure alters zebrafish and human miRNAs associated with angiogenesis, cancer, and neurodevelopment
#> 724                                                                                                                                                                                              Epigenomic landscapes of human primary pancreatic cell types
#> 725                                                                                                                                                                                                                         Study of Topoisomerase I in human
#> 726                                                                                                                                                                             Methylome-wide analysis of chronic HIV infected patients and healthy controls
#> 727                                                                                                                                                                                     Generation of Stem Cell-Derived β Cells from Type 1 Diabetic Patients
#> 728                                                                                                                           Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients [methylome analysis]
#> 729                                                                                                                       Altered DNA methylation of glycolytic and lipogenic genes in liver from obese and type 2 diabetic patients [transcriptome analysis]
#> 730                                                                                                                                                                                   fibroblasts and iPS cells from patients with insulin receptor mutations
#> 731                                                                                                                                                                           Omics profiling of 21 novel primary and metastatic colorectal cancer cell lines
#> 732                                                                                                                                SNP-array profiling of 21 novel primary and metastatic colorectal cancer cell lines [Illumina HumanExome-12 v1.2 BeadChip]
#> 733                                                                                                                                SNP-array profiling of 21 novel primary and metastatic colorectal cancer cell lines [Illumina HumanExome-12 v1.0 BeadChip]
#> 734                                                                                                                                                        Systematic Evaluation Of Genes And Genetic Variants Associated With Type 1 Diabetes Susceptibility
#> 735                                                                                                                                                                                                   Gene expression response to mitochondrial DNA depletion
#> 736                                                                                                                                Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid [human]
#> 737                                                      Perivascular Progenitor Cells Derived from Human Embryonic Stem Cells Exhibit Functional Characteristics of Pericytes, and Improve the Retinal Vasculature in a Rodent Model of Diabetic Retinopathy
#> 738                                                                                                                   Integrated Analysis of Dysregulated lncRNA and mRNA Expression profiles of myocardial sleevesof pulmonary veins in  atrial fibrillation
#> 739                                                                                                                                                                                   Maternal-diabetes induced gene expression changes in the umbilical cord
#> 740                                                                                                                                                                                     Palmitate-induced gene expression in human gingival fibroblasts (HGF)
#> 741                                                                                                                                              An integrative analysis of renal miRNA- and mRNA-expression signatures in progressive chronic kidney disease
#> 742                                                                                                                          An integrative analysis of renal miRNA- and mRNA-expression signatures in progressive chronic kidney disease [validation cohort]
#> 743                                                                                                                           An integrative analysis of renal miRNA- and mRNA-expression signatures in progressive chronic kidney disease [discovery cohort]
#> 744                                                                                                                                                                                Altered microRNA expression in individuals at high risk of type 1 diabetes
#> 745                                                                                                                                                             Integration of ATAC-seq and RNA-seq Identifies Human Alpha Cell and Beta Cell Signature Genes
#> 746                                                                                                                                     Tetraspanin-2 promotes glucotoxic apoptosis by regulating JNK/β-catenin signaling pathway in human pancreatic β-cells
#> 747                                                                                                                                                                                                                                     Rader HHDL genotyping
#> 748                                                                                                              Human skeletal muscle gene expression analysis on Lean, obese insulin sensitive, obese insulin resistant and obese Type II diabetic subjects
#> 749                                                                                                                                               Tissue Transcriptome Driven Identification of Epidermal Growth Factor as a Chronic Kidney Disease Biomarker
#> 750                                                                                                                                                                                                                       Mexican Patients with Breast Cancer
#> 751                                                                                                                                                                                                    Gene Expression of Mexican Patients with Breast Cancer
#> 752                                                                                                                                                                                                  miRNAs Expression of Mexican Patients with Breast Cancer
#> 753                                                                                                                                          Capture Hi-C reveals novel candidate genes and complex long-range interactions with related autoimmune risk loci
#> 754                                                                                                                       Blood transcriptional biomarkers for active TB among US patients: A case-control study with systematic cross-classifier evaluation.
#> 755                                                                                                                                Peripheral blood transcriptome profiles from an RNA Pilot Study within the United States Health and Retirement Study (HRS)
#> 756                                                                                                         Near-whole-genome transcriptome analysis of gene expression in human skeletal muscle tissue at baseline in obese individuals with Type 2 Diabetes
#> 757                                                                                                                                                         Pancreatic Beta Cell Enhancers Regulate Rhythmic Transcription of Exocyst Triggering and Diabetes
#> 758                                                                                                                                          Genome-wide Circadian Control of Transcription at Active Enhancers Regulates Insulin Secretion and Diabetes Risk
#> 759                                                                                                                                                                                                                Expression data from MSC-treated monocytes
#> 760                                                                                                                                                                  Transcriptome profile of peripheral blood from pancreatic ductal adenocarcinoma patients
#> 761                                                                                                                                                                             miRNA profile in the vitreous of proliferative vitreoretinal disease patients
#> 762                                                                                                                                                  Gene expression in the pancreas of healthy control, auto-antibody positive, and type 1 diabetic subjects
#> 763                                                                                                                           Chlorella ingestion and suppression of resistin gene expression in borderline diabetics: a randomized, placebo-controlled study
#> 764                                                                                                                                                                       Genetic and epigenetic variation in the lineage specification of regulatory T cells
#> 765                                                                                                                Plasma induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment naïve inflammatory bowel disease
#> 766                                                                                                                                      Canakinumab treatment for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
#> 767                                                                                                                          Interleukin-1 receptor antagonist for recent-onset type 1 diabeties mellitus: a multicenter randomized, placebo-controlled trial
#> 768                                                                                                                                                                                                          Influence of muscle activity on paralyzed muscle
#> 769                                                                                                                                                      Preserved DNA Damage Checkpoint Pathway Protects From Complications in Long-standing Type 1 Diabetes
#> 770                                                                                                          Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex
#> 771                                                                                        Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [gene expression]
#> 772                                                                                            Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [methylation]
#> 773                                                                                                                                    Expression data from insulin-treated human primary fibroblasts and effects of U0126 on insulin-induced gene expression
#> 774                                                                                                                                                          Gene Expression Profiling in Omental Adipose Tissue of Morbidly Obese Diabetic African Americans
#> 775                                                                                                                                                          Inhibition of ZEB1 expression induces redifferentiation of adult human β cells expanded in vitro
#> 776                                                                                                                                               Comparative analysis of gene expression profiles in lymphoma cells after treatment by Dexamethasone or CpdA
#> 777                                                                                                                                        Comparative analysis of gene expression profiles in prostate cancer cells after treatment by Dexamethasone or CpdA
#> 778                                                                                                                                                                                                          BisPCR2 method for targeted bisulfite sequencing
#> 779                                                                                                                                                               Gene expression annalysis of peripheral blood cells in patients with chronic kidney disease
#> 780                                                                                                                                                                  Genome-wide blood transcriptional profiling in critically ill patients - MARS consortium
#> 781                                                                                                                                                                  Cold acclimation improves insulin sensitivity in patients with type 2 diabetes mellitus.
#> 782                                                                                                                                                                      Effect of type 2 diabetes on transcriptional signatures during exercise and recovery
#> 783                                                                                                                                                Differences in platelet miRNA profiles between patients with coronary artery disease and healthy controls.
#> 784                                                                                                                                                                                            miRNA regulation in diabetes associated impaired wound healing
#> 785                                                                                                                                        Novel Observations from Next Generation RNA Sequencing of Highly Purified Human Adult and Fetal Islet Cell Subsets
#> 786                                                                                                                                                                                       A Blood Transcriptional Diagnostic Assay for Septicemic Melioidosis
#> 787                                                                                                                                                                                                                Genetic background of immune complications
#> 788                                                                                                                                                                                    Differential mRNA expression profile regulated by HNF4α in Hep3B cells
#> 789                                                                 Fibroblast growth factor 21 is elevated in metabolically unhealthy obesity and affects lipid deposition, adipogenesis, and adipokine secretion of human abdominal subcutaneous adipocytes
#> 790                                                                                                                                                         Skeletal muscle gene expression changes with exercise mode, duration and intensity: STRRIDE study
#> 791                                                                                                                                                        caArray_beer-00153: Gene-expression profiles predict survival of patients with lung adenocarcinoma
#> 792                                                                                                                                                                                           Gene expression responses to chronic low dose arsenite exposure
#> 793                                                                                                                                  Comparative genomic, microRNA, and tissue analyses reveal subtle differences between non-diabetic and diabetic foot skin
#> 794                                                                                       Comparative genomic, microRNA, and tissue analyses reveal subtle differences between non-diabetic and diabetic foot skin [nanoString nCounter miR expression assay]
#> 795                                                                                                             Comparative genomic, microRNA, and tissue analyses reveal subtle differences between non-diabetic and diabetic foot skin [microRNA PCR panel]
#> 796                                                                                                                Comparative genomic, microRNA, and tissue analyses reveal subtle differences between non-diabetic and diabetic foot skin [gene expression]
#> 797                                                                                                                                                                       MicroRNA signature in skeletal muscle in type 2 Diabetes and insulin resistant rats
#> 798                                                                                                                                                                                          MicroRNA signature in skeletal muscle in type 2 Diabetes [human]
#> 799                                                                                                          Differential adipose tissue gene expression profiles in abacavir treated patients that may contribute to cardiovascular risk: a microarray study
#> 800                                                                                                                                                                                                 Salivary Transcriptomic Biomarkers for Insulin Resistance
#> 801                                                                                                                                                                                                         RNA-sequencing of healthy human skeletal myocytes
#> 802                                                                                                                                                                                       Transcriptome analysis of Myotonic Dystrophy type 2 (DM2) patients.
#> 803                                                                                                                                                                  Noncoding RNAs in human intervertebral disc degeneration: an integrated microarray study
#> 804                                                                                                                                                     Mitoscriptome analysis to understand the pathogenesis of Diabetic Retinopathy using tissue microarray
#> 805                                                                                                                                                               Age-associated DNA methylation changes within 5 years after birth in human blood leukocytes
#> 806                                                                                                                                           Genome-Wide Gene Expression Profiles in the Pancreatic Lymph Nodes of At-Risk Autoantibody Positive Individuals
#> 807                                                                                                                     A Whole Blood Molecular Signature for the Identification of Acute Myocardial Infarction Without Relying Upon Myonecrosis (microarray)
#> 808                                                                                                                                                 Blood methylomic signatures of pre-symptomatic dementia in elderly subjects with Type 2 Diabetes Mellitus
#> 809                                                                                                                                                                                           Genome wide analysis of copy number variation in NAFLD spectrum
#> 810                                                                                         Differential microarray expression profile analysis of long non-coding RNAs in umbilical cord vein plasma from normal and gestational diabetes-induced macrosomia
#> 811                                                                                                                                Imporatance of substantial weight loss for altering gene expression during intensive cardiovascular lifestyle modification
#> 812                                                                                                                                                                                                     miRNA expression profiling of primary melanoma tumors
#> 813                                                                                                                                                                                          miRNA expression profiling of primary melanoma tumors (cohort I)
#> 814                                                                                                             The effects of moderate weight gain in adipose tissue gene expression in metabolically-normal (MNO) and metabolically-abnormal (MAO) subjects
#> 815                                                                                                                                        Mouse-human experimental epigenetic analysis unmasks dietary targets and genetic liability for diabetic phenotypes
#> 816                                                                                                                                                                                   Next generation sequencing of human immune cell subsets across diseases
#> 817                                                                                         MicroRNA Expression Profiles identify genes of apoptosis, anabolism and catabolism in patients with Intervertebral Disc Degeneration different from Spinal Trauma
#> 818                                                                                                                                                                           Gene expression profiling in blood of patients with chronic respiratory failure
#> 819                                                                                                                                                         Determinants of excess genetic risk of acute myocardial infarction – a matched case-control study
#> 820                                                                                                                        p38 MAPK activation upregulates pro-inflammatory pathways in skeletal muscle cells from insulin resistant type 2 diabetic patients
#> 821                                                                                                                                             Differential regulation of microRNAs in skeletal muscle from monozygotic twins discordant for type 2 diabetes
#> 822                                                                                                                                     The long noncoding RNA expression profile of human intervertebral disc degeneration identified by microarray analysis
#> 823                                                                                                                                                                                 White-to-brown metabolic conversion of human adipocytes by JAK inhibition
#> 824                                                                                                                                                                                   Gene expression profiling of myxoid liposarcomas (validation set INT-B)
#> 825                                                                                                                                                                                     Gene expression profiling of myxoid liposarcomas (training set INT-A)
#> 826                                                                                                                 Gene expression profiles of HMEC-1 after exposure to the chemotherapeutic drugs bleomycin and cisplatin with untreated samples as control
#> 827                                                                                                                                           PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies [expression array]
#> 828                                                                                                                                                   PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies [ChIP-seq]
#> 829                                                                                                                                                                                           SNP genotyping data from human iPSCs and human fibroblast cells
#> 830                                                                                                                                                                                             Generation of functional human pancreatic beta cells in vitro
#> 831                                                                                                                                                              Global mRNA/LncRNA expression analysis of pancreatic tumors causing type3C Diabetes Mellitus
#> 832                                                                                                                                                                   Exonic variants associated with development of Aspirin Exacerbated Respiratory Diseases
#> 833                                                                                                                                                  Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta
#> 834                                                                                                                                 Using RNA sequencing for identifying gene imprinting and random monoallelic expression in human placenta (SNP genotyping)
#> 835                                                                                                                                                               Redifferentiation of adult human β cells expanded in vitro by inhibition of the WNT pathway
#> 836                                                                                                                          Molecular and cellular characterization of Cord Blood derived, IDO expressing human fibrocystic Myeloid Derived Suppressor Cells
#> 837                                                                                                                                             Ras-induced epigenetic inactivation of RRAD promotes glucose uptake in a human ovarian cancer model [DGE-Seq]
#> 838                                                                                                                                            Ras-induced epigenetic inactivation of RRAD promotes glucose uptake in a human ovarian cancer model (RRBS-Seq]
#> 839                                                                                                                             FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance
#> 840                                                                                                                                                      Gene Expression Profile of Fibrovascular Membrane Associated with Proliferative Diabetic Retinopathy
#> 841                                                                                                                                                          Peripheral blood mononuclear cell in patients with type 1 diabetes compared with normal controls
#> 842                                                                                                                          microRNA expression data from peripheral blood mononuclear cell in patients with type 1 diabetes  compared with normal controls.
#> 843                                                                                                                                    Expression data from peripheral blood mononuclear cell in patients with type 1 diabetes  compared with normal controls
#> 844                                                                                                                                               Identification of Novel Auto-antibodies in Type 1 Diabetic Patients using a High-density Protein Microarray
#> 845                                                                                                                           Global transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism [expression array]
#> 846                                                                                                                       microRNA profiling of HepG2 cells: control vs treatment with cacao, grape seed proanthocyanidin extract or epigallocatechin gallate
#> 847                                                                                                                                                                             Human cells infected with Mucormycosis-causing strains from clinical settings
#> 848                                                                                                                                           Maternal microRNAs secreted by the endometrium act as  transcriptomic regulators of the pre-implantation embryo
#> 849                                                                                                                                                                Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin
#> 850                                                                                                                              Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks
#> 851                                                                                                                                                                              Molecular signatures differentiate immune states in Type 1 Diabetes families
#> 852                                                                                                                                 Dietary fat quality, more than dietary fat quantity, impacts genome-wide DNA methylation patterns in Greek preadolescents
#> 853                                                                                                  Resveratrol improves adipose insulin signaling and reduces the inflammatory response in adipose tissue of rhesus monkeys on a high-fat, high-sugar diet.
#> 854                                                   Risk of T1D progression in islet autoantibody positive children can be further stratified using expression patterns of multiple genes implicated in peripheral blood lymphocyte activation and function
#> 855                                                                                                                                            Identification of Type 1 Diabetes-Associated DNA Methylation Variable Positions That Precede Disease Diagnosis
#> 856                                                                                                                                                                                              A conditionally immortalized human pancreatic beta cell line
#> 857                                                                                                                                                                                                 Platelet micro-RNA expression in type 2 diabetes mellitus
#> 858                                                                                                                                                                               Whole Blood Transcriptional Modules generated on Illumina Hu-6 V2 Beadchips
#> 859                                                                                                                                                                           Expression microarray analysis of human pancreatic islets reveals CD59 function
#> 860                                                                                                                                                                                  Expression data of Participants of Ornish intervention and Control group
#> 861                                                                             Genome-wide expression kinetics of children with Type 1 diabetes (T1D) -associated autoantibodies or progression towards clinical T1D, compared to healthy matched controls .
#> 862                                                                                                                                                                                               Gene expression changes during Type 1 diabetes pathogenesis
#> 863                                                                                                                                                                Genome-wide espression kinetics of children progressing to clinical Type 1 diabetes (T1D).
#> 864                                                                                                                                    Genome-wide expression kinetics of children with T1D-associated autoantibodies compared to healthy matched controls II
#> 865                                                                                                                                     Genome-wide expression kinetics of children with T1D-associated autoantibodies compared to healthy matched controls I
#> 866                                                                                                                                     Differential miRNA expression profiling of urinary exosomes from normo- and microalbuminuric type 1 diabetic patients
#> 867                                                                                                                                                        Genome wide analysis of Visceral adipose tissue CD14+ cells from Obese and obese diabetic subjects
#> 868                                                                                                                                                       Prenatal arsenic exposure and the epigenome: altered gene expression profiles in newborn cord blood
#> 869                                                                                                                                                      Prenatal arsenic exposure and the epigenome: altered miRNA expression profiles in newborn cord blood
#> 870                                                                                                                                 RNA-sequencing identifies dysregulation of the human pancreatic islet transcriptome by the saturated fatty acid palmitate
#> 871                                                                                                                                                               gene expression Fulminant type 1 diabetes vs classical type 1A diabetes vs healthy controls
#> 872                                                                                                                                                                                   Gene expression Fulminant type 1 diabetes vs classical type 1A diabetes
#> 873                                                                                                                                                                                                                 mRNA and microRNA profile in colon cancer
#> 874                                                                                                             Complementary Strand MicroRNAs Mediate Acquisition of Metastatic Potential in Colonic AdenocarcinomamRNA and microRNA profile in colon cancer
#> 875                                                                                                                                                                                                     mRNA and microRNA profile in colon cancer [mRNA data]
#> 876                                                                                                                                                                               Impact of Visceral Fat on Gene Expression Profile in Peripheral Blood Cells
#> 877                                                                                                                          Epigenomic Approaches to explaining Metabolic Memory in the Epidemiology of Diabetes Intervention and Complications (EDIC) Study
#> 878                                                                                                                                                                                                         Human islets exposed to cytokines IL-1β and IFN-γ
#> 879                                                                                                                                             Expression of the placental transcriptome in fetal growth restriction in the Baboon is Dependent on Fetal Sex
#> 880                                                                                                                                                                            Molecular signatures of human iPSCs highlight sex differences and cancer genes
#> 881                                                                                                                                                                   Epigenetic regulation of the MEG3-DLK1 microRNA cluster in human Type 2 diabetic islets
#> 882                                                                                                                                                          DNA methylation differences between multiple sclerosis and controls in frontal lobe white matter
#> 883                                                                                                     Differential genes in adipocytes induced from polycystic ovary syndrome-derived and non- polycystic ovary syndrome-derived human embryonic stem cells
#> 884                                                                                                                                                                   Epigenetic regulation of the MEG3-DLK1 microRNA cluster in human Type 2 diabetic islets
#> 885                                                                                                                                                                     Differentially Expressed Wound Healing-Related microRNAs in the Human Diabetic Cornea
#> 886                                                                                                                                   Chromatin stretch enhancer states drive cell-specific gene regulation and harbor human disease risk variants (ChIP-seq)
#> 887                                                                                                                                    Chromatin stretch enhancer states drive cell-specific gene regulation and harbor human disease risk variants (RNA-seq)
#> 888                                                                                                                                            Increases in Insulin Sensitivity among Obese Youth are Associated with Gene Expression Changes in Whole Blood.
#> 889                                                                                                                                                       SBV - Gene Expression Profiles of Lung Cancer Tumors - Adenocarcinomas and Squamous Cell Carcinomas
#> 890                                                                                                                                                                Adipose tissue gene expression associated with weight gain in kidney transplant recipients
#> 891                                                                                                                                     Effects of 30 days resveratrol supplementation on adipose tissue morphology and gene expression patterns in obese men
#> 892                                                                                                                                                                                            Expression data from kidney biopsies of liver disease patients
#> 893                                                                                                                                                                     DNA methylation differences between human regulatory T cells and conventional T cells
#> 894                                                                                                                                                                             Gene expression profiles in 74 laser microdissected colorectal cancer tissues
#> 895                                                                                                                                                                           Epigenomic plasticity enables human pancreatic alpha to beta cell reprogramming
#> 896                                                                                                                                                                            Expression data from open bariatric surgery patients - various adipose samples
#> 897                                                                                                                                                               Ficolin-1 is upregulated in leukocytes and glomeruli from microscopic polyangiitis patients
#> 898                                                                                                                         Differential expression profiles of human primary endothelial cells (HUVECs) from umbilical cords of Gestational Diabetic mothers
#> 899                                                                                                                  Analyses of a deactivation genetic variation in Ha-Ras proto oncogene identified in a patient wit premature aging and insulin resistance
#> 900                                                                                                                                                                         A mutation in the c-Fos gene associated with congenital generalized lipodystrophy
#> 901                                                                                                                                                       In silico nano-dissection: defining cell type specificity at transcriptional level in human disease
#> 902                                                                                                                                  In silico nano-dissection: defining cell type specificity at transcriptional level in human disease (tubulointerstitium)
#> 903                                                                                                                                           In silico nano-dissection: defining cell type specificity at transcriptional level in human disease (glomeruli)
#> 904                                                                                                                                                                        Cyclodextrin protects podocytes in diabetic kidney disease [HumanHT-12 V4.0 array]
#> 905                                                                                                                                                                                               Cyclodextrin protects podocytes in diabetic kidney disease.
#> 906                                                                                                                                                                         Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]
#> 907                                                                                                                                                                          The Heritage (HEalth, RIsk factors, exercise Training And GEnetics) family study
#> 908                                                                                                                                                                                       miRNA-sequencing of human pancreatic islets and enriched beta-cells
#> 909                                                                                                                                 Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes
#> 910                                                                                                                         Temporal induction of immunoregulatory processes coincides with age-dependent resistance to viral-induced type 1 diabetes [human]
#> 911                                                                                                                   Cluster analysis reveals differential transcript profiles associated with resistance training-induced human skeletal muscle hypertrophy
#> 912                                                                                                                                                                       Genetic Risk Factors for Type 2 Diabetes:  A Trans-Regulatory Genetic Architecture?
#> 913                                                                                                                                          A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v3.0]
#> 914                                                                                                                                          A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v2.0]
#> 915                                                                                                                                                                                               A stem cell model of diabetes due to glucokinase deficiency
#> 916                                                                                                                                                                                                               Gene expression from human pancreatic islet
#> 917                                                                                                                                                                               Transcription dependent dynamic supercoiling is a short-range genomic force
#> 918                                                                                                                                                                                Transcription dependent dynamic supercoiling in Raji human B cells in vivo
#> 919                                                                                                                                                                                                             Gene expression assay from Raji human B cells
#> 920                                                                                                                                           Gene expression profiling in endothelial precursor cells of patients protected from microvascular complications
#> 921                                                                                                                  Human transcriptome analysis of acute responses to glucose ingestion reveals a role of leukocytes in hyperglycemia induced inflammation.
#> 922                                                                                                                                                                                                                               PBEF Knockdown in HMVEC-LBI
#> 923                                                                                                                               Genome-Wide Analysis of DNA Methylation Differences in Muscle and Fat from Monozygotic Twins Discordant for Type 2 Diabetes
#> 924                                                                                                                                           The anti-inflammatory IL-1 receptor antagonist (IL-1ra) protects against the development of islet autoimmunity.
#> 925                                                                                                                                                                                                       An eQTL study in the Japanese population [genotype]
#> 926                                                                                                                                                                                              An eQTL study in the Japanese population [gene expression_3]
#> 927                                                                                                                                                                                              An eQTL study in the Japanese population [gene expression_2]
#> 928                                                                                                                                                                                              An eQTL study in the Japanese population [gene expression_1]
#> 929                                                                                                                                                                     Global Gene Expression Profiles of  Visceral Adipose in Females with Type 2 Diabetes.
#> 930                                                                                                                                                                  Global Gene Expression Profiles of Subcutaneous Adipose in Females with Type 2 Diabetes.
#> 931                                                                                                                                                                        Global Gene Expression Profiles of  Skeletal Muscle in Males with Type 2 Diabetes.
#> 932                                                                                                                                                                                Global gene expression profile of coronary artery disease in Asian Indians
#> 933                                                                                                                                                         Dynamic regulation of miRNA and mRNA signatures during in vitro pancreatic differentiation (mRNA)
#> 934                                                                                                                                                        Dynamic regulation of miRNA and mRNA signatures during in vitro pancreatic differentiation (miRNA)
#> 935                                                         Differential Gene Expression in Granulosa Cells from Polycystic Ovary Syndrome Patients with and without Insulin Resistance:  Identification of Susceptibility Gene Sets through Network Analysis
#> 936                                                                                                                                      Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [T1D_114]
#> 937                                                                                                                        Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [Pneu_S3S24_10Pneu_4HC]
#> 938                                                                                                                                                Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes
#> 939                                                                                                                             Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [H1N1_S5_5Pre_5D0]
#> 940                                                                                                                      Transcriptional Signatures as a Disease-Specific and Predictive Inflammatory Biomarker for Type 1 Diabetes [CF_S1S3_5Auto_20CF_10HC]
#> 941                                                                                                                                                                                  microRNAs expression profile in Myotonic Dystrophy type-2 (DM2) patients
#> 942                                                                                                                                 Genomic Multivariate Predictors of Response to Adjuvant Chemotherapy in Ovarian Carcinoma: Predicting Platinum Resistance
#> 943                                                                                                                                                                           microRNA profiling of formalin-fixed, paraffin-embedded human sarcoma specimens
#> 944                                                                                                                                                                     Plasticity of adult human pancreatic duct cells by neurogenin3-mediated reprogramming
#> 945                                                                                                                                                                                                              Expression data from human pancreatic islets
#> 946                                                                                                                                                                                                                                         Paradigm Test Set
#> 947                                                                                                                                                                                                                        Paradigm Test Set Expression Array
#> 948                                                                                                                                            Cell type-specific binding patterns reveal that TCF7L2 can be tethered to the genome by association with GATA3
#> 949                                                                                                                                                                              Dermal lymphatic endothelial cell response to type 2 diabetes [Homo sapiens]
#> 950                                                                                                                                                      Profiles of Epigenetic Histone Post-translational Modifications at Type 1 Diabetes Susceptible Genes
#> 951                                                                                                                                                                  ChIP-chip of lymphocytes using H3K9Ac, H3K4me3, H3K9me3, H3K27me3 and H4K16Ac antibodies
#> 952                                                                                                                                                                              ChIP-chip of monocytes using H3K9Ac, H3K4me3, H3K9me2 and H4K16Ac antibodies
#> 953                                                                                                                                                                                                               Gene expression data from human lymphocytes
#> 954                                                                                                                                                                                 Peripheral Blood Monocyte Gene Expression in Recent-Onset Type 1 Diabetes
#> 955                                                                                                                                                                                     Incisional hernia recurrence through genomic profiling: a pilot study
#> 956                                                                                                                                         Transcriptome analysis of circulating monocytes in obese patients before and three months after bariatric surgery
#> 957                                                                                                                                                                                   microRNA expression analysis of circulating monocytes in obese patients
#> 958                                                                                                                                                                               Evaluation of a novel clinical platform for cardiovascular drug development
#> 959                                                                                                                                                                   Mid-gestational gene expression profile in placenta and link to pregnancy complications
#> 960                                                                                                                                                                              Amorfrutins are selective PPARγ agonists with potent antidiabetic properties
#> 961                                                                                                                                   Blood biomarkers of pancreatic cancer associated diabetes identified by peripheral blood-based gene expression profiles
#> 962                                                                                                                               Genome-wide analysis of SPARC(secreted protein acidic and rich in cysteine)-responsive gene expression in HTR-8/SVneo cells
#> 963                                                                                                                                                             DNA methylation profiling of male human pancreatic islets identifies loci for type 2 diabetes
#> 964                                                                                                                                Gene expression analysis of bone biospies from nine patients with endogenous Cushings syndrome before and after  treatment
#> 965                                                                                                                                       Hyperglycemia and a Common Variant of GCKR Are Associated with the Levels of Eight Amino Acids in 9,371 Finnish Men
#> 966                                                                                                                                                                                 RNA-sequencing of TGF-ß1-driven gene expression in human kidney cell line
#> 967                                                                                                                                                                                           Expression data from cytoplasmic hybrid (cybrid) and rho0 cells
#> 968                                                                                                                                                      Transcriptome analysis of diabetic and non diabetic patients affected by post-ischemic heart failure
#> 969                                                                                                                                                                Personal Omics Profiling Reveals Dynamic Molecular Phenotypes and Actionable Medical Risks
#> 970                                                                                                                                                                                                                    Autoantibody profile timecourse of UNK
#> 971                                                                                                                                                                            The human pancreatic islet transcriptome: impact of pro-inflammatory cytokines
#> 972                                                                                                       Polyunsaturated fatty acids acutely affect triacylglycerol-derived skeletal muscle fatty acid uptake and increases postprandial insulin sensitivity
#> 973                                                                                                             Expression data from peripheral blood mononuclear cell in patients with type 1 diabetes before and after peripheral stem cell transplantation
#> 974                                                                                                                                        Differential gene expression in adipose tissue from obese human subjects during weight loss and weight maintenance
#> 975                                                                                                                                      Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.
#> 976                                                                                                                                                                  MicroRNAs expression profiling of human nucleus pulposus cells: control vs. degeneration
#> 977                                                                                                                                                                                                 Blood genomic expression profile for ischemic stroke (IS)
#> 978                                                                                                                                                                                Gene expression profiling in arterial tissue from type 2 diabetic patients
#> 979                                                                                                                     Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans
#> 980                                                                                                                                                                                    Molecular markers of predictive value associated with low birth weight
#> 981                                                                                                                                      Genome-wide survey reveals predisposing diabetes type 2-related DNA methylation variations in human peripheral blood
#> 982                                                                                                                                                                                              Human oocytes reprogram somatic cells to a pluripotent state
#> 983                                                                                                                                                                         Gene expression in blastomeres after transfer of somatic cells into human oocytes
#> 984                                                                                                                                                   Gene expression in pluripotent stem cells derived after somatic cell genome transfer into human oocytes
#> 985                                                                                                                                                          To investigate how the glycosylation of podocyte proteins changes during diabetic kidney disease
#> 986                                                                                                                                                                              Formalin Fixation at Low Temperature Better Preserves Nucleic Acid Integrity
#> 987                                                                                                                                                                                              Correlation between maternal age and newborn DNA methylation
#> 988                                                                                                                                                                            Gene expression profiles in 132 laser microdissected colorectal cancer tissues
#> 989                                                                                                                                                     A gene signature in histologically normal surgical margins is predictive of oral carcinoma recurrence
#> 990                                                                                                                                                            Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli)
#> 991                                                                                                                                                                   Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli)
#> 992                                                                                                                                                             Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli)
#> 993                                                                                                                                                                                                   Transcriptome Analysis of Human Diabetic Kidney Disease
#> 994                                                                                                                                            Differences in subcutaneous adipose tissue gene expression between obese African Americans and Hispanic Youths
#> 995                                                                                                                                             Genome-wide mRNA profiling of adult human pancreatic beta and duct cells in comparison to other human tissues
#> 996                                                                                                                                                     Insulin-producing cells generated from dedifferentiated human pancreatic beta cells expanded in vitro
#> 997                                                                                                                                                         HIV Infection and Antiretroviral Therapy Have Divergent Effects on Mitochondria in Adipose Tissue
#> 998                                                                                                                                                                  Expression in Huh7 cells 72 hours after treatment with scramble, SPTLC123, or DEGS siRNA
#> 999                                                                                                                                                       Gene-chip studies of adipogenesis-regulated microRNAs in mouse primary adipocytes and human obesity
#> 1000                                                                                                                                                                                An early inflammatory gene profile in visceral adipose tissue in children
#> 1001                                                                                                                                         Gene-chip studies of adipogenesis-regulated microRNAs in mouse primary adipocytes and human obesity (Affymetrix)
#> 1002                                                                                                                                                    Genome-wide profiling of H3K56 acetylation and transcription factor binding sites in human adipocytes
#> 1003                                                                                                                                                                              TGFß1-driven epithelial to mesenchymal transition in human kidney cell line
#> 1004                                                                                                                                                                 Comparative miRNA Expression Profiles in Individuals with Latent and Active Tuberculosis
#> 1005                                                                                                                             Transcriptome profile of peripheral blood mononuclear cells in patients with type I diabetes and their first grade relatives
#> 1006                                                                                                                                                                                                 Expression Data from HNF4a RNAi Knockdown in HepG2 cells
#> 1007                                                                                                                                                     Increased SRF Transcriptional Activity is a Novel Signature of Insulin Resistance in Humans and Mice
#> 1008                                                                                                                                                    Mapping of INS promoter interactions reveals its role in long-range  regulation of SYT8 transcription
#> 1009                                                                                                       Dioxin exposure of human CD34+ hemopoietic cells induces gene expression modulation that recapitulates its in vivo clinical and biological effects
#> 1010                                                                                                                                                                                                           Adenosine-treated endothelial progenitor cells
#> 1011                                                                                                                                      Resolution of Type 2 Diabetes Following Bariatric Surgery is Associated with Changes in Whole Blood Gene Expression
#> 1012                                                                                                                           Growth hormone receptor deficiency is associated with a major reduction in pro-aging signaling, cancer, and diabetes in humans
#> 1013                                                                                                                                                             Genomic expression profiles of blood and placenta in Chinese women with gestational diabetes
#> 1014                                                                                                                                                                                                       Type 2 Diabetes mellitus: mRNA and miRNA profiling
#> 1015                                                                                                                          MicroRNA 144 impairs insulin signaling by inhibiting the expression of insulin receptor substrate 1 in Type 2 Diabetes mellitus
#> 1016                                                                                                                                                                                                     DNA methylation patterns associated with arsenicosis
#> 1017                                                                                                                                                                                               Investigation of somatic copy number variation in MZ twins
#> 1018                                                                                                                                                                              Expression data from type 2 diabetic and non-diabetic isolated human islets
#> 1019                                                                                                                                                   Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array
#> 1020                                                                                                                                                                      Effect of insulin on the stromal and adipocyte cells within hMSC derived adipocytes
#> 1021                                                                                                                                                                                           Skeletal muscle mitochondrial dysfunction is secondary to T2DM
#> 1022                                                                                                                                     Genome-wide binding of the orphan nuclear receptor TR4 suggests its general role in fundamental biological processes
#> 1023                                                                                                                                    BI Human Reference Epigenome Mapping Project: Characterization of chromatin modification by ChIP-Seq in human subject
#> 1024                                                                                                                                 Global epigenomic analysis of primary human pancreatic islets provides insights into type 2 diabetes susceptibility loci
#> 1025                                                                                                                                                                                   Analysis of transcriptome in ectopic versus orthotopic thyroid tissue.
#> 1026                                                                                                                                                                       microRNA and mRNA expression profiles of human pancreatic islet-like cell clusters
#> 1027                                                                                                                                                                              Sural nerve of progressive and non-progressive diabetic neuropathy patients
#> 1028                                                                                                                    Insulin resistance induced by physical inactivity is associated with multiple transcriptional changes in skeletal muscle in young men
#> 1029                                                                                                                                                                                     Sera-induced transcriptional signatures in human leukemia cell lines
#> 1030                                                                                                                                              DNA methylation data from non-immortalized lymphocyte samples from participants of the AGES Reykjavik Study
#> 1031                                                                                                                                             Peripheral blood gene expression profiles in metabolic syndrome, coronary artery disease and type 2 diabetes
#> 1032                                                                                                                                    Phenothiazine Neuroleptics Signal To The Human Insulin Promoter As Revealed By A Novel Human b-Cell Line Based Screen
#> 1033                                                                                                                                                                                                  Human lung squamous cell carcinoma expression profiling
#> 1034                                                                                                                                                        Gene expression changes in Peripheral Blood Mononuclear cells (PBMC) induced by physical activity
#> 1035                                                                                                                                 Effect of IL6 level on gene expression changes in Peripheral Blood Mononuclear cells (PBMC) induced by physical activity
#> 1036                                                                                                                                                                                         Expression data from human liver with or without type 2 diabetes
#> 1037                                                                                                                                                                                                  Systematic analysis of a human renal transcript dataset
#> 1038                                                                                                                                                                                                               Expression data from human skeletal muscle
#> 1039                                                                                                                                                                    Transcriptional response in human umbilical vein endothelial cells exposed to insulin
#> 1040                                                                                                                                                                                                   miRNA expression profile of human subcutaneous adipose
#> 1041                                                                                                                                                          Blood microRNA profiles and upregulation of hsa-miR-144 in males with type 2 diabetes mellitus.
#> 1042                                                                                                                                        A Transcriptional Signature and Common Gene Networks Link Cancer with Metabolic Syndrome and Auto-immune Diseases
#> 1043                                                                                                                                                       Human skeletal muscle - type 2 diabetes and family history positive individuals - Mexican American
#> 1044                                                                                                                                                      Expression levels in immortalized B cells from unrelated individuals and twins undergoing ER stress
#> 1045                                                                                                                       Gene expression profiles of beta-cell enriched tissue obtained by Laser Capture Microdissection from subjects with type 2 diabetes
#> 1046                                                                                                                                                                Genome wide DNA methylation profiling of diabetic nephropathy in type 1 diabetes mellitus
#> 1047                                                                                                                                            A restricted repertoire of cytosine methylation changes in neonates following intrauterine growth restriction
#> 1048                                                                                                                                                            C-peptide and/or transforming growth factor beta 1 effect on human proximal tubular cell line
#> 1049                                                                                                                                                                                             mRNA expression data from skeletal muscle of type 2 diabetes
#> 1050                                                                                                                                                         miRNA expression signatures for human stomach biopsy samples, H. pylori positive versus negative
#> 1051                                                                                                                                                                                       University of Washington Human Reference Epigenome Mapping Project
#> 1052                                                                                                                                        Preadipocytes of T2DM patients display an intrinsic gene expression profile of decreased differentiation capacity
#> 1053                                                                                                                                     Folic acid supplementation normalizes the endothelial progenitor cell transcriptome of patients with type 1 diabetes
#> 1054                                                                                                                                                               Differential Expression of MicroRNAs in Mouse Liver under Aberrant Energy Metabolic Status
#> 1055                                                                                                                                                                 Mitochondrial dysregulation and oxidative stress in patients with chronic kidney disease
#> 1056                                                                                                                                                  Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry
#> 1057                                                                                                                                                                                              THE EFFECTS OF ALCOHOLISM ON THE HUMAN BASOLATERAL AMYGDALA
#> 1058                                                                                                                                               Gene expression analysis of chronically inflamed human peri-implant and periodontal ligament cells in vivo
#> 1059                                                                                                                                                                               Thrombospondin-1: A Pro-Atherosclerotic Protein Augmented by Hyperglycemia
#> 1060                                                                                                                                                                                                           UCSD Human Reference Epigenome Mapping Project
#> 1061                                                                                                                                                                               Meta analysis of gene expression in human islets after in vitro expansion.
#> 1062                                                                                                                                                                   Expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes
#> 1063                                                                                                                                                             MiRNA expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes
#> 1064                                                                                                                                                                                                                 miRNA prognostic profiles in lung cancer
#> 1065                                                                                                                                     Genomic Transcriptional Profiling Identifies a Blood Biomarker Signature for the Diagnosis of Septicemic Melioidosis
#> 1066                                                                                                                                                   A synthetic gene-metabolic circuit preferentially increased fatty acid metabolism in human hepatocytes
#> 1067                                                                                                                                                            Genome wide gene expression profiling of visceral adipose tissue among Asian Indian diabetics
#> 1068                                                                                                                                                           Expression data from liver of obese (with or without type 2 diabetes) and lean human subjects.
#> 1069                                                                                                                                                                                           Gene expression of innate immune response in endothelial cells
#> 1070                                                                                                                                                              Acetaminophen-induced gene expression profiles in sandwich-cultured primary rat hepatoctyes
#> 1071                                                                                                                                                                                                   MicroRNA expression profiling in diabetic GK rat model
#> 1072                                                                                                                                                                                                  Transcriptomes in Healthy and Diseased Gingival Tissues
#> 1073                                                                                                                                                                                                Circulating Cells in Coronary Collateral Artery Growth II
#> 1074                                                                                                                                                                          Gene expression profiling in skeletal muscle of PCOS after pioglitazone therapy
#> 1075                                                                                                                                                                                   Transcription profiling of myotubes from patients with type 2 diabetes
#> 1076                                                                                                                                                                                  Construction of a modular analysis framework for blood Genomics Studies
#> 1077                                                                                                                                                     A Modular Analysis Framework for Blood Genomics Studies: Application to Systemic Lupus Erythematosus
#> 1078                                                                                                                                     Transcriptional changes in blood from metabolic syndrome patients after a period of high intensity interval training
#> 1079                                                                                                                                                                                       Mapping the Genetic Architecture of Gene Expression in Human Liver
#> 1080                                                                                                                                            Profiling Gene Expression in Human Placentae of Different Gestational Ages: an OPRU Network and UW SCOR Study
#> 1081                                                                                                                                                      Gene expression data on human optic nerve head astrocytes in normal Caucasian and African americans
#> 1082                                                                                                                                                                                 Expression profiles of peripheral blood monocytes in periodontal therapy
#> 1083                                                                                                                                                                                                    gene expression in monkey aorta with aging and gender
#> 1084                                                                                                                                                     Reduced expression of mitochondrial oxidative metabolism genes in skeletal muscle of women with PCOS
#> 1085                                                                                                                                               Expression profiling of human adipose tissue in obese and lean subjects and in various clinical conditions
#> 1086                                                                                                                                                                     Expression profile of human preadipocytes cultured with activated macrophages medium
#> 1087                                                                                                                                                         Effect of Acute Physiologic Hyperinsulinemia on Gene Expression in Human Skeletal Muscle in vivo
#> 1088                                                                                                                                                                                                     Gene expression in PBMCs from children with diabetes
#> 1089                                                                                                                                    Myocardial gene expression of hibernating and control tissue from patients with ischemic left ventricular dysfunction
#> 1090                                                                                                                                                                Specific inhibition of p300-HAT alters Global Gene Expression and Repress HIV replication
#> 1091                                                                                                                                                                                                      Effect of insulin infusion on human skeletal muscle
#> 1092                                                                                                                                                                      Changes in transcription profile in pelvic organ fibroblasts in response to stretch
#> 1093                                                                                                                                                               Dysregulation of the circulating and tissue-based renin-angiotensin system in preeclampsia
#> 1094                                                                                                                                                                    Effects of laughter on gene expression profiles patients with type 2 diabetes (Tenri)
#> 1095                                                                                                                                                                          Comparison of expression profile between human Müller cells, HMCL-I and HMCL-II
#> 1096                                                                                                                                                                         Effects of laughter on gene expression profiles of patients with type 2 diabetes
#> 1097                                                                                                                                                                                                                        PCOS patients vs control subjects
#> 1098                                                                                                                                                                                                              Skeletal muscle and insulin regulated genes
#> 1099                                                                                                                                          Target genes of the transcription factors HNF1beta and HNF1alpha in the human embryonic kidney cell line HEK293
#> 1100                                                                                                                                                                 Gene Expression Signature Shared in Autoimmune Diseases Not in Unaffected Family Members
#> 1101                                                                                                                                                                                                        Comparative profiling in 13 muscle disease groups
#> 1102                                                                                                                                                                                                                                   Colon cancer profiling
#> 1103                                                                                                                                                                Gestational Diabetes Induces Placental Genes for Chronic Stress and Inflammatory Pathways
#> 1104                                                                                                                                                                                 laughter regulates postprandial blood glucose levels and gene expression
#> 1105                                                                                                                                                                                                                                     Diabetic nephropathy
#> 1106                                                                                                                                                                                                            Muscle - atypical diabetes protein expression
#> 1107                                                                                                                                                                                                                   Type 2 diabetes and insulin resistance
#>                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Summary
#> 1                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Genome-wide DNA methylation profiling of bead-enriched total monocytes collected from Native Hawaiian participants with known type 2 diabetes mellitus enrolled in a 3 month diabetes-specific social support education intervention. DNA methylation profiling was performed across ~450,000 CpGs from monocytes using the Illumina Infinium HumanMethylation450 BeadChip. Samples included 8 participants with paired DNA methylation data collected at pre-intervention and post-intervention (3 months), and 2 non-diabetic donors.
#> 2                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                We identified lncRNA expression profiles in vitreous samples between proliferative diabetic retinopathy (PDR) patients and idiopathic macular hole (IMH) patients, and between PDR patients who had received preoperative anti-vascular endothelial growth factor (anti-VEGF) therapy and PDR patients who had received surgery alone. There had been the systemic expression differences in vitreous at the microarray level from PDR patients and IMH patients, and from PDR patients after anti-VEGF treatment and untreated PDR patients.
#> 3                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Cardiovascular disease (CVD) accounts for the majority of deaths in patients with type 1 diabetes (T1D); however, the determinants of plaque composition are unknown in this population. MicroRNAs (miRNAs), the most abundant class of circulating small non-coding RNA (sncRNAs) regulating gene expression, participate in the development of atherosclerosis and represent promising biomarkers of CVD.  This study analyzed the circulating miRNA expression profile in T1D with carotid calcified and fibrous plaque. more...
#> 4                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Studies in genetically identical individuals indicate that as much as 50% of complex trait variation cannot be traced to either genetics or to the environment. The mechanisms that generate this ‘unexplained’ phenotypic variation (UPV) remain largely unknown. Here, we identify neuronatin (NNAT) as a conserved factor that buffers against unexplained phenotypic variation. We find that Nnat deficiency in isogenic F1 mice triggers the emergence of a novel, bi-stable polyphenism, where isogenic littermates emerge into adulthood either ‘normal’ or ‘overgrown’, without intermediates. more...
#> 5                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Non-alcoholic fatty liver disease is continuum of disorders among which non-alcoholic steatohepatitis (NASH) is particularly associated with a negative prognosis. Hepatocyte lipotoxicity is one of the main pathogenic factors of liver fibrosis and NASH. However, the molecular mechanisms regulating this process are poorly understood. Here, we integrated transcriptomic and chromatin accessibility analyses from human liver and mouse hepatocytes to identify lipotoxicity-sensitive transcription factors. more...
#> 6                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Non-alcoholic fatty liver disease is continuum of disorders among which non-alcoholic steatohepatitis (NASH) is particularly associated with a negative prognosis. Hepatocyte lipotoxicity is one of the main pathogenic factors of liver fibrosis and NASH. However, the molecular mechanisms regulating this process are poorly understood. Here, we integrated transcriptomic and chromatin accessibility analyses from human liver and mouse hepatocytes to identify lipotoxicity-sensitive transcription factors. more...
#> 7                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here we unravel a fundamental role for exercise-responsive cytokines (exerkines) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. more...
#> 8                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Metformin is one of the first-line drugs for clinical treatment of type II diabetes, and recent studies have found that metformin can inhibit the development of multiple malignant tumors. When metformin is combined with chemotherapeutic drugs to treat head and neck squamous cell carcinoma(HNSCC), it can effectively enhance the efficacy of chemotherapy. The aim of this study was to define the signaling pathways regulated by metformin in HNSCC, and the underlying mechanisms by which metformin sensitizes HNSCC chemotherapy. more...
#> 9                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We investigate the effects of GLP-1 on diabetic cardiomyocytes (DCMs) model established by human induced pluripotent stem cells-derived cardiomyocytes (iPSC-CMs). Two subtypes of GLP-1, GLP-17-36 and GLP-19-36, were evaluated for their efficacy on hypertrophic phenotype, impaired calcium homeostasis and electrophysiological properties. RNA-seq was performed to reveal the underlying molecular mechanism of GLP-1. more...
#> 10                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Epigenetics was reported to mediate the effects of environmental risk factors on disease pathogenesis. To unleash the role of DNA methylation modification in the pathological process of cardiovascular diseases in diabetes, we screened differentially methylated genes by methylated DNA immunoprecipitation chip (MeDIP-chip) among the enrolled participants.
#> 11                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Aims: Metformin is a widely used, primary drug of choice to treat individuals with type 2 diabetes (T2D). Clinically, inter-individual variability of drug response is of significant  concern. The targets and precise mechanisms of action for metformin is still under interrogation. In the present study, a whole transcriptome analysis was performed with an  intent to identify predictive biomarkers of metformin response in T2D individuals. more...
#> 12                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 To understand the role of adipose tissue senescence in NAFLD/NASH,  RNA sequencing was performed in the visceral adipose tissue of NAFLD and NASH pateints.
#> 13                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Single-cell transcriptomes of corpus cavernosum from three males with normal erections and five organic erectile dysfunction (ED) patients.
#> 14                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Gestational diabetes mellitus (GDM) “program” an elevated risk of metabolic syndrome in the offspring.  Epigenetic alterations are a suspected mechanism. GDM has been associated with placental DNA methylation changes in some epigenome-wide association studies. It remains unclear which genes or pathways are affected, and whether any placental differential gene methylations are correlated to fetal growth or circulating metabolic health biomarkers. more...
#> 15                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Adipocytes are key regulators of human metabolism, and their dysfunction in insulin signaling is central to metabolic diseases including type II diabetes mellitus (T2D). However, the progression of insulin resistance into T2D is still poorly understood. This limited understanding is due, in part, to the dearth of suitable models of insulin signaling in human adipocytes. Traditionally, adipocyte models fail to recapitulate in vivo insulin signaling, possibly due to exposure to supraphysiological nutrient and hormone conditions. more...
#> 16                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         In this dataset, we utilized the db/db, uninephrectomy and renin-hypertension mouse model. We performed bulk RNA-seq and compared vehicle to ACE inhibitor, Rosiglitizone, SGLT2 inhibitor, ACEi + Rosiglitizone and ACEi + SGLT2i at two time points (2 days and 2 weeks). To study the mechanism, we also performed bulk RNA-seq on human primary tubular epithelial cells with or without SRSF7 siRNA knockdown.
#> 17                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      To reveal the expression profiles of transfer RNA-derived small RNA (tsRNA)s and microRNA (miRNA)s in the vitreous humour of proliferative diabetic retinopathy (PDR).
#> 18                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Objectives: This study was undertaken to understand the mechanistic basis of response to anti-TNF therapies and determine if transcriptomic changes in the synovium are reflected in peripheral protein markers. Methods: Synovial tissue from 46 RA patients was profiled with RNA sequencing before and 12 weeks after treatment with anti-TNF therapies.  Pathway and gene signature analyses were performed on RNA expression profiles of synovial biopsies to identify mechanisms that could discriminate among EULAR good, moderate and non-responders. more...
#> 19                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Abnormal mechanical load is a main risk factor of intervertebral disc degeneration (IDD), and cellular senescence is a pathological change in IDD. Additionally, extracellular matrix (ECM) stiffness promotes human nucleus pulposus cells (hNPCs) senescence. However, the molecular mechanism underlying mechano-induced cellular senescence and IDD progression is not yet fully elucidated. First, we demonstrated that mechano-stress promoted hNPCs senescence via NF-κB signaling. more...
#> 20                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Patients with NEUROGENIN3 mutations have enteric endocrinopathy and diabetes mellitus. We generated pluripotent stem cells from a patient’s fibroblasts to investigate if gene editing restores endocrine differentiation. Corrected cell lines differentiated into all pancreatic lineages while native cell lines failed to activate pancreatic progenitor and lineage determination genes, suggesting that the mutation disrupts pancreatic organogenesis and results in endocrine and exocrine dysfunction. more...
#> 21                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Among 226 morbidly obese patients who underwent gastric bypass surgery between 2013 and 2014 as part of the A Biological Atlas of Severe Obesity (ABOS) study (ClinicalTrials.gov; NCT01129297), 18 women who gave informed consent were recruited in this study for immunophenotyping and microarray analyses of omental adipose tissue (AT). We characterized T and NK cell populations in omental AT from morbidly obese women with varying levels of IR. more...
#> 22                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Objective: To explore the characteristics and underlying molecular mechanisms of genome-scale expression profiles of women with- or without- GDM and their offspring.  Materials and Methods: We recruited a group of 21 pregnant women with GDM and 20 healthy pregnant women as controls. For each pregnant women, RNA-seq were performed using the placenta and paired neonatal umbilical cord blood specimens. more...
#> 23                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Objective: To explore the characteristics and underlying molecular mechanisms of genome-scale expression profiles of women with- or without- gestational diabetes mellitus and their offspring.  Materials and Methods: We recruited a group of 21 pregnant women with gestational diabetes mellitus (GDM) and 20 healthy pregnant women as controls. For each pregnant women, RRBS were performed using the placenta and paired neonatal umbilical cord blood specimens. more...
#> 24                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 25                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          To systemically investigate the role of ZnT8 in β cell maturation, we performed single cell RNA-seq in both WT and KO β cells at both S6 (immature) and S7 (mature) stages.  Both WT and KO β cells were obtained from FACS as positive for both INS and NKX6.1. Single cell RNA-seq results revealed that SLC30A8 is mainly involved in β cell maturation process, and further showed that SLC30A8 LOF accelerates β cell maturation and upregulates insulin secretion pathway in mature β cells.
#> 26                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      The antisense non-coding RNA in the INK locus (ANRIL), which originates from the CDKN2A/B (INK4-ARF) locus, has been identified as a hotspot for genetic variants associated with cardiometabolic disease including coronary artery disease (CAD) and Type 2 diabetes (T2D). We recently found that ANRIL abundance in human pancreatic islets was increased in donors carrying certain T2D risk-SNPs, and that a T2D risk-SNP located within exon2 of ANRIL conferred reduced beta cell proliferation index, pointing to a role for ANRIL in the regulation of T2D pathogenicity via an impact on insulin secretory capacity. more...
#> 27                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Long noncoding RNAs (lncRNAs) are involved in diabetes related diseases. However, the role of lncRNAs in the pathogenesis of type 2 diabetes with macrovascular complication (DMC) has seldomly been recognized. This study screened lncRNA profiles of leukocytes from DMC patients and explored protective role of lncRNA LYPLAL1-DT in endothelial cells (EC) under high glucose (HG) and inflammatory conditions (IS). more...
#> 28                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 29                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and post-operative atrial fibrillation (POAF) is a major healthcare burden, contributing to an increased risk of stroke, kidney failure, heart attack and death. Genetic studies have identified associations with AF, but no molecular diagnostic exists to predict POAF based on pre-operative measurements. Such a tool would be of great value for perioperative planning to improve patient care and reduce healthcare costs. more...
#> 30                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and post-operative atrial fibrillation (POAF) is a major healthcare burden, contributing to an increased risk of stroke, kidney failure, heart attack and death. Genetic studies have identified associations with AF, but no molecular diagnostic exists to predict POAF based on pre-operative measurements. Such a tool would be of great value for perioperative planning to improve patient care and reduce healthcare costs. more...
#> 31                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        We profiled manually microdissected tubulointerstitial tissue from 43 IgA nephropathy, 3 diabetes mellitus nephropathy, 3 focal segmental glomerulosclerosis, 3 lupus nephritis, 4 membranous nephropathy, and 9 minimal change disease biopsy cores and 22 nephrectomy controls by RNA sequencing. The 3 outliers which were not included in our main analysis were also uploaded in this database.
#> 32                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Serum miRNAs could be powerful classifiers for the detection of patients with postmenopausal osteoporosis.
#> 33                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            The pancreas and liver arise from a common pool of progenitors in the foregut endoderm; however, the underlying molecular mechanisms driving this lineage diversification are not fully understood. We combined human pluripotent stem cell guided differentiation and sequential CRISPR-Cas9 loss-of-function screening to uncover regulators of  pancreatic specification. Here we report the discovery of a cell-intrinsic requirement for HHEX, a transcription factor (TF) associated with diabetes susceptibility. more...
#> 34                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            The pancreas and liver arise from a common pool of progenitors in the foregut endoderm; however, the underlying molecular mechanisms driving this lineage diversification are not fully understood. We combined human pluripotent stem cell guided differentiation and sequential CRISPR-Cas9 loss-of-function screening to uncover regulators of  pancreatic specification. Here we report the discovery of a cell-intrinsic requirement for HHEX, a transcription factor (TF) associated with diabetes susceptibility. more...
#> 35                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The pancreas and liver arise from a common pool of progenitors in the foregut endoderm; however, the underlying molecular mechanisms driving this lineage diversification are not fully understood. We combined human pluripotent stem cell guided differentiation and sequential CRISPR-Cas9 loss-of-function screening to uncover regulators of pancreatic specification. Here we report the discovery an unexpected, cell-intrinsic requirement for HHEX, a transcription factor (TF) associated with diabetes susceptibility. more...
#> 36                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Every year, about 18 million babies are born from mothers with gestational diabetes mellitus (GDM). While diabetic symptoms usually resolve after delivery, lasting complications can occur for both mother and child, including fetal overgrowth, type 2 diabetes (T2D), cardiovascular diseases, and obesity. The rapid progression of GDM is unique to pregnancies, and likely arises from placental dysfunction. more...
#> 37                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Regenerating pancreatic b-cells is a potential curative approach for diabetes. We previously identified the small molecule CID661578 as a potent inducer of b-cell regeneration but its target and mechanism of action have remained unknown. We now screened 257 million yeast clones and determined that CID661578 targets MAP kinase-interacting serine/threonine kinase 2 (MNK2), an interaction that was genetically validated in vivo. more...
#> 38                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We have reported differntial abundance of miRNAs present in the secretory Extracellular vesicles during Gestetional Diabetes Mellitus or Ischemic placental disease
#> 39                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           The aim of this study was to conduct a baseline comparison of serum-circulating miRNA in diabetic patients with and without ischemic heart disease. We analysed the expression levels of 798 serum miRNAs using the NanoString nCounter Technology Platform. The prediction of the putative miRNAs targets was performed by the Ingenuity Pathway Analysis (IPA) software. Receiver operating characteristic (ROC) analysis was used to assess the diagnostic value of identified miRNAs. more...
#> 40                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              We performed RNA-seq on tissue biopsies derived from patients with DFU and compared it to healthy controls who had similar foot surgery to identify the significant immune related differentially expressed genes between normal and DFU samples. Our results identified that there was a total of 8800 DEGs detected by RNA-seq data analysis, among which 2351 were upregulated and 6449 downregulated genes in DFU. more...
#> 41                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Studies of monogenic diabetes are particularly useful as we can gain insight into the molecular events of pancreatic β-cell failure. Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes form, caused by a mutation in the HNF4A gene. Human induced pluripotent stem cells (hiPSC) provide an excellent tool for disease modelling by subsequent directed differentiation toward desired pancreatic islet cells, but cellular phenotypes in terminally differentiated cells are notoriously difficult to detect. more...
#> 42                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Background:  Long-term complications of type 2 diabetes (T2D) are the major causes for T2D-related disability and mortality. Notably, diabetic nephropathy (DN) has become the most frequent cause of end-stage renal disease (ESRD) in most countries. Understanding epigenetic contributors to DN can provide novel insights into this complex disorder and lay the foundation for more effective monitoring tools and preventive interventions, critical for achieving the ultimate goal of improving patient care and reducing healthcare burden.
#> 43                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Diabetic kidney disease (DKD) is the leading cause of both chronic kidney disease (CKD) and end-stage renal disease (ESRD). In this study, we performed transcriptome gene expression profiling of kidney tissues in human renal proximal epithelial tubular cell line (HK-2) treated with high D-glucose (HG) for 7 days before the addition of 40 mM oxamate for a further 24 hours in the presence of HG. Afterwards, we analyzed the differentially expressed (DE) genes and investigated gene relationships based on weighted gene co-expression network analysis (WGCNA). more...
#> 44                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Background: Pre-diabetes condition precedes the Diabetes Mellitus (DM) disease and is a critical period for hyperglycemia treatment, especially for menopausal women, considering all metabolic alterations due to hormonal changes. Recently, the literature has demonstrated the role of physical exercise in epigenetic reprogramming to modulate the gene expression patterns of metabolic conditions, such as hyperglycemia, preventing DM development. more...
#> 45                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              To investigate whether aberrant lncRNA expression in the placenta is involved in the pathogenesis of NDFMS and to elucidate its biological mechanisms. The expression profile of lncRNAs in the placentas of pregnant women with NDFMS was investigated using an Agilent Human LncRNA Microarray. Differentially expressed lncRNAs were selected for validation using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). 
#> 46                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Dysregulated neurite outgrowth and synapse formation underlie many psychiatric disorders. Wolfram syndrome (WS) mainly caused by WFS1 deficiency is a monogenic genetic disease manifested by severe psychiatric disorders. Due to athe lack of proper human disease models, the underlying mechanism is poorly understood. Particularly, whether and how WFS1 deficiency affects synapse formation remain elusive. more...
#> 47                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 48                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Type 1 diabetes (T1D) usually has a preclinical phase identified by the presence of circulating autoantibodies to pancreatic islet antigens, and most young children who have multiple autoantibodies progress to diabetes within 10 years. While autoantibodies denote underlying islet autoimmunity, how this process is initiated and then progresses to clinical diabetes on a background of genetic susceptibility is not clearly understood. more...
#> 49                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Type 1 diabetes (T1D) usually has a preclinical phase identified by the presence of circulating autoantibodies to pancreatic islet antigens, and most young children who have multiple autoantibodies progress to diabetes within 10 years. While autoantibodies denote underlying islet autoimmunity, how this process is initiated and then progresses to clinical diabetes on a background of genetic susceptibility is not clearly understood. more...
#> 50                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Microglia are the tissue-resident macrophages of the retina and brain, being critically involved in organ development, tissue homeostasis, and response to cellular damage. Until now, little is known about the transcriptional profile of human retinal microglia and how they differentiate from peripheral monocytes, as well as from brain microglia. Additionally, the degree to which mice are suitable models for human retinal microglia is still not clear. more...
#> 51                             BACKGROUND.  The incidence of Type 1 Diabetes (T1D) has significantly increased in recent decades and coincides with lifestyle changes that have likely altered the composition of the gut microbiota.  Dysbiosis and gut barrier dysfunction are associated with T1D, and notably, our studies have identified an inflammatory state in T1D families that is consistent microbial antigen exposure.     METHODS.  We conducted a 6-week, single-arm, open-label trial to investigate whether daily multi-strain probiotic (Bifidobacteria, Lactobacillus, and Streptococcus) supplementation could reduce the familial inflammatory state in 25 unaffected siblings of diabetes patients.    RESULTS.  Probiotic supplementation was found safe and well-tolerated; there were no adverse events and participant adherence was 93%.  Bacterial 16S rDNA gene sequencing of stool revealed that community alpha and beta diversity were not altered between the pre- and post-supplement samplings.  LEfSe analyses identified post-supplement enrichment of the family Lachnospiraceae, producers of the anti-inflammatory short chain fatty acid butyrate.  Systemic inflammation was measured by plasma induced transcription and quantified with a gene ontology-based composite inflammatory index (I.I.com).  After supplementation, I.I.com was reduced (p=0.017), and pathway analysis predicted inhibition of IL17A, lipopolysaccharide, NFkB, IL1B, and TNF (Z-score≤-2.0) and activation of IL10RA (Z-score=2.0).  Post-supplement plasma levels of IL12p40, IL-13, IL-15, IL-18, CCL2, CCL24 were reduced (p<0.05), while butyrate levels trended 2.4-fold higher (p=0.06).    CONCLUSION.  There is a substantial need for safe, broadly applicable therapies to reduce T1D susceptibility.  This study indicates that investigations of prebiotic and probiotic strategies are warranted as they may be efficacious either alone or in combination with other therapeutic agents.
#> 52                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We used the latest technology, BD Rhapsody, to analyze the pairing of α and β chains that constitute the TCR of PBMCs from patients with type 1 diabetes at the single-cell level.
#> 53                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Background: Despite the established relation between energy restriction and metabolic health, the most beneficial nutrient composition of a weight-loss diet is still subject of debate. Objectives: The aim of the study was to examine the additional effects of nutrient quality on top of energy restriction(ER). Methods: A parallel-designed 12-week 25%ER dietary intervention study was conducted. Participants aged 40-70 years with abdominal obesity were randomized over three groups: a 25%ER high nutrient quality diet (n = 40); a 25%ER low nutrient quality diet (n = 40); or a habitual diet (n = 30). more...
#> 54                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The ability to detect and target β cells in vivo can drastically refine the way diabetes is studied and treated. By an unsupervised Systematic evolution of ligands by exponential enrichment (SELEX) we identified two RNA aptamers  that specifically recognize mouse and human β cells in vitro and in vivo.  Here we took advantage of commercially available high density protein arrays to identify putative target of the two islet specific aptamers. more...
#> 55                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Bariatric surgery mediated weight loss has been shown to significantly reduce breast cancer incidence in women. We hypothesize that loss of excessive adiposity, reduces net Estrogen Receptor Alpha activation which in turn lowers breast cancer risk. A differential gene expression analysis and subsequent pathway enrichment analysis would reveal the relevant molecular mechanism behind the preventive effect of weight loss. more...
#> 56                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Colorectal cancer (CRC) is one of the most frequently diagnosed and lethal malignancy. Several key factors including poor dietary habits, smoking, alcohol consumption, genetic predisposition, obesity, diabetes mellitus, and sedentary lifestyle – all result in a significantly increased risk for developing CRC. Current treatment modalities for patients with CRC include surgery, which is often followed with adjuvant chemotherapy, especially in patients with a stage II and III disease. more...
#> 57                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We used WGCNA to construct a co‐expression network and obtain modules related to blood glucose, thus detecting key lncRNAs, and providing a reference for searching potential biomarkers of prediabetes and T2DM in hypertriglyceridemia patients.
#> 58                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   A rare truncating p. Arg138* variant (R138X) in zinc transporter is associated with a 65% reduced risk for type 2 diabetes. To address the mechanism of how this variant protects from type 2 diabetes, we derived human pluripotent stem cells carrying this mutation and differentiated them into insulin-producing cells. We found that human pluripotent stem cells with R138X mutation and the null mutation have normal efficiency of differentiation towards insulin-producing cells, but these cells were depleted of zinc and presented large diffused insulin granules. more...
#> 59                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  This study aimed to identify the crucial molecules and explore the function of noncoding RNAs and related pathways in IDD. We randomly selected 3 samples each from an IDD and a spinal cord injury group (control) for RNA-sequencing. We identified 463 differentially-expressed long noncoding RNAs (lncRNAs), 47 differentially-expressed microRNAs (miRNAs), and 1,334 differentially-expressed mRNAs in IDD. more...
#> 60                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Proteinuria, the spillage of serum proteins into the urine, is a feature of glomerulonephritides, podocyte disorders and diabetic nephropathy. However, the response of tubular epithelial cells to serum protein exposure has not been systematically characterized. Using transcriptomic profiling we studied serum-induced changes in primary human tubular epithelial cells cultured in 3D microphysiological devices. more...
#> 61                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Proteinuria, the spillage of serum proteins into the urine, is a feature of glomerulonephritides, podocyte disorders and diabetic nephropathy. However, the response of tubular epithelial cells to serum protein exposure has not been systematically characterized. Using transcriptomic profiling we studied serum-induced changes in primary human tubular epithelial cells cultured in 3D microphysiological devices. more...
#> 62                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Non-mesenchymal pancreatic cells are a potential source for cell replacement therapies aiming to restore the endocrine capacity lost during diabetes mellitus. Although a highly complex network of transcription factors underlies the differentiation, growth, and specification of pancreatic precursors, several studies indicated that the transdifferentiation of non-mesenchymal cells can be achieved by epigenetic regulation. more...
#> 63                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 64                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Pluripotent stem cell-derived islets (hPSC-islets) are a promising cell resource for diabetes treatment. Here, we demonstrate that transplantation of pluripotent stem cell-derived islets into diabetic nonprimates effectively restored endogenous insulin secretion and improved glycemic control. Single-cell RNA sequencing analysis of S6D2 clusters confirmed the existence of the three major pancreatic endocrine cell populations (β cells, α-like cells and δ-like cells) and their proportions, which altogether accounted for 80%. more...
#> 65                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Human pluripotent stem cell-derived islets (hPSC-islets) are a promising cell resource for diabetes treatment. Here, we demonstrate that transplantation of human pluripotent stem cell-derived islets into diabetic nonhuman primates effectively restored endogenous insulin secretion and improved glycemic control. Single-cell RNA sequencing analysis of S6D2 clusters confirmed the existence of the three major pancreatic endocrine cell populations (β cells, α-like cells and δ-like cells) and their proportions, which altogether accounted for 80%. more...
#> 66                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                We profiled three prominent ATM subtypes from human visceral omental adipose tissue in obesity by RNA-seq. In the related manuscript, we evaluated differences in their signatures and their relationship to type 2 diabetes:  Visceral (VAT) and subcutaneous (SAT) adipose tissue samples were collected from diabetic and non-diabetic obese subjects to evaluate cellular content and gene expression. VAT CD206+CD11c− ATMs were increased in diabetic subjects, scavenger receptor-rich with low intracellular lipids, secreted proinflammatory cytokines, and diverged significantly from two CD11c+ ATM subtypes, which were lipid-laden, lipid antigen presenting, and overlapped with monocyte signatures. more...
#> 67                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Up until now, no study has looked specifically at epigenomic landscapes throughout twin samples, discordant for Anorexia nervosa (AN). Our goal was to find evidence to confirm the hypothesis that epigenetic variations play a key role in the aetiology of AN. In this study, we quantified genome-wide patterns of DNA methylation using the Infinium Human DNA Methylation EPIC BeadChip array (850K) in DNA samples isolated from whole blood collected from a group of 7 monozygotic twin pairs discordant for AN. more...
#> 68                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Genome wide DNA methylation profiling of blood samples collected from patients after diagnosis with hepatocellular carcinoma (HCC) (cases) vs. blood samples collected from healthy individuals without family history of cancer (controls). The Illumina Infinium 450K Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in human samples corresponding to cases (post-diagnostic HCC) and controls. more...
#> 69                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Genome wide DNA methylation profiling of blood samples collected from patients prior to diagnosis with hepatocellular carcinoma (HCC) vs. blood samples collected from healthy individuals without family history of cancer. The Illumina Infinium 450K Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in human samples corresponding to cases (pre-diagnostic HCC) and controls. more...
#> 70                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 β cell proliferation rates decline with age and adult β cells have limited self-duplicating activity for regeneration, which predisposes to diabetes. Here we show that, among MYC family members, Mycl was expressed preferentially in proliferating immature endocrine cells. Genetic ablation of Mycl caused a modest reduction in cell proliferation of pancreatic endocrine cells in neonatal mice. By contrast, systemic expression of Mycl in mice stimulated proliferation in pancreatic islet cells and resulted in expansion of pancreatic islets without forming tumors in other organs. more...
#> 71                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Fibrous membrane (FM), the hallmark for proliferative diabetic retinopathy (PDR) and proliferative vitreoretinopathy (PVR), can cause hemorrhages and retinal detachment, which may lead to blindness if not properly treated. However, little is known about the pathophysiology of FM. In this study, we successfully employed single-cell RNA sequencing on the small-sized vitreous FMs, and generated a comprehensive cell atlas of FMs derived from PVR and PDR. more...
#> 72                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Purpose: Short chain fatty acids (SCFAs) produced by the gut microbiota have dual beneficial anti-inflammatory and anti-dysbiotic effects associated with the prevention of type 1 diabetes (T1D) in mice. We have conducted a single-arm trial of a dietary supplement (HAMSAB), to determine the effects of increasing SCFA delivery  in adults with long-standing T1D. Particularly, we examined blood transcriptome in these patients using RNA-seq. more...
#> 73                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Purpose: The goal of this study is to conduct and compare NGS-derived transcriptome profiling (RNA-seq) of progenitor lines derived from 3 HNF1A-WT and 3 HNF1A-CRISPR (with p291fsinsC mutation) human induced pluripotent stem cell lines. Methods: mRNA profiles of WT/CRISPR pancreatic progenitor cells obtained after in-vitro differentiation for 14 days were generated by deep sequencing using Illumina HiSeq 2000 sequencer. more...
#> 74                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Several studies have suggested a relationship between SARS-CoV-2 infection and diabetes. This study examined the consequences of infection of human pancreatic islets with SARS-CoV-2 virus. This GEO submission contains the raw and processed data from single-cell RNA sequencing (scRNAseq) experiments evaluating the tropism of SARS-CoV-2 in pancreatic islets and transcriptional changes induced by infection of these cells. more...
#> 75                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Exosomal RNAs in cord blood may allow intercellular communication between  maternal and fetus. We aimed to establish exosomal RNA expression profiles in cord blood exosomes from gestational diabetes mellitus (GDM) patients with macrosomia.We used microarray technology to establish the differential mRNA, lncRNA and circRNA expression profiles in cord blood exosomes from GDM patients with macrosomia compared with normal controls. more...
#> 76                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       To compare the circRNA expression profile of diabetic retinopathy with that of diabetes mellitus and controls, peripheral blood mononuclear cell samples were obtained and extracted from healthy controls and diabetes mellitus patients (with or without diabetic retinopathy). CircRNA Capital Bio Technology Human CircRNA Array v2 was performed to detect circRNA expression profiles. To further check differentiate circRNA, qRT_PCR assay was performed to detect the level of 5 candidates.
#> 77                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Purpose:Metabolic syndrome (MetS) is associated with a group of conditions including diabetes, obesity, insulin resistance etc. The goal of our study is to identify the differentially regulated genes under metabolic syndromes induced by TNF-α. Methods:A Homosapines Reference based Transcriptome sequencing is performed to understand the genes that are diffrerentially regulated under metabolic synromes with TNF-α as upstream. more...
#> 78                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Type 1 diabetes (T1D) results from autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas from diabetic NOD mice treated with anti-CD3 monoclonal antibody and IL-1 receptor antagonist (IL-1RA). more...
#> 79                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Ex-vivo pharmacological modulation enhances the immunoregulatory and trafficking properties of HSCs which mitigated autoimmune diabetes and other autoimmune disorders. We used GeneChip microarrays to compare the whole transcriptomes of vehicle (DMSO) and dmPGE2 (10uM) + Dexamenthasone (uM) modulated human CD34+ HSPCs.
#> 80                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Aims/hypothesis. Ectopic calcification is a typical feature of diabetic vascular disease and resembles an accelerated aging phenotype. We previously found an excess of myeloid calcifying cells (MCCs) in diabetic patients. We herein examined molecular and cellular pathways linking atherosclerotic calcification with calcification by myeloid cells in the diabetic milieu. Methods. We first examined the associations among coronary calcification, MCC levels, and mononuclear cell gene expression in a cross-sectional study of 87 type 2 diabetic patients undergoing elective coronary angiography. more...
#> 81                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Objective: To explore the mechanism of Jiangtang Tiaozhi Recipe in the treatment of obese T2DM patients with dyslipidemia based on transcriptomics.  Methods: We chose 6 patients with obese type 2 diabetes mellitus and dyslipidemia (syndrome of excess of gastrointestinal heat) who were treated by JTTZR for 24 weeks, while 6 cases included in the healthy control group. We selected 6 cases in each group (disease group before treatment, disease group after treatment and healthy control group) to start the research of lncRNA microarray. more...
#> 82                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             White adipose tissue (WAT), once regarded as morphologically and functionally bland, is now recognized to be dynamic, plastic, heterogenous, and involved in a wide array of biological processes including energy homeostasis, glucose and lipid handling, blood pressure control, and host defense.  High fat feeding and other metabolic stressors cause dramatic changes in adipose morphology, physiology, and cellular composition, and alterations in adiposity are associated with insulin resistance, dyslipidemia, and Type 2 diabetes (T2D). more...
#> 83                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We report single-cell RNA-seq (Drop-seq) data from the stromal vascular fraction (SVF) of human subcutaneous adipose tissue (SAT).
#> 84                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Development of insulin resistance is a key pathogenic component underlying metabolic syndrome and Type 2 diabetes (T2DM). Despite its importance, the molecular mechanisms underlying insulin resistance are poorly understood. Genome-wide association studies for T2DM and other metabolic traits have led to the identification of many candidate SNPs, but the majority of these SNPs are noncoding and determination of associated causal genes and/or specific tissue sites of action have been difficult. more...
#> 85                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Background Changes in innate and adaptive immunity occurring in/around pancreatic islets had been observed in peripheral blood mononuclear cells (PBMC) of Caucasian T1D patients by some, but not all researchers. The aim of our study was to investigate whether gene expression patterns of PBMC of the highly admixed Brazilian population could add knowledge about T1D pathogenic mechanisms.  METHODS: We assessed global gene expression in PBMC from two groups matched for age, sex and BMI: 20 patients with recent-onset T1D (≤ 6 months from diagnosis, in a time when the autoimmune process is still highly active), testing positive for one or more islet autoantibodies and 20 islet autoantibody-negative healthy controls. more...
#> 86                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Changes in innate and adaptive immunity occurring in and around pancreatic islets can also be observed in peripheral  blood mononuclear cells (PBMC) of T1D patients  in Caucasians. The aim of our study was to investigate whether gene expression patterns of PBMC could complement islet autoantibodies for T1D pathogenic mechanisms in the higlty admixed Brazilian population. Methods: We assessed global gene expression in PBMC from  two groups mached for age, sex and BMI: The T1D group with 20 patients with recent-onset T1D (≤ 6 months from diagnosis, in a time  when the autoimmune process is still highly active), testing positive for one or more  islet autoantibodies and 20 islet autoantibody-negative healthy controls (Control group). more...
#> 87                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 88                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          GDM is a multi-system disorder that is primarily characterised by new-onset hypertension accompanied by proteinuria during gestation. This disease is one of the leading causes of maternal and perinatal morbidity and mortality. In this work, placental samples were collected from GDM and control patients. RNA-seq was performed to identify differences in gene expression. Significantly differentially expressed genes between the GDM and control samples included 64 up-regulated and 296 down-regulated genes. more...
#> 89                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             N6-methyladenosine (m6A) is the most prevalent modification in eukaryotic mRNA and potential regulatory functions of m6A have been shown by mapping the RNA m6A modification landscape. M6A modification in active gene regulation manifests itself as altered methylation profiles. However, the profiling of m6A modification and its potential role in gestational diabetes mellitus (GDM) has not yet been studied. more...
#> 90                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Intervertebral disc degeneration (IDD) is majorly resulted from disordered extracellular matrix (ECM) metabolism, including decreased anabolism and increased catabolism activities in the nucleus pulposus (NP) cells of discs. Pro-inflammatory cytokines such as interleukin-1β (IL-1β) are considered to be potent mediators of ECM loss. We reported previously that hemeoxygenase-1 (HO-1) inducer cobalt protoporphyrin IX (CoPP) could attenuate the ECM breakdown which induced by IL-1β, however, the underlying mechanism remains elusive. more...
#> 91                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Background. Diabetes mellitus (DM) increases tuberculosis (TB) severity. We previously reported baseline blood microarray data in a South Indian pulmonary TB cohort with or without DM, finding no qualitative or quantitative differences in immune pathway gene expression. To extend those observations, we compared baseline and longitudinal blood gene expression in TB patients from South India and Brazil. more...
#> 92                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Introduction.  Epigenetic modifications have been implicated to mediate several complications of diabetes mellitus (DM), especially nephropathy and retinopathy. Our aims were to ascertain if epigenetic alterations in whole blood discriminate among DM patients with normal, delayed and rapid gastric emptying (GE). Methods.  Using ChIP-seq (Chromatin immunoprecipitation combined with next generation sequencing) assays, we compared the genome-wide enrichment of three histone modifications (ie, H3K4me3, H3K9ac and H3K27ac) in buffy coats from 20 DM patients with normal (n=6), delayed (n=8), or rapid (n=6) GE. more...
#> 93                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Type 2 diabetes (T2D) is associated with cardiovascular-renal complications and premature death. Although most patients with T2D are obese, not all obese individuals develop T2D. Thus, an understanding of the mechanistic relationships between obesity and T2D is crucial. In this study, using subcutaneous (SAT) and visceral adipose tissues (VAT) from obese individuals with or without T2D collected during metabolic surgery, integration of the transcriptomes and methylomes of VAT and SAT with publicly available tissue-specific regulatory networks, we discovered the close relation between T2D and inflammatory response in both SAT and VAT in obese individuals, although less differences were observed respectively in transcriptome or methylome. more...
#> 94                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This SuperSeries is composed of the SubSeries listed below.
#> 95                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Purpose:  The goals of this study is to compare and profile the smallRNA transcriptome of the placenta in preeclamptic and normal patients using RNA sequencing. Methods: Placental and Placental vesicles (STB-EVs)  smallRNA profiles of normal and preeclamptic patients were generated by deep sequencing using Illumina HISEQ. FASTq.gz files were compressed with OASIS compressor and alignment was done with OASIS 2.0 ( by trimmimng with trimmomatic, aligning using default OASIS 2.0 aligning papameters). more...
#> 96                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Purpose:  The goals of this study is to compare and profile the transcriptome of the placenta in preeclamptic and normal patients using RNA sequencing. Methods: Placental and Placental vesicles (STB-EVs)  mRNA profiles of normal and preeclamptic patients were generated by deep sequencing using Illumina HISEQ. The sequence reads that passed quality filters were analyzed at the gene level HISAT2 followed by featureCounts. more...
#> 97                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Enteroviruses, particularly the group B Coxsackieviruses have been associated with the development of type 1 diabetes. Several CVB serotypes can establish chronic infection in human cells in vivo and in vitro. However, the mechanisms of leading to enterovirus persistency and, possibly, bell-cell autoimmunity are not fully understood. We established a carrier-state persistent infection model in human pancreatic ductal-like cell line PANC-1 using two distinct CVB1 strains and profiled infection-induced changes in cellular transcriptome. more...
#> 98                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Human islet antigen reactive CD4+ memory T cells (IAR T cells) play a key role in the pathogenesis of autoimmune type 1 diabetes (T1D). Using single cell RNA-sequencing (scRNA-seq) to identify T cell receptors (TCRs) in IAR T cells, we have identified a class of TCRs that share TCR alpha chains between individuals (“public”).
#> 99                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Fungiform papillae (FP) are visible protrusions on the anterior tongue surface that contain taste buds, their nerves, and capillaries, epithelial cells, stromal cells, and immune-surveilling cells. As FP are easily biopsied in a minimally invasive procedure and have been shown to regrow, we compared three different mechanical methods of FP protein extraction and found that mechanical disruption of FP under liquid nitrogen or bead beating were more efficient than mincing in terms of yield and proteomic profile. more...
#> 100                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Fetal progenitor endothelial cells (endothelial colony forming cells; ECFC) are recruited for repair, vascular growth and angiogenesis and their high abundance perinatally suggests a function in postnatal vasculogenesis and angiogenesis. In this study we profiled ECFCs from pregnancies of control, overweight and diabetic mothers to study if adverse pregnancies are associated with epigenetic variation in ECFCs.
#> 101                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The establishment and function of the human placenta is dependent on specialized cells called trophoblasts. Unfortunately, little is known about the cellular and molecular processes controlling human trophoblast stem cell maintenance and differentiation into mature trophoblast sub-populations/cell states. To address this, we here report transcriptomic data from n=7 first trimester human placental tissues, n=3 regenerative human trophoblast stem cell (hTSC) derived trophoblast organoids, and n=3 EVT-differentiated hTSC derived organoid cultures at single-cell resolution. more...
#> 102                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Physical training improves insulin sensitivity and can prevent type 2 diabetes. However, approximately 20% of individuals lack a beneficial outcome in glycemic control. TGF-β, identified as a possible upstream regulator involved in this low response is also a potent regulator of microRNAs (miRs). Aim of this study was to elucidate the potential impact of TGF-β-driven miRNAs on individual exercise response. more...
#> 103                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Physical training improves insulin sensitivity and can prevent type 2 diabetes. However, approximately 20% of individuals lack a beneficial outcome in glycemic control. TGF-β, identified as a possible upstream regulator involved in this low response is also a potent regulator of microRNAs (miRs). Aim of this study was to elucidate the potential impact of TGF-β-driven miRNAs on individual exercise response. more...
#> 104                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Arterial media calcification caused by diabetes is an important cause of vascular calcification. Dipeptidyl peptidase-4 (DPP4) is associated with diabetic arterial media calcification. At the same time, long non-coding RNA(lncRNA) is closely related to the evolution of a variety of cardiovascular diseases, but the involvement of lncRNA in vascular calcification induced by DPP4 has not been reported in details. more...
#> 105                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             MODY8 (maturity-onset diabetes of the young, type 8) is a dominantly inherited monogenic form of diabetes associated with frameshift mutations in the carboxyl ester lipase (CEL) gene expressed by pancreatic acinar cells. Patients carrying the mutation develop childhood-onset exocrine pancreas dysfunction followed by the manifestation of diabetes during adulthood. However, it is unclear how CEL mutations cause diabetes. more...
#> 106                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Currently, no oral medications are available for individuals suffering from type 1 diabetes (T1D). Our randomized placebo-controlled phase 2 trial recently revealed that oral verapamil has short- term beneficial effects in subjects with new-onset type 1 diabetes (T1D) 1. However, what exact biological changes verapamil elicits in humans with T1D, how long they may last, and how to best monitor any associated therapeutic success has remained elusive. more...
#> 107                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           About 20% of youth are obese with higher risk for cardiovascular disease and type 2 diabetes (T2D). We have recently reported that in obese adolescents altered pattern of fat distribution is associated with insulin resistance and T2D. In particular, the high ratio of visceral AT depot (VAT) to abdominal subcutaneous AT depot (SAT) (high VAT/(VAT+SAT)) was associated with a metabolically unhealthy phenotype with high risk for insulin resistance and T2D. more...
#> 108                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 109                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We conducted prospective clinical studies to validate the importance of CD4+ T cells in 13 diseases from the following ICD-10-CM chapters: Neoplasms (breast cancer, chronic lymphocytic leukemia); endocrine, nutritional and metabolic diseases (type I diabetes, obesity); diseases of the circulatory system (atherosclerosis); diseases of the respiratory system (acute tonsillitis, influenza, seasonal allergic rhinitis, asthma); diseases of the digestive system (Crohn’s disease [CD], ulcerative colitis [UC]); and diseases of the skin and subcutaneous tissue (atopic eczema, psoriatic diseases). more...
#> 110                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Salivary exsomal miRNAs may play important role in the pathogenesis of chronic inflammatory disease, such as periodontitis. There are many studies which suggested the connection between periodontitis and systemic disease, however, the role of specific miRNA as a intersection of periontitis and diabetes are not elucidated. We suggested miR-25-3p as possible common mediator in the pathogenesis of periodontitis and diabetes.
#> 111                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Diabetic retinopathy (DR) is a common microvascular complication that may cause severe visual impairment and blindness in patients with type 2 diabetes mellitus (T2DM). Early detection of DR will provide opportunities for more treatment options and better control of disease progression. Effective biomarkers, which are not currently available, may improve clinical outcomes through precise diagnosis and prognosis. more...
#> 112                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 113                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   First-degree relatives (FDRs) of type 2 diabetics (T2D) feature dysfunction of subcutaneous adipose tissue (SAT) long before T2D onset. miRNAs have a role in adipocyte precursor cells (APC) differentiation and in adipocyte identity. Thus, impaired miRNA expression may contribute to SAT dysfunction in FDRs. In the present work, we have explored changes of miRNA expression associated with T2D family history which may affect gene expression in SAT APCs from FDRs. more...
#> 114                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   First-degree relatives (FDRs) of type 2 diabetics (T2D) feature dysfunction of subcutaneous adipose tissue (SAT) long before T2D onset. miRNAs have a role in adipocyte precursor cells (APC) differentiation and in adipocyte identity. Thus, impaired miRNA expression may contribute to SAT dysfunction in FDRs. In the present work, we have explored changes of miRNA expression associated with T2D family history which may affect gene expression in SAT APCs from FDRs. more...
#> 115                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Using next generation RNA sequencing (RNA-seq), this study evaluated the whole transcriptome of subcutaneous (SC) and omental (OM) adipose tissues from patients with gestational diabetes (GD) and healthy matching controls that were collected during cesarean delivery (C-section). Results show a strong separation of the transcriptomic profiles based on anatomical location and reveal specific RNA expression patterns unique to GD patients
#> 116                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 117                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Most obese and insulin resistant individuals do not develop diabetes. This is the result of the capacity of β-cells to adapt and produce enough insulin to cover the needs of the organism. The underlying mechanism of β-cell adaptation in obesity, however, remains unclear. Previous studies have suggested a role for STAT3 in mediating β-cell development and human glucose homeostasis, but little is known about its role in β-cells in obesity. more...
#> 118                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Type 2 diabetes is associated with defective insulin secretion and reduced β-cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of b-cell failure is a key translational question. Here, we reverse-engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic-inflexibility and endocrine-progenitor/stem cell features. more...
#> 119                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Type 2 diabetes is associated with defective insulin secretion and reduced β-cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of b-cell failure is a key translational question. Here, we reverse-engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic-inflexibility and endocrine-progenitor/stem cell features. more...
#> 120                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Type 2 diabetes is associated with defective insulin secretion and reduced β-cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of b-cell failure is a key translational question. Here, we reverse-engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic-inflexibility and endocrine-progenitor/stem cell features. more...
#> 121                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The expression of SEMA3E isoforms changes in mouse circulation with type 1 diabetes. The alterations in the transcriptional profiles of human aortic endothelial cells (HAECs) in response to PCS1 (Processing consensus sequences)-cleaved SEMA3E and PCS1-uncleaved SEMA3E were examined.
#> 122                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Diabetic foot ulcers (DFUs) are a devastating complication of diabetes. In order to identify systemic and local factors associated with DFU healing, we examined the cellular landscape of DFUs by single-cell RNA-seq analysis of foot and forearm skin specimens, as well as PBMC samples, from 10 non-diabetic subjects, and 17 diabetic patients, 11 with, and 6 without DFU. Our analysis shows enrichment of a unique inflammatory fibroblast population in DFU patients with healing wounds. more...
#> 123                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Background: Proliferative diabetic retinopathy (PDR) is hallmarked by the formation of retinal neovascularization (RNV) membranes, which can lead to a tractional retinal detachment, the primary reason for severe vision loss in end-stage disease. The aim of this study was to characterize the molecular and cellular features of RNV in order to unravel potential novel drug treatments for PDR.  Methods: A total of 42 patients undergoing vitrectomy for PDR, macular pucker or macular hole (control patients) were included in this study. more...
#> 124                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Preclinical models of type 1 diabetes mellitus exhibit marked declines in skeletal muscle health including significant impairments in muscle repair. The present study investigated, for the first time, whether muscle repair was altered in young adults with uncomplicated type 1 diabetes (T1D) following damaging exercise.In this cohort study, eighteen physically-active young adults (M=22.1, SEM=0.9 years) with T1D (n, male/female=4/5; MHbA1c= 58, SEMHbA1c=5.9 mmol/mol) and without T1D (n, male/female=4/5) performed 300 unilateral eccentric contractions (90°s-1) of the knee extensors. more...
#> 125                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Diabetic foot ulcers (DFUs) are a devastating complication of diabetes. To better understand the molecular mechanisms and cell types implicated in DFU healing, we used NanoString’s GeoMx Digital Spatial profiling platform on DFU tissue sections and compared gene expression of areas within the same ulcer as well as between patients who in 12 weeks following surgery healed their DFU (Healers, N=2) vs those who did not (Non-Healers, N=2).
#> 126                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 127                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Long non-coding RNAs (lncRNAs) are widely involved in gene transcription regulation and which act as epigenetic modifiers. To determine whether lncRNAs are involved in ischemic stroke (IS), we analyzed the expression profile of lncRNAs and mRNAs in IS. RNA sequencing was performed on the blood of three pairs of IS patients and heathy controls. Differential expression analysis was used to identify differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs). more...
#> 128                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Cardiovascular disease (CVD) is the leading cause of mortality in diabetes mellitus (DM). However, the molecular factors that cause this disproportiona increase in CVD in the DM/chronic kidney disease (CKD) population are still unknown.Human endothelial cells treated with high glucose to mimic DM and with the uremic toxin indoxyl sulfate (IS) to mimic the endothelial injury associated with CKD. Differentially expressed lncRNAs in these conditions were analyzed by RNA sequencing.Lnc-SLC15A1-1 expression was significantly increased upon IS treatment versus high glucose alone.
#> 129                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The pathogenesis of non-alcoholic fatty liver disease is not fully understood. Transcriptomic analysis of a large cohort of 318 patients provides evidence of gene perturbations related to inflammation, complement and coagulation pathways, and tissue remodeling in distinct states of NAFLD.
#> 130                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 N6-methyladnine, which is the most abundant post-transcriptional RNA modification in eukaryotic mRNA, has been proved to be essential in various biological processes and related to numerous diseases. Transcriptome-wide m6A profiling by next generation sequencing is widely used to explore the distributions as well as quantity of m6A modifications. As traditional m6A-seq demands large amount of starting RNA which limited its application to clinical samples, we present a strategy of low input multi-barcode m6A-seq (SLIM-m6A-seq) to realize simplified m6A profiling of mixed clinical samples. more...
#> 131                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Stem cell derived beta-like cells (sBC) carry the promise of providing an abundant source of insulin-producing cells for use in cell replacement therapy for patients with diabetes, potentially allowing widespread implementation of a practical cure. To achieve their clinical promise, sBC need to function comparably to mature adult beta cells, but as yet they display varying degrees of maturity. Indeed, detailed knowledge of the events resulting in human beta cell maturation remains obscure. more...
#> 132                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The goal of this study is to compare RNA-seq of wild-type fibroblasts and patient fibroblasts bearing the m.3243A>G mutatioin. When comparing patient fibroblasts to wild-type ones and using a significance level of false discovery rate (FDR) < 0.05, we identified 3394 transcripts of which 1849 were upregulated and 1545 were downregulated.
#> 133                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Heterozygous human INS gene mutations are known to promote ER stress, leading to β-cell dysfunction and neonatal diabetes. Recent literature challenged the long-standing notion that neonatal diabetes occurs due to ER stress-induced β-cell apoptosis. Importantly, mechanisms of β-cell failure during the disease progression and why the other wild-type (WT) INS allele is unable to function still remain unclear. more...
#> 134                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     The objective of this study is to investigate alveolar bone gene expression in health and diabetes through RNA-sequencing and bioinformatics analysis.
#> 135                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    The mechanisms of obesity and type 2 diabetes (T2D)-associated impaired fracture healing are poorly studied. In a murine model of T2D reflecting both hyperinsulinemia induced by high fat diet (HFD) and insulinopenia induced by treatment with streptozotocin (STZ), we examined bone healing in a tibia cortical bone defect. A delayed bone healing was observed during hyperinsulinemia as newly formed bone was reduced by – 28.4±7.7% and was associated with accumulation of marrow adipocytes at the defect site +124.06±38.71%, and increased density of SCA1+ (+74.99± 29.19%) but not Runx2+osteoprogenitor cells. more...
#> 136                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              BACKGROUND AND AIMS: It is proposed that impaired expansion of subcutaneous adipose tissue (SAT), caused in part by an increase in adipose tissue fibrosis, redirects fatty acids to the liver and other organs, leading to ectopic lipid accumulation and insulin resistance. We therefore evaluated whether a decrease in SAT expandability, assessed by measuring SAT lipogenesis (triglyceride production), and an increase in SAT fibrogenesis (collagen production) are associated with nonalcoholic fatty liver disease (NAFLD) and insulin resistance in people with obesity. more...
#> 137                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Retinal neovascularization is a severe complication of proliferative diabetic retinopathy. We have previously identified that miRNAs is directly involved in the development of retinal neovascularization. Here, we explored the role of miRNAs and its underlying mechanism in modulating angiogenesis.
#> 138                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Background: A previous Phase I study showed that the infusion of autologous Treg cells expanded ex-vivo into recent onset Type 1 Diabetes (T1D) patients had an excellent safety profile, however, the majority of the infused Tregs could no longer be detected in the peripheral blood three months post-infusion (NCT01210664-Treg-T1D Trial). Interleukin-2 (IL-2) is a well-characterized cytokine that has been shown to enhance human Treg cell survival and expansion at low doses in vivo. more...
#> 139                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Developmental alteration in brain wiring that would make it more susceptible to later pathological processes has been suggested as a basis for the occurrence of neurodegenerative diseases, but mechanisms have remained elusive. A recent series of magnetic resonance imaging studies have demonstrated that, in Wolfram syndrome, neurodegenerative processes appear during childhood and adolescence on top of a clinically silent global defect in brain development. more...
#> 140                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The aim of this study is to investigate the impact of the metabolic status on the transcriptome of isolated preadipocytes and in vitro differentiated adipocytes. We identified 38654 transcripts in pancreatic fat cells. We report that preadipocyte differentiation increased the abundance of mRNA levels of proteins related to adipogenesis and lipid metabolism. These changes in the transcriptome were absent or less pronounced in fat cells obtained from patients with prediabetes and type 2 diabetes. more...
#> 141                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Type 2 diabetes is a complex, systemic disease affected by both genetic and environmental factors. Previous research has identified genetic variants associated with type 2 diabetes risk, however gene regulatory changes underlying progression to disease are still largely unknown. We investigated RNA expression changes that occur during diabetes progression using a two-stage approach. In our discovery stage, we compared changes in gene expression using two longitudinally collected blood samples from subjects who transitioned to type 2 diabetes between the time points against those who did not with a novel analytical network approach. more...
#> 142                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Free fatty acids (FFAs) are often stored in lipid droplet (LD) depots for eventual metabolic and/or synthetic use in many cell types, such a muscle, liver, and fat. In pancreatic islets, overt LD accumulation was detected in humans but not mice. LD buildup in islets was principally observed after roughly 11 years of age, increasing throughout adulthood under physiologic conditions, and also enriched in type 2 diabetes. more...
#> 143                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Dysregulation of macrophage populations at the wound site is responsible for the non-healing state of chronic wounds. The molecular mechanisms underlying macrophage dysfunction and its control in diabetes are largely unexplored on an epigenetic level. Here, we report that acetyl histone-H3 (Lys27), an epigenetic mark regulating the macrophage transcriptome, is lost in the hostile tissue microenvironment in diabetes. more...
#> 144                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Permutational analysis of immune landscape reveals advanced immune aging in people with Down syndrome and in people with type 1 diabetes.
#> 145                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Islet-enriched transcription factors (TFs) exert broad control over cellular processes in pancreatic α and β cells and changes in their expression are associated with developmental state and diabetes. However, the implications of heterogeneity in TF expression across islet cell populations are not well understood. To define this TF heterogeneity and its consequences for cellular function, we profiled >40,000 cells from normal human islets by scRNA-seq and stratified α and β cells based on combinatorial TF expression. more...
#> 146                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Purpose: Excess oxidative stress (OS) impairs endothelial function and plays an important role in vascular diseases, diabetes, and neuronal disorders. Several consequences of OS including cell recovery and apoptosis have been described previously. In this study, we report systems model of the temporal dynamics of the oxidative stress response in Human Umbilical Vein Endothelial Cells (HUVECs) and characterize HMOX1 as a master regulator in orchestrating the response to oxidative stress. more...
#> 147                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      ATAC-seq (assay for transposase-accessible chromatin followed by sequencing) is widely used to decode chromatin accessibility. Here we performed high-sensitive ATAC-seq in 9 human liver samples from normal and T2D donors, and identified a set of differentially accessible regions (DARs). DARs were overlapped with publicly available CREs databases and integrated with multi-omics data to identify candidates for further experimental validations. more...
#> 148                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Single nuclei sequencing of grafts developed 14 weeks post transplantation of human embryonic stem cell derived pancreatic progenitors alone (PP) or with rat adipose derived microvessels (PPMV) into the subcutaneous pocket of diabetic (STZ-induced) Scid-beige mice.
#> 149                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 150                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is mainly the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. more...
#> 151                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Persons living with HIV (PLWH) are at increased risk of tuberculosis (TB). HIV-associated TB is mainly the result of recent infection with Mycobacterium tuberculosis (Mtb) followed by rapid progression to disease. Alveolar macrophages (AM) are the first cells of the innate immune system that engage Mtb, but how HIV and antiretroviral therapy (ART) impact on the anti-mycobacterial response of AM is not known. more...
#> 152                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Circular RNA can regulate blood glucose levels by targeting mRNA expression, but the role of circRNA in GDM is still unknown. Therefore, a joint microarray analysis of circRNAs and their targeting mRNAs using the peripheral blood of GDM patients and healthy pregnant women was carried out for the first time. In our study, high-throughput microarray sequencing technique was used to analyze the expression profile of circRNA and transcripts mRNA in the peripheral blood of GDM patients, in order to comprehensively evaluate the role of circRNAs targets and their parents genes in the signal pathways related to the pathogenesis of GDM. more...
#> 153                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To improve the power of mediation in high-throughput studies, here we introduce High-throughput mediation analysis (Hitman), which accounts for direction of mediation and applies empirical Bayesian linear modeling. We apply Hitman in a retrospective, exploratory analysis of the SLIMM-T2D clinical trial in which participants with type 2 diabetes were randomized to Roux-en-Y gastric bypass (RYGB) or nonsurgical diabetes/weight management, and fasting plasma proteome and metabolome were assayed up to 3 years. more...
#> 154                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Congenital generalized lipodystrophy (CGL) is an autosomal recessive disorder characterized by defective adipose tissue, extreme insulin resistance, and early onset of diabetes. There are four types of congenital generalized lipodystrophy based on the causative genetic alterations. The symptoms and the degrees of disease progression are varied among all affected individuals, which might be due to unknown genetic modifiers. more...
#> 155                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 156                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Circadian rhythms are generated by an auto-regulatory feedback loop composed of transcriptional activators and repressors. Disruption of circadian rhythms contributes to Type 2 diabetes (T2D) pathogenesis. We elucidated whether altered circadian rhythmicity of clock genes is associated with metabolic dysfunction in T2D. Transcriptional cycling of core clock genes BMAL1, CLOCK, and PER3 was altered in skeletal muscle from individuals with T2D and this was coupled with reduced number and amplitude of cycling genes and disturbed circadian oxygen consumption. more...
#> 157                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Circadian rhythms are generated by an auto-regulatory feedback loop composed of transcriptional activators and repressors. Disruption of circadian rhythms contributes to Type 2 diabetes (T2D) pathogenesis. We elucidated whether altered circadian rhythmicity of clock genes is associated with metabolic dysfunction in T2D. Transcriptional cycling of core clock genes BMAL1, CLOCK, and PER3 was altered in skeletal muscle from individuals with T2D and this was coupled with reduced number and amplitude of cycling genes and disturbed circadian oxygen consumption. more...
#> 158                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       we apply miRNA sequencing from blood samples of 10 DMED patients and 10 DM controls to study the mechanism of miRNAs action on DMED.
#> 159                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Genome Wides Association Studies (GWAS) have identified tens of thousands of associations between human genetic variation and common disease. The majority of causative variants lie in regulatory elements that are located some distance from their target genes. High resolution chromosome conformation capture (3C) has proven useful for identifying enhancer-promoter interaction. We employed targeted Capture-C at loci with GWAS for severe COVID-19, Type-1 Diabetes (T1D), Ankylosing spondylitis (AS) and red blood cell traits (RBC)
#> 160                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Severe angiopathy is a major driver for diabetes associated secondary complications. Knowledge on underlying mechanisms essential for advanced therapies to attenuate these pathologies is limited. Injection of ABCB5+ stromal precursors (SPs) at the edge of non-healing diabetic wounds in a murine db/db model, closely mirroring human type II diabetes, profoundly accelerates wound closure. Strikingly, enhanced angiogenesis was substantially enforced by the release of the ribonuclease angiogenin from ABCB5+ SPs. more...
#> 161                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Hepatic lipid accumulation is a hallmark of type 2 diabetes (T2D) and associated with hyperinsulinemia, insulin resistance, and hyperphagia. Hepatic synthesis of GABA, catalyzed by GABA-transaminase (GABA-T), is upregulated in obese mice. To assess the role of hepatic GABA production in obesity-induced metabolic and energy dysregulation, we treated mice with two pharmacologic GABA-T inhibitors and also knocked down hepatic GABA-T expression using an antisense oligonucleotide. more...
#> 162                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Dysregulation of glucagon secretion in type 1 diabetes (T1D) involves hypersecretion during postprandial states, but insufficient secretion during hypoglycemia. The sympathetic nervous system regulates glucagon secretion. To investigate islet sympathetic innervation in T1D, sympathetic tyrosine hydroxylase (TH) axons were analyzed in control non-diabetic organ donors, non-diabetic islet autoantibody-positive individuals (AAb), and age-matched persons with T1D. more...
#> 163                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We employed a microarray as a discovery platform to identify the differential gene expressions between hND islets and hT2DM islets. 4805 genes with differential expression (fold change >2) were manifested in hT2DM islets. Inflammatory response and immune response were the mostly upregulated biological processes distinguished betwee hND islets and T2DM islets. Results provided insight into the molecular mechanisms in T2DM.
#> 164                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Epidemiological evidence has identified an association between breast cancer (BC) and systemic dysregulation of glucose metabolism. However, how BC influences glucose homeostasis remains unknown. Here we show that BC-derived extracellular vesicles (EVs) suppress pancreatic endocrine secretion to systemically reset glucose homeostasis. In pancreatic β-cells, miR-122 delivered in BC-derived EVs targets PKM to suppress glycolysis and ATP-dependent insulin exocytosis. more...
#> 165                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Heterozygous mutations in HNF1B in humans result in a multi-system disorder, including pancreatic hypoplasia and diabetes mellitus. The underlying mechanisms that contribute to disease pathogenesis remain largely unknown, partially accounted by the fact that mouse models with heterozygous deletions in Hnf1b do not develop diabetes, in contrast to the phenotypes observed in MODY patients. Here we used a well-controlled human induced pluripotent stem cell pancreatic differentiation model to elucidate the molecular mechanisms underlying HNF1B-associated diabetes and pancreatic hypoplasia. more...
#> 166                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the  effect of body mass index (BMI) which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in BD and BMI interaction remained unclear. more...
#> 167                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the  effect of body mass index (BMI) which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in BD and BMI interaction remained unclear. more...
#> 168                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Background: Tumor stage predicts pancreatic cancer (PDAC) prognosis, but prolonged and short survivals have been described in patients with early-stage tumors. Circulating microRNA (miRNA) are an emerging class of suitable biomarkers for PDAC prognosis. Our aim was to identify whether serum miRNA signatures predict survival of early-stage PDAC. Methods: Se-rum RNA from archival 15 stage I-III PDAC patients and 4 controls was used for miRNAs ex-pression profile (Agilent microarrays). more...
#> 169                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Myometrial biopsies were collected from 31 women undergoing primary cesarean sections and were carefully phenotyped with respect to gestational age (GA), circumstances of labor onset, and clinical status at the start and end of the intervention. Cases were aggregated into groups as follows: Group 1: term birth following spontaneous onset of term labor (TL, n=5); Group 2: term birth by elective cesarean section not in labor (TNL, n=5); Group 3: PTB following spontaneous preterm labor with intact membranes (n=6); Group 4: preterm birth following PPROM (n=8); and Group 5: provider-initiated preterm birth in the absence of active labor contractions, cervical dilation or membrane rupture (n=7). more...
#> 170                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 171                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Background: Cardiovascular disease had a global prevalence of 523 million cases and 18.6 million deaths in 2019.  The current standard for diagnosing coronary artery disease (CAD) is coronary angiography.  Surprisingly, despite well-established clinical indications, up to 40% of the one million invasive cardiac catheterizations return a result of ‘no blockage’.  The present studies employed RNA sequencing of whole blood to identify an RNA signature in patients presenting with a clinical suspicion of CAD. more...
#> 172                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Human pancreatic islets, including insulin secreting beta-cells are a major focus of transplantation strategies aimed at identifying new therapeutic approaches to counteract hyperglycemia in patients with diabetes. Identifying the transcriptomic signature of human islet cells provides insights into regulatory pathways that can be harnessed for planning therapeutic strategies. In this context, single-cell RNA-sequencing (scRNA-seq) has been used mostly in vitro. more...
#> 173                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The objective of this study was to perform a global, non-targeted gene expression analysis by microarray, to understand the immune cell gene regulation at fasting and in response to oral glucose load and how this regulation is different in Asian-Indian men with normal glucose tolerance (NGT) and pre-diabetes (PD). Through observing real-time gene expression changes, this study highlights 1. the importance of acute metabolic challenges like oral glucose load in regulating the immune cell gene expression and function. more...
#> 174                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             In our genome-wide association study, we searched for an association of genetic variants with colorectal cancer, type 1 diabetes, Hodgkin lymphoma and  Diffuse large B-cell lymphoma among Polish population.
#> 175                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Stem and progenitor cells in the adult human pancreas provide an under-explored resource for regenerative medicine. Using micro-manipulation and methylcellulose-containing colony/organoid assays, we identified cells within the human cadaveric exocrine pancreas that fulfill the definition of a stem cell: able to self-renew and differentiate. Exocrine tissues were collected after the isolation of endocrine cells, dissociated into single cells, and plated into a 3-dimensional semisolid medium. We found that some pancreatic ductal cells gave rise to cystic colonies/organoids containing pancreatic duct, acinar, and endocrine lineage cells. These cells self-renewed and expanded approximately 300-fold over 9 weeks. When transplanted into diabetic mice, colonies/organoids lowered blood glucose levels and gave rise to insulin-expressing endocrine cells. Thus, stem/progenitor-like cells capable of self-renewal and differentiation either preexist in the adult human pancreas or readily adapt in culture. more...
#> 176                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Betel-nut consumption is the fourth most common addictive habit  globally and there is good evidence linking the habit to obesity, type 2 diabetes (T2D)  and the metabolic syndrome. The aim of our pilot study was to identify gene expression  relevant to obesity, T2D and the metabolic syndrome using a genome-wide  transcriptomic approach in a human monocyte cell line incubated with arecoline and its  nitrosated products.
#> 177                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Generation of mature cells with stable functional identities is crucial for developing cell-based replacement therapies. Current global efforts to produce insulin-secreting beta-like cells to treat diabetes are hampered by the lack of tools to reliably assess cellular identity. We conducted a thorough single-cell transcriptomics meta-analysis to generate robust genesets defining the identity of human adult alpha-, beta-, gamma- and delta-cells. more...
#> 178                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               This study aimed to analyze the mutated genes of primary and recurrent SSs (PRSSs), to discover whether these sarcomas exhibit some potential mutated genes between primary and recurrent cases Illumina Infinium whole genome genotyping (WGG) arrays are increasingly being applied in cancer genomics to study gene copy number alterations and allele-specific aberrations such as loss-of-heterozygosity (LOH). more...
#> 179                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Purpose: To detect serum exosomal ncRNA profiles of proliferative diabetic retinopathy (PDR) by High-throughput sequencing Methods: serum exosomal non-coding RNA (ncRNA) profiles profiles of PDR and MH were generated by deep sequencing, only in once, using IlluminaHiSeq 3000. After analyzing the base composition and quality of the data, according to the analysis results of the original data, the data were filtered  to remove the joint sequence and the contaminated part, and to remove  low-quality base sequences.If it is paired-ended sequencing data, the filtered data should be further screened to retain the paired sequences and obtain clean data. more...
#> 180                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Four male patients were enrolled for this study in collaboration with the Cardiology Unit of Policlinico Tor Vergata-Fondazione PTV (Rome). We have performed RNA-Sequencing using NextSeq 500 ILLUMINA platform on PBMCs of patients with clinically proven healthy coronary arteries (CTR) and patients with chronic coronary artery disease (CAD) confirmed by coronary angiography. RNA sequencing results showed differentially Altenative Splicing (AS) events and filtering for a statistically significant Splicing-Index Fold-Change≥ ±1.5 (p≤0.05) we observed 113 differentially regulated AS events (24 up and 89 down-regulated) from 86 genes. more...
#> 181                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Skeletal muscle accounts for the largest proportion of human body mass, on average, and is a key tissue in complex diseases and mobility. It is composed of several different cell and muscle fiber types. Here, we optimize single-nucleus ATAC-seq (snATAC-seq) to map skeletal muscle cell-specific chromatin accessibility landscapes in frozen human and rat samples, and single-nucleus RNA-seq (snRNA-seq) to map cell-specific transcriptomes in human. more...
#> 182                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Skeletal muscle accounts for the largest proportion of human body mass, on average, and is a key tissue in complex diseases and mobility. It is composed of several different cell and muscle fiber types. Here, we optimize single-nucleus ATAC-seq (snATAC-seq) to map skeletal muscle cell-specific chromatin accessibility landscapes in frozen human and rat samples, and single-nucleus RNA-seq (snRNA-seq) to map cell-specific transcriptomes in human. more...
#> 183                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 184                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We identified a novel lncRNA DRAIR that is downregulated in CD14+ monocytes from type 2 diabetes relative to controls. Functional studies showed that DRAIR regulates anti-inflammatory genes and its knockdown enhances proinflammatoory phentype of monocytes. To examine mechanisms of DRAIR actions, we performed Chromatin isolation by RNA purification (ChIRP) assays using DRAIR biotinylated tiling oligonucleotides to identify chromatin inding sites in THP-1 monocytes.
#> 185                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Monocyte activation by high glucose and free fatty acids promotes inflammation implicated in vascular complications associated with Type 2 diabetes (T2D). Emerging evidence shows that long non coding RNA (lncRNA)s regulate inflammation, but their  role in  T2D induced monocyte dysfunction is unclear. To examine this, we profiled the transcriptome of CD14+ monocytes from volunteers with T2D and without diabetes (n=5 each) using strand-specific RNA-seq on Illumina HiSeq 2500. more...
#> 186                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Genome wide DNA methylation profiling of cord blood cells obtained from gestational diabetes mellitus (GDM) pregnancies. The Illumina EPIC methylation beadchip array was used to obtain DNA methylation profiles across approximately 850,000 CpG dinucleotide methylation loci in DNA isolated from cord blood. Samples include 165 GDM subjects.
#> 187                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Pancreatic beta cell senescence occurs during the development of Type 1  Diabetes. To model the transcriptional responses of islet cells to DNA damage, we previously developed a human islet culture model in which the DNA damage response and senescence can be induced via double strand-breaks with the agent bleomycin. Here, we report the transcriptome-wide changes in human pancreatic islet cells following bleomycin exposure.
#> 188                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        We investigated  the role of SNO-GNIA2 in HG+oxLDL-induced endothelial inflammation during the development of diabetes-accelerated atherosclerosis and found that SNO-GNAI2 could promote endothelial inflammation through dysregulating Hippo-YAP .  We hypothesized that SNO-GNAI2 induced Hippo-YAP dysfunction through enhancing coupling and activating  G-protein coupling receptors (GPCRs).
#> 189                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We describe an unusual course of Ketosis Prone Diabetes and investigate potential mechanisms using induced pluripotent stem cell technology with high throughput mRNA sequencing and validation of a lecuine sensitive mTOR pathway.
#> 190                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Hyperhomocysteinemia (HHcy) is an established and potent independent risk factor for degenerative diseases, including cardiovascular disease (CVD), Alzheimer disease, type II diabetes mellitus, and chronic kidney disease. HHcy has been shown to inhibit proliferation and promote inflammatory responses in endothelial cells (EC), and impair endothelial function, a hallmark for vascular injury. However, metabolic processes and molecular mechanisms mediating HHcy-induced endothelial injury remains to be elucidated. more...
#> 191                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Hyperhomocysteinemia (HHcy) is an established and potent independent risk factor for degenerative diseases, including cardiovascular disease (CVD), Alzheimer disease, type II diabetes mellitus, and chronic kidney disease. HHcy has been shown to inhibit proliferation and promote inflammatory responses in endothelial cells (EC), and impair endothelial function, a hallmark for vascular injury. However, metabolic processes and molecular mechanisms mediating HHcy-induced endothelial injury remains to be elucidated. more...
#> 192                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The aim of this study was to establish the exosomal miRNA profile across gestation in normal and GDM pregnancies and to determine the signaling pathways associated with the changes in the miRNA profile in GDM.
#> 193                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Purpose: Whole-transcriptome sequencing technology and bioinformatics analysis were applied to systematically analyze the differentially expressed mRNAs, lncRNAs, circRNAs and miRNAs in adipose stem cells (ASCs) from diabetic, old and young patients. Methods: MRNAs, lncRNAs and cirRNAs profiles of adipose stem cells were generated by RNA sequencing, in triplicate, using Illumina HiSeq X Ten . MiRNAs profiles of adipose stem cells were generated by RNA sequencing, in triplicate, using BGISEQ-500. more...
#> 194                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Patients with hypertension alone, hypertension plus controlled diabetes and hypertension plus uncontrolled diabetes, and control patients without these conditions underwent coronary artery bypass grafting surgery. Skeletal muscle biopsy specimens were taken at the beginning ('pre-operative') and at the end ('post-operative') of the surgery.
#> 195                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Skeletal muscle aging is characterized by a progressive decline in muscle mass and function, which is referred to as sarcopenia. Aging is also a primary risk factor for metabolic syndrome (SX), which is a cluster of risk factors for cardiovascular diseases and type 2 diabetes. However, the molecular mechanisms implicated in sarcopenia and changes in muscle proteome associated with SX in elderly men remain unclear. more...
#> 196                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The placenta is a highly heterogeneous organ and is closely related to adverse pregnancy. The previous bulk sequencing of whole tissue  could not show the characteristics of individual cells and the interactions between cells. Here, we select the placental tissues of the gestational diabetes group(GDM), preeclampsia group(PE), advanced age group(GL) and normal control group for single-cell sequencing in order to explain the mechanism of related diseases in more depth.nated spatial and temporal regulation of gene expression in the murine hindlimb determines the identity of mesenchymal progenitors and the development of diversity of musculoskeletal tissues they form. more...
#> 197                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Studies in rodents have shown obesity and aging impair tissue nicotinamide adenine dinucleotide (NAD+) biosynthesis, which contributes to metabolic dysfunction. The availability of nicotinamide mononucleotide (NMN) is an important rate-limiting factor in mammalian NAD+ biosynthesis. We conducted a 10-week, randomized, placebo-controlled, double-blind trial to evaluate the effect of NMN supplementation on metabolic function in 25 postmenopausal women with prediabetes who were overweight/obese. more...
#> 198                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Recent clinical data has suggestedsed a bi-directional relationship  between Coronavirus disease 19 (COVID-19) and diabetes. Here, we showdemonstrateed the detection of SARS-CoV-2 in pancreatic endocrine cells in autopsy samples derived fromof COVID-19 patients. Single cell RNA-seq and immunostaining confirmed that multiple types of pancreatic islet cells can be infected byare susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. more...
#> 199                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 200                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Diabetic Retinopathy (DR) is among the major global causes for vision loss. With the rise in diabetes prevalence, an increase in DR incidence is expected. Current understanding of both the molecular etiology and pathways involved in the initiation and progression of DR is limited. Here we analyzed mRNA and miRNA expression profiles of 80 human post-mortem retinal samples from 80 patients diagnosed with various stages of DR. more...
#> 201                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Diabetic Retinopathy (DR) is among the major global causes for vision loss. With the rise in diabetes prevalence, an increase in DR incidence is expected. Current understanding of both the molecular etiology and pathways involved in the initiation and progression of DR is limited. Here we analyzed mRNA and miRNA expression profiles of 80 human post-mortem retinal samples from 80 patients diagnosed with various stages of DR. more...
#> 202                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             By functionally dissecting  densest enhancer cluster in the gene desert at 9P21 locus, we identified a non-redundant inter-dependent enhancer network that functions over long distances, the perturbation in any enhancer in the network results in the complete collapse of entire enhancer cluster and target genes activity. The enhancer network can be targeted to regulate INK4a/ARF locus in associated pathophysiologies and cancers.
#> 203                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          To gain insight into the history of islet cell deterioration along the progression from normal glycemic regulation to T2D, we collected surgical pancreatic tissue samples from 133 metabolically phenotyped pancreatectomized patients (PPP). Gene expression profiles of islets isolated by laser capture microdissection (LCM) from resected and snap-frozen pancreas samples were assessed by RNA sequencing.
#> 204                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 205                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          High blood levels of free fatty acids link obesity with type-2 diabetes, but this connection remains poorly understood. We have investigated lipolysis and glucose homeostasis in recently diagnosed obese type-2 diabetics; in obese insulin resistant non-diabetic subjects (obese-IR) matched for age, sex, body composition and fasting insulin levels; and in healthy lean individuals. Our results show that obese-IR dissociate lipolysis from glycemic control, revealing that the action of compensatory hyperinsulinemia on blood glucose is not mediated by reduced lipolysis. more...
#> 206                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            In a randomized controlled trial, 82 older adults (>65y) with (or at risk of) undernutrition (n=82) were randomly allocated to 12 weeks of supplementation with a novel supplement (586 kcal, 22 g protein of which 50% whey and 50% casein, 206 mg ursolic acid, 7 g free BCAAs, 11 µg vitamin D) or standard care (600 kcal, 24g protein of which 100% casein, 4 µg vitamin D). Body weight increased significantly in the 12 weeks, both in the intervention group (+1.6 ± 0.2 kg, p<.0001) and in the standard care group (+1.8 ± 0.2 kg, p<.0001). more...
#> 207                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Despite the central role of chromosomal context in gene transcription, human noncoding DNA variants are generally studied outside of their endogenous genomic location. This limits our understanding of disease-causing regulatory variants. INS promoter mutations cause recessive neonatal diabetes. We studied 60 patients with such mutations, and show that all single base mutations disrupt a CC dinucleotide, while none affect elements important for INS promoter function in episomal assays. more...
#> 208                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Our transcriptomic phenotyping of pancreatic cell types provides novel insights into pancreas biology, as well as the initial pathogenic events in T1D.
#> 209                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 210                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 A multi-omic approach in a clinical experimental study identified circulating biomarkers reflecting glucocorticoid exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study. more...
#> 211                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 A multi-omic approach in a clinical experimental study identified circulating biomarkers reflecting glucocorticoid exposure. Background: Endogenous glucocorticoids (GC) are mechanistically linked to common diseases and are important as drugs in the treatment of many disorders. There is no marker that can measure and quantify GC action. Our aim was to identify circulating biomarkers of GC action using a clinical experimental study. more...
#> 212                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Type 2 diabetes mellitus is mainly affected by genetic and environmental factors, and long noncoding RNAs (lncRNAs) have been shown to be correlated with diabetes.LncRNA is expected to be a target for the treatment and prediction of type 2 diabetes. We used microarrays to detail the lncRNAs and mRNAs expression in type 2 diabetes patients and healthy controls and obtained differentially expressed genes. more...
#> 213                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Over 90% of disease associated single nucleotide polymorphisms (SNPs) identified by genome wide association studies (GWAS) are noncoding variants. Platform to efficiently validate the biological function of variants thus discovered remain distinctly lacking. Here, we used β-like cells derived from isogenic human pluripotent stem cells (hPSCs), carrying the type 1 diabetes (T1D)-associated noncoding SNP rs2542151T>G or the knockout of the SNP-associated gene PTPN2−/−, to systematically examine the role of the T1D associated noncoding variant in β cell function and survival. more...
#> 214                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Glucocorticoids are key regulators of glucose homeostasis and pancreatic islet function. In this study we used ATAC-seq and RNA-seq to map chromatin accessibility and gene expression from eleven primary human islet samples cultured in vitro with the glucocorticoid dexamethasone at multiple doses and durations. We identified thousands of accessible chromatin sites and genes with significant changes in activity in response to glucocorticoids. more...
#> 215                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The objective of this study was to investigate whether placental exosomes in gestational diabetes mellitus (GDM) carries a specific set of miRNAs associated with skeletal muscle insulin sensitivity. Exosomes were isolated from chorionic villi-conditioned media and plasma from normal and GDM pregnancies. A specific set of miRNAs was identified to be selectively enriched within exosomes when compared to their cells of origin indicating specific packaging of miRNAs into exosomes. more...
#> 216                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The aging of pancreatic beta-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging beta-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to beta-cell failure. Herein, we defined the beta-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from human senescent beta-cells. more...
#> 217                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Genetic risk variants identified in genome-wide association studies (GWAS) of complex disease are primarily non-coding, and translating risk variants into mechanistic insight requires detailed gene regulatory maps in disease-relevant cell types. Here, we combined a GWAS of type 1 diabetes (T1D) in 520,580 samples with candidate cis-regulatory elements (cCREs) in pancreas and peripheral blood mononuclear cell types defined using single nucleus ATAC-seq (snATAC-seq) of 131,554 nuclei. more...
#> 218                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Obesity is a major risk factor for a high number of secondary diseases, including cancer. Specific insights into the role of gender differences and secondary co-morbidities, such as type 2 diabetes (T2D) and cancer risk, are yet to be fully obtained. The aim of this study is thus to find a correlation between the transcriptional deregulation present in the subcutaneous adipose tissue of obese patients and the risk of cancer, in the presence of T2D, and considering gender differences. more...
#> 219                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 220                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Introduction. Hindered by a limited understanding of the molecular mechanisms responsible for diabetic gastroenteropathy (DGE), patients are managed by symptom-based therapies.  We investigated the duodenal mucosal expression of protein-coding genes and miRNAs in DGE and related these abnormalities to clinical features. Methods. mRNA and micro RNA (miRNA) expression and ultrastructure of duodenal mucosal biopsies were investigated in 39 DGE patients and 21 healthy controls. more...
#> 221                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Introduction. Hindered by a limited understanding of the molecular mechanisms responsible for diabetic gastroenteropathy (DGE), patients are managed by symptom-based therapies.  We investigated the duodenal mucosal expression of protein-coding genes and miRNAs in DGE and related these abnormalities to clinical features. Methods. mRNA and micro RNA (miRNA) expression and ultrastructure of duodenal mucosal biopsies were investigated in 39 DGE patients and 21 healthy controls. more...
#> 222                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 223                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           This study was designed to simulate the effect of hyperglycemia on the proximal tubule.  This portion of the kidney is responsible for reabsorption of the filtered glucose, and thus, the amount reabsorbed is not regulated by insulin.  A long-term exposure was designed to model aspects of renal demise seen in diabetes.  We utilized mortal cultures of human renal tubule epithelial cells isolated from renal cortical tissue. more...
#> 224                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The association between T2 DM and BMSCs osteogenic differentiation has been documented in experimental settings. We examine miRNA expression specific for BMSCs from human jaw in Type 2 diabetics.
#> 225                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Single-cell RNAseq (10x Genomics) analysis of human CD4+ T cells in IPEX patients, healthy donors and heterozygous mothers (blood). Human CD4+T cells from IPEX, HD and mothers were isolated from frozen peripheral blood mononuclear cells by flow cytometry as DAPI–CD3+CD4+ cells. In cohort 1, cells from separate donor were encapsulated in separate channel following 10x Genomics Single Cell 3′ Reagent Kit (V2 chemistry). more...
#> 226                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Mitochondrial respiration and gene expression related to mitochondrial function were measured from the peripheral blood of infection and sepsis patients as well as healthy controls
#> 227                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Despite reduced function and volume of the exocrine pancreas in type 1 diabetes, literature describing the histology and the molecular biological profile in this area is limited. Here, the density of acinar cells was examined adjacent to and at varying distances from islets and the transcriptome was analyzed on laser capture microdissected (LCM) tissue from organ donors with and without type 1 diabetes. more...
#> 228                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Islet function diminishes with age and as such the incidence of type 2 diabetes increases. The cause of this is unknown. In this study whole islets were extracted with laser capture microdissection from organ donors 1-81 years of age. Increasing age was associated with a downregulation of pathways associated with the cell cycle and increase in markers of senescence e.g. CDKN2A. Among novel genes increasing with age was SPP1.
#> 229                                                                                         Aims/hypothesis: Recurrent hypoglycaemia (RH) is a major side-effect of intensive insulin therapy for people with diabetes. Changes in hypoglycaemia sensing by the brain contribute to the development of impaired counterregulatory responses to and awareness of hypoglycaemia. Little is known about the intrinsic changes in human astrocytes in response to acute and recurrent low glucose (RLG) exposure.  Methods: Human primary astrocytes (HPA) were exposed to zero, one, three or four bouts of low glucose (0.1 mmol/l) for three hours per day for four days to mimic RH.  On the fourth day, DNA and RNA were collected. Differential gene expression and ontology analyses were performed using DESeq2 and GOseq respectively. DNA methylation was assessed using the Infinium MethylationEPIC BeadChip platform.  Results: 24 differentially expressed genes (DEGs) were detected (after correction for multiple comparisons). One bout of low glucose exposure had the largest effect on gene expression. Pathway analyses revealed that endoplasmic-reticulum (ER) stress-related genes such as HSPA5, XBP1, and MANF, involved in the unfolded protein response (UPR), were all significantly increased following LG exposure, which was diminished following RLG. There was little correlation between differentially methylated positions and changes in gene expression yet the number of bouts of LG exposure produced distinct methylation signatures.  Conclusions/interpretation: These data suggest that exposure of human astrocytes to transient LG triggers activation of genes involved in the UPR linked to endoplasmic reticulum (ER) stress. Following RLG, the activation of UPR related genes was diminished, suggesting attenuated ER stress. This may be mediated by metabolic adaptations to better preserve intracellular and/or ER ATP levels, but this requires further investigation.
#> 230                                                                                         Aims/hypothesis: Recurrent hypoglycaemia (RH) is a major side-effect of intensive insulin therapy for people with diabetes. Changes in hypoglycaemia sensing by the brain contribute to the development of impaired counterregulatory responses to and awareness of hypoglycaemia. Little is known about the intrinsic changes in human astrocytes in response to acute and recurrent low glucose (RLG) exposure.  Methods: Human primary astrocytes (HPA) were exposed to zero, one, three or four bouts of low glucose (0.1 mmol/l) for three hours per day for four days to mimic RH.  On the fourth day, DNA and RNA were collected. Differential gene expression and ontology analyses were performed using DESeq2 and GOseq respectively. DNA methylation was assessed using the Infinium MethylationEPIC BeadChip platform.  Results: 24 differentially expressed genes (DEGs) were detected (after correction for multiple comparisons). One bout of low glucose exposure had the largest effect on gene expression. Pathway analyses revealed that endoplasmic-reticulum (ER) stress-related genes such as HSPA5, XBP1, and MANF, involved in the unfolded protein response (UPR), were all significantly increased following LG exposure, which was diminished following RLG. There was little correlation between differentially methylated positions and changes in gene expression yet the number of bouts of LG exposure produced distinct methylation signatures.  Conclusions/interpretation: These data suggest that exposure of human astrocytes to transient LG triggers activation of genes involved in the UPR linked to endoplasmic reticulum (ER) stress. Following RLG, the activation of UPR related genes was diminished, suggesting attenuated ER stress. This may be mediated by metabolic adaptations to better preserve intracellular and/or ER ATP levels, but this requires further investigation.
#> 231                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               DNA methylation data throughout human muscle cell differentiation in n=14 individuals with type 2 diabetes and n=14 controls
#> 232                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             DNA methylation data for both proliferating myoblasts and differentiated myotubes from n=14 individuals with type 2 diabetes and n=14 controls
#> 233                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               mRNA expression data throughout human muscle cell differentiation in n=13 individuals with type 2 diabetes and n=13 controls
#> 234                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             mRNA expression data for both proliferating myoblasts and differentiated myotubes from n=13 individuals with type 2 diabetes and n=13 controls
#> 235                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 236                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Preterm or small for gestational age (SGA) infants are to be at high risk of noncommunicable diseases in adolescence, because they are exposed to hypoxia and malnutrition in and ex utero during perinatal period. Epigenetics could be one of the most important mechanisms of DOHaD.In the field of premature babies, previous studies investigated the methylation alterations related to gestational age and birthweight by using cord blood samples. more...
#> 237                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               We profiled scRNA-seq of 284 samples collected from 196 individuals, including 22 patients with mild/moderate symptoms, 54 hospitalized patients with severe symptoms, and 95 recovered convalescent persons, as well as 25 healthy controls. The samples were obtained from various tissue types, including human peripheral blood mononuclear cells (249), bronchoalveolar lavage fluid (12) and pleural pleural effusion (1)/sputum (22).
#> 238                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We performed single cell transcriptomic analysis on 17 urine samples obtained from five subjects at two different occasions using both spot and 24-hour urine collection. In addition, we used a combined spot urine samples of five healthy individuals as a control sample. We sequenced a total of 71,667 cells. After quality control and downstream analysis, we found that epithelial cells were the most common cell types in the urine. more...
#> 239                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We performed RNA-sequencing in uninfected, SARS-CoV-2-infected, and additionally remdesivir treated ex vivo cultured human islets from two donors to shed light on the transcriptional changes occurring upon viral infection.
#> 240                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Previously, we developed a new model of diabetes-induced wound healing impairment in skin-humanized mice models that faithfully recapitulates the major histo-physiological features of such skin repair-deficient condition. Aiming to dissect the molecular mechanisms responsible for the delayed wound closure, global gene expression studies were performed.
#> 241                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 242                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Genome wide DNA Methylation in fetal cord blood and placenta from mother with GDM compared to mother with normal glucose tolerance
#> 243                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Genome wide DNA Methylation in fetal cord blood and placenta from mother with GDM compared to mother with normal glucose tolerance
#> 244                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Genetic variants associated with type 2 diabetes (T2D) risk affect gene regulation in metabolically relevant tissues, such as pancreatic islets. Here, we investigated contributions of regulatory programs active during pancreatic development to T2D risk. Interrogation of chromatin maps from developmental precursors throughout pancreatic differentiation of human embryonic stem cells (hESCs) identifies enrichment of T2D variants in pancreatic progenitor-specific stretch enhancers that are not active in islets. more...
#> 245                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            The increased usage of alternative Ayurvedic treatments as potential health-beneficial therapies emphasizes the importance of studying its efficacy in sound placebo-controlled intervention trials. An example of such a traditional Ayurvedic herbal preparation is Mohana Choorna, a mixture composed of 20 different herbs and used to prevent and treat type 2-diabetes (T2D). We studied the efficacy of “Mohana Choorna” on T2D-related parameters in subjects with impaired glucose tol-erance. more...
#> 246                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Single-nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq) creates new opportunities to dissect cell type-specific mechanisms of complex diseases. Since pancreatic islets are central to type 2 diabetes (T2D), we profiled 15,298 islet cells by using combinatorial barcoding snATAC-seq and identified 12 clusters, including multiple alpha, beta and delta cell states. We cataloged 228,873 accessible chromatin sites and identified transcription factors underlying lineage- and state-specific regulation. more...
#> 247                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Single-nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq) creates new opportunities to dissect cell type-specific mechanisms of complex diseases. Since pancreatic islets are central to type 2 diabetes (T2D), we profiled 15,298 islet cells by using combinatorial barcoding snATAC-seq and identified 12 clusters, including multiple alpha, beta and delta cell states. We cataloged 228,873 accessible chromatin sites and identified transcription factors underlying lineage- and state-specific regulation. more...
#> 248                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Single-nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq) creates new opportunities to dissect cell type-specific mechanisms of complex diseases. Since pancreatic islets are central to type 2 diabetes (T2D), we profiled 15,298 islet cells by using combinatorial barcoding snATAC-seq and identified 12 clusters, including multiple alpha, beta and delta cell states. We cataloged 228,873 accessible chromatin sites and identified transcription factors underlying lineage- and state-specific regulation. more...
#> 249                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Single-nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq) creates new opportunities to dissect cell type–specific mechanisms of complex diseases. Since pancreatic islets are central to type 2 diabetes (T2D), we profiled 15,298 islet cells by using combinatorial barcoding snATAC-seq and identified 12 clusters, including multiple alpha, beta and delta cell states. We cataloged 228,873 accessible chromatin sites and identified transcription factors underlying lineage- and state-specific regulation. more...
#> 250                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Type 2 diabetes mellitus (T2D), characterised by peripheral insulin resistance, is a risk factor for dementia. In addition to its contribution to small and large vessel disease, T2D may directly damage cells of the brain neurovascular unit. In this study, we investigated the transcriptomic changes in cortical neurones, and associated astrocytes and endothelial cells of the neurovascular unit, in the ageing brain
#> 251                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            It has been well established that the presence of diabetes is accompanied by a chronic inflammatory state promoting various diabetes-associated complications. One potential driver of this enhanced inflammatory state in patients with diabetes is hyperglycemia. Even after blood glucose control is achieved, diabetes-associated complications persist, suggesting the presence of a “hyperglycemic memory.” Innate immune cells, critically involved in various complications associated with diabetes, can build nonspecific, immunological memory (trained immunity) via epigenetic regulation. more...
#> 252                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Adipose tissue is found throughout the human body. The diversity of physiological specialization of fat depots is reflected in the depot-specific alterations seen in lipodystrophies and links between specific patterns of fat distribution and susceptibility to diseases, including Type II Diabetes. We compared gene expression patterns in seven anatomically diverse fat depots and in adipocytes and stromal-vascular cells isolated from each sample. more...
#> 253                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We report the high-throughput miRNA sequencing of plasma isolated from human patients with type 2 diabetes & gastroparesis, idiopathic gastroparesis alone, and healthy control patients.
#> 254                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Pericardial sac surrounding the heart contains pericardial fluid (PF), which is rich in exosomes. PF exosomes increase angiogenesis in hypoxic endothelial cells and in animal model of hindlimb ischemia by passing the proangiogenic miRNAs to recipient cells. However, under pathological conditions such as diabetes, exosome cargo composition changes and harmful miRNAs can be transferred to the recipient cells and induce more deleterious effects in target tissues. more...
#> 255                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Improving the early diagnosis and treatment of type 2 diabetes (T2D) can effectively control blood glucose. To investigate new long non-coding RNAs (lncRNAs) as molecular markers we used microarrays to identify differentially expressed lncRNAs and mRNAs in peripheral blood mononuclear cells from T2D patients and controls.
#> 256                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Glucagon-like peptide-1 (GLP-1) is an incretin hormone that potentiates glucose  stimulated insulin secretion. GLP-1 is classically produced by gut L cells; however, under  certain circumstances alpha-cells can express the prohormone convertase required for  proglucagon processing to GLP-1, prohormone convertase 1/3 (PC1/3), and can produce  GLP-1. However, the mechanisms through which this occurs are poorly defined. more...
#> 257                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 258                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      The downregulation of diabetes susceptibility gene GLIS3 contributes to pancreatic beta cell demise, at least in part, through downregulation of the  splicing factor SRSF6. Here, we used individual-nucleotide UV crosslinking and immunoprecipitation (iCLIP)  to map the RNA binding landscape of SRSF6 in pancreatic beta cells.
#> 259                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              The gene expression signature of the human kidney interstitium is not fully understood. Transcript expression of laser microdissected cortical interstitium (excluding tubules, glomeruli and large vessels) in 9 human reference nephrectomies was compared to 6 human diabetic kidney biopsy specimens. This transcriptomic data revealed novel interstitial markers and enrichment of relevant pathways. Analysis of diabetic interstitium uncovered genes with unchanged as well as down-regulated expression when compared to reference samples. more...
#> 260                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Glycemic control is a strong predictor of long-term cardiovascular risk in patients with diabetes mellitus, and poor glycemic control influences long-term risk of cardiovascular disease even decades after optimal medical management. This phenomenon, termed glycemic memory, has been proposed to occur due to stable programs of cardiac and endothelial cell gene expression. This transcriptional remodeling has been shown to occur in the vascular endothelium through a yet undefined mechanism of cellular reprogramming. more...
#> 261                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Bulk RNA-sequencing of sorted CD8 T cells from recent-onset T1D subjects treated with alefacept.
#> 262                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Idiopathic nodular mesangial sclerosis, also called idiopathic nodular glomerulosclerosis (ING) is a rare clinical entity with unclear pathogenesis. The hallmark of this disease is the presence of nodular mesangial sclerosis on histology without clinical evidence of diabetes mellitus or other predisposing diagnoses. To achieve insights into its pathogenesis, we queried the clinical, histopathologic and transcriptomic features of ING and nodular diabetic nephropathy (DN)
#> 263                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Comparative genomic hybridization analysis for detection of recurring gene copy number variation (CNV) among a set of lung cancer mestastatic brain tumors DNA was isolated and analyzed in a two-color experiment using Cancer CGH+SNP 180Kx4 arrays from Agilent and Agilent SureScan system: Cy5-labeled specimen DNA and Cy3-labeled Agilent characterized normal human reference DNA
#> 264                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is one of the leading causes of cancer-related deaths worldwide. The multi‐target inhibitor sorafenib is a first-line treatment for patients with advanced unresectable HCC. Recent clinical studies have evidenced that patients treated with sorafenib together with the anti-diabetic drug metformin have a survival disadvantage compared to patients receiving sorafenib only. more...
#> 265                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Women with diabetes have a higher prevalence of cardiovascular complications than men, suggesting that sex-steroid hormones like estrogen may impact on female health in diabetes. Here we demonstrate that estrogen suppletion and insulin resistance in male-to-female transgenders coincides with lower plasma levels of miR-224 and miR-452 carried in extracellular vesicles. Systemic silencing of miR-224 and miR-452 in mice triggered a prediabetic phenotype with higher plasma insulin levels, increased white adipose lipogenesis and less glucose uptake and mitochondrial respiration in brown adipose tissue. more...
#> 266                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           This study aimed to examine the postprandial transcriptome of adipose tissue middle-aged men selectively recruited on the basis of MetS (defined by the International Diabetes Federation (IDF) criteria) and healthy control participants. Two breakfast meals that provided different macronutrient composition, and were indicative of major patterns of dietary habits (animal-based versus plant-based) were given, postprandial adipose gene expression was measured by microarray at fasting (0 h) and 4 hours post-meal.
#> 267                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Transcriptional profiling of human PBMCs comparing healthy controls, patients with diabetic nephropathy and patients with ESRD. PBMCs were analyzed as they mediate inflammatory injury. Goal was to determine effects of increasing severity of diabetic nephropathy on global PBMC gene expression. Microarray analysis of PBMCs taken from patients with varying degrees of diabetic nephropathy.
#> 268                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            We previously reported a child with transient neonatal diabetes mellitus (TNDM), who upon molecular diagnosis was homozygous for a one base-pair deletion in ZFP57, inheriting the mutations from both heterozygous parents. Methylation profiling at diagnosis revealed severe hypomethylation at PLAGL1 and mosaic loss-of-methylation (LOM) at GRB10, NAP1L5 and GNAS-XL DMRs.  Some years after the first child, a second sibling was born with a comparable clinical presentation. more...
#> 269                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Understanding the process of immune remodeling and regulation in SARS-CoV-2 infected patients from hospitalization to rehabilitation is crucial for therapy of patients with COVID-19. Here, we performed a longitudinal whole-transcriptome RNA sequencing on peripheral blood mononuclear cell (PBMC) samples of 18 patients with mild, moderate or severe COVID-19 symptoms during the treatment, convalescence and rehabilitation stages. more...
#> 270                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Maternal metabolic disorders such as obesity and diabetes are detrimental factors that compromise fertility and the success rates of medically assisted procreation (MAP) procedures. During metabolic stress, adipose tissue is more likely to release free fatty acids (FFA) in the serum resulting in an increase of FFA levels not only in blood, but also in follicular fluid (FF). In humans, high concentrations of palmitic acid (PA) and stearic acid (SA) reduced granulosa cell survival and were associated with poor cumulus-oocyte complex (COC) morphology. more...
#> 271                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The aim of this study was therefore to investigate molecular mechanisms associated with insulin sensitivity in skeletal muscle by relating global skeletal muscle gene expression with a surrogate measure of insulin sensitivity, i.e. homeostatic model assessment of insulin resistance (HOMA-IR). To identify genes with skeletal muscle expression related to insulin sensitivity, we obtained muscle biopsies from 38 non-diabetic participants in study A. more...
#> 272                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We studied 9 healthy young non-diabetic men without any family history of diabetes. The mean age and body mass index (BMI) were 25.33 ± 0.33 years and 24.57 ± 0.62 kg/m2, respectively, and the mean 1/ homeostatic model assessment of insulin resistance (HOMA-IR) was 1.17 ± 0.12. We included baseline gene expression profile data (i.e. only before bed rest)
#> 273                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To identify genes correlated to insulin sensitivity in skeletal muscle, we studied 38 non-diabetic men from Malmö, Sweden. Briefly, the Malmö Exercise Intervention cohort consists of sedentary but otherwise healthy male subjects from southern Sweden. They all have European ancestry and 18 of them have a first-degree family member with T2D. The mean age and body mass index (BMI) were 37.71 ± 0.71 years and 28.47 ± 0.48 kg/m2, respectively, and the mean 1/the homeostatic model assessment-insulin resistance (HOMA-IR) was 0.69 ± 0.04
#> 274                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         The mechanisms underlying Roux-en-Y gastric bypass (RYGB) surgery-induced weight loss and the immediate postoperative beneficial metabolic effects associated with the operation remain uncertain. We aimed to identify novel gut-derived peptides with therapeutic potential in obesity and/or diabetes by determining genome-wide expression patterns in isolated human small intestinal enteroendocrine cells (EECs) obtained from 20 obese subjects undergoing RYGB and again three months later by upper enteroscopy. more...
#> 275                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             RNA-seq data of monocyte-derived human Dendritic cells (huDCs) cultured with PSAB-liposomes and/or Liraglutide
#> 276                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Genome-wide DNA methylation profiling of umbilical cord blood buffy coat DNA samples. The Illumina Infinium MethylationEPIC array was used to obtain DNA methylation profiles across approximately 850,000 CpGs. Samples included 557 cord blood samples born to obese women in the UPBEAT trial, with and without gestational diabetes mellitus (GDM), to determine the association between maternal GDM and hyperglycaemia during pregnancy on the methylation in the infant.
#> 277                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 278                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We report novel epigenetic mechanisms of epigenetic memory and its role in regulation of transporter genes in diabetic renal proximal tubules. We have generated RNA-seq, ATAC-seq and Infinium EPIC methylation array datasets from human primary proximal tubule epithelial cells from non-diabetic healthy controls and from patients with history of Type II Diabetes.
#> 279                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We report novel epigenetic mechanisms of epigenetic memory and its role in regulation of transporter genes in diabetic renal proximal tubules. We have generated RNA-seq, ATAC-seq and Infinium EPIC methylation array datasets from human primary proximal tubule epithelial cells from non-diabetic healthy controls and from patients with history of Type II Diabetes. Analyses of RNA-seq, ATAC-seq and Methylaiton EPIC array data.
#> 280                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Deglycosylated-leucine-rich α-2-glycoprotein1 (DG-LRG1) as well as LRG1 was discovered to promote angiogenesis under diabetes mellitus condition through TGF-β independent binding to endoglin. To examine the signaling pathways triggered by DG-LRG1, we subjected whole-cell protein lysates of control and DG-LRG1 treated HUVECs to a Phospho Explorer antibody array analysis using commercial antibody array assay kit (Full Moon Biosystems, Inc.). more...
#> 281                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Pancreatic β-cell failure is key to type 2 diabetes (T2D) onset and progression. We assessed whether human β-cell dysfunction induced by metabolic stress is reversible, evaluated the molecular pathways underlying persistent or transient damage, and explored the relationships with T2D islet traits. Twenty-six human islet preparations were exposed to several lipo- and/or glucotoxicity conditions, some of which impaired insulin release depending on stressor type, concentration and combination. more...
#> 282                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Persons with HIV have a disproportionate burden of metabolic disease, including type 2 diabetes. We hypothesized that the accumulation of chronically activated T cells in the adipose tissue of HIV+ persons is a central mechanism promoting local macrophage activation, impaired adipocyte function, and the development of HIV-associated glucose intolerance. Prior studies of immune activation and HIV-associated metabolic disease have only measured circulating T cell subsets. more...
#> 283                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 284                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Although analysis of maternal plasma cell-free content has been employed for screening of genetic abnormalities within a pregnancy, limited attention has been paid to its use for the detection of adverse pregnancy outcomes (APOs) based on placental function. We investigated the cell-free RNA content of 102 maternal, 25 cord plasma samples and 7 non pregnant women as control. using cell-free RNA sequencing, APOs revealed seventy-one differentially expressed genes early in pregnancy. more...
#> 285                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Although analysis of maternal plasma cell-free content has been employed for screening of genetic abnormalities within a pregnancy, limited attention has been paid to its use for the detection of adverse pregnancy outcomes (APOs) based on placental function. Here we investigated cell-free DNA and RNA content of 102 maternal and 25 cord plasma samples. Employing a novel deconvolution methodology, we found that during the first trimester, placenta-specific DNA increased prior to the subsequent development of gestational diabetes with no change in patients with preeclampsia while decreasing with maternal obesity. more...
#> 286                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Obesity and type 2 diabetes (T2D) can be associated with altered secretion of enterohormones in condition that remains to be understood in depth. Here, we aimed to decipher the mechanisms by which a major enterohormone GLP-1, is decreased in human obese patients according to their diabetic status.
#> 287                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Metformin is a classic type II diabetes drug which has possessed anti-tumor properties for various cancers. However, different cancers do not respond to metformin with the same effectiveness or acquire resistance. Thus, searching for vulnerabilities of metformin-resistant prostate cancer is a promising strategy to improve the therapeutic efficiency. A genome-scale CRISPR-Cas9 activation library targeting 23430 genes is conducted to identify the genes that confer resistance to metformin in prostate cancer cells.
#> 288                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Diabetes mellitus is associated with serious long-term complications, including increased cardiovascular risk and a higher occurrence of infections. These diabetes-related complications are suggestive of altered responses of the innate immune system. Recent studies have shown that energy metabolism of monocytes is a crucial determinant of their functionality. Here we investigate whether metabolism and function of monocytes are changed in patients with diabetes and aim to identify diabetes-associated factors driving these alterations. more...
#> 289                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Dedifferentiation of pancreatic beta cells may reduce islet function in type 2 diabetes (T2D). However, the prevalence, plasticity and functional consequences of this cellular state remain unknown.  We employed single-cell RNAseq to detail the maturation program of alpha and beta cells during human ontogeny. We show that although both alpha and beta cells mature in part by repressing non-endocrine genes, alpha-cells retain hallmarks of an immature state, while beta-cells attain a full beta-cell specific gene expression program. more...
#> 290                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             In vitro differentiation of human ES cells into insulin-producing β-like cells offers new opportunities for pancreatic development modeling and potential diabetes therapy. However, the precise molecular events associated with this multi-stage process remain unclear. Here, we generated 95,308 single cell transcriptome data encompassing the entire differentiation process, and reconstructed a tree delineating the fate choices of all major cell populations in both endocrine and non-endocrine lineages. more...
#> 291                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Type 1 diabetes (T1D) is characterized by immune mediated destruction of insulin producing β cells. Biomarkers capable of identifying T1D risk and dissecting disease-related heterogeneity represent an unmet clinical need. Aims: Towards the goal of informing T1D biomarker strategies, we profiled different classes of RNAs in human islet-derived exosomes and identified RNAs that were differentially expressed under cytokine stress conditions. more...
#> 292                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We performed RNA-seq on tissue biopsies derived from patients with DFUs and compared it to human oral and skin wounds to identify the molecular mechanisms and transcriptional networks that are deregulated in DFUs. Our results identified a unique inflammatory transcriptional signature unique to oral and skin wounds involved in promoting cell proliferation and cell survival of immune cells that are deficient in DFUs. more...
#> 293                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Immune responses in lungs of Coronavirus Disease 2019 (COVID-19) are poorly characterized. We conducted transcriptomic, histologic and cellular profiling of post mortem COVID-19 and normal lung tissues. Two distinct immunopathological reaction patterns were identified. One pattern showed high expression of interferon stimulated genes (ISGs) and cytokines, high viral loads and limited pulmonary damage, the other pattern showed severely damaged lungs, low ISGs, low viral loads and abundant immune infiltrates. more...
#> 294                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We investigated whether circulating microRNAs (miRNAs) are associated with residual insulin secretion at diagnosis and predict the severity of its future decline. We studied 53 newly diagnosed subjects enrolled in placebo groups of TrialNet clinical trials.  We measured serum levels of 2,083 miRNAs using RNAseq technology, in fasting samples from the baseline visit (<100 days from diagnosis), during which residual insulin secretion was measured with a mixed meal tolerance test (MMTT). more...
#> 295                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Histone deacetylases (HDACs) are important regulators of epigenetic gene modification that are involved in the transcriptional control of metabolism. In particular class IIa HDACs have been shown to affect hepatic gluconeogenesis and previous approaches revealed that their inhibition reduces blood glucose in type 2 diabetic mice. In the present study, we aimed to evaluate the potential of class IIa HDAC inhibition as a therapeutic opportunity for the treatment of metabolic diseases. more...
#> 296                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      IL-12 and IL-18 synergize to promote TH1 responses and have been implicated as accelerators of autoimmune pathogenesis in type 1 diabetes (T1D). We therefore investigated the influence of these cytokines on phenotype and function of immune cells that are involved in disease progression. To understand how IL-12 and IL-18 may synergize to impair Treg function and phenotype, we conducted transcriptional profiling of Treg expanded under normal conditions or in the presence of IL-12 and IL-18. more...
#> 297                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We identified that PBMC of individuals simultaneously affected by a combination of T2DM, dyslipidemia and periodontitis, showed altered molecular profile mainly associated to inflammatory response, immune cell trafficking, and infectious disease pathways Patients were divided into: T2DMpoorly-DL-P (n=5, Grupo 1), T2DMwell-DL-P (n=7, Grupo 2), DL-P (n=6, Grupo 3), P (n=6, Grupo 4) and Healthy (n=6, Control). more...
#> 298                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The growth hormone plays a significant role in normal renal function and overactive growth hormone signaling has been implicated in proteinuria in diabetes. Earlier studies from our group have shown that the glomerular podocytes, which play an essential role in renal filtration, express the growth hormone receptor, suggesting the direct action of growth hormone on these cells. Nevertheless, the precise mechanism and the downstream pathways that are induced by the excess growth hormone in these podocytes leading to diabetic nephropathy are not clearly established. more...
#> 299                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The incidence of new onset diabetes after transplant (NODAT) has increased over the past decade, likely due to calcineurin inhibitor-based immunosuppressants, including tacrolimus (TAC) and cyclosporin (CsA). Voclosporin (VCS), a next generation calcineurin inhibitor is reported to cause fewer incidences of NODAT but the reason is unclear. Whilst calcineurin signaling plays important roles in pancreatic beta-cell survival, proliferation, and function, its effects on human beta-cells remain understudied. more...
#> 300                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 301                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We perfomed transcriptomic and methylomic analysis of sural nerve biopsies from type 2 diabetic patients with neuropathy. Sural nerve transcriptomic and methylomic profiles were integrated and subsequent biological meaning investigated using KEGG pathway analysis of overlapping differentially expressed genes (DEGs) and differentially methylated genes (DMGs). A gene interation network was also generated including DEGs and DMGs, and common biological pathways were identified.
#> 302                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We perfomed transcriptomic and methylomic analysis of sural nerve biopsies from type 2 diabetic patients with neuropathy. Sural nerve transcriptomic and methylomic profiles were integrated and subsequent biological meaning investigated using KEGG pathway analysis of overlapping differentially expressed genes (DEGs) and differentially methylated genes (DMGs). A gene interation network was also generated including DEGs and DMGs, and common biological pathways were identified.
#> 303                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Gene expression plasticity is central for macrophages? timely responses to cues from the microenvironment permitting phenotypic adaptation from pro-inflammatory (M1) to wound healing and tissue-regenerative (M2, with several subclasses). Regulatory macrophages (Mreg) are a distinct macrophage type, partially sharing some functionalities with both M1 and M2 cells. Mreg possess immunoregulatory, anti-inflammatory, and angiogenic properties, and are considered as a potential allogeneic cell therapy product to treat clinical conditions, e.g., non-healing diabetic foot ulcers. more...
#> 304                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 305                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Background: Cold acclimation and exercise training were previously shown to increase peripheral insulin sensitivity in human volunteers with type 2 diabetes. Although cold is a potent activator of brown adipose tissue, the increase in peripheral insulin sensitivity by cold is largely mediated by events occurring in skeletal muscle and at least partly involves GLUT4 translocation, as is also observed for exercise training. more...
#> 306                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Background: Cold acclimation and exercise training were previously shown to increase peripheral insulin sensitivity in human volunteers with type 2 diabetes. Although cold is a potent activator of brown adipose tissue, the increase in peripheral insulin sensitivity by cold is largely mediated by events occurring in skeletal muscle and at least partly involves GLUT4 translocation, as is also observed for exercise training. more...
#> 307                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 308                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 309                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 310                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 311                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 312                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 313                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. more...
#> 314                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Background: Prolonged exposure to elevated free fatty acids induces β-cell failure (lipotoxicity) and contributes to the pathogenesis of type 2 diabetes. In vitro exposure of β-cells to the saturated free fatty acid palmitate is a valuable model of lipotoxicity, reproducing features of β-cell failure observed in type 2 diabetes. In order to map the β-cell response to lipotoxicity, we combined RNA-sequencing of palmitate-treated human islets with iTRAQ proteomics of insulin-secreting INS-1E cells following a time course exposure to palmitate. more...
#> 315                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Circulating cell-free unmethylated DNA fragments arising from the human INS gene have been proposed as biomarkers of β-cell death for the presymptomatic detection of diabetes. However, given the variability of CpG methylation in the INS gene in different cell types, this gene alone may not yield sufficiently specific information to unambiguously report β-cell damage. We employed an unbiased approach using data from a human DNA methylation gene array to identify the CHTOP gene as a candidate biomarker whose CpGs show a greater frequency of unmethylation in human islets. more...
#> 316                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Proliferative diabetic retinopathy (PDR) is the advanced stage of diabetic retinopathy (DR), coupling with irregular neovascularization, and is the leading cause of blindness in working-age people; but the molecular mechanism of vascular differentiation in PDR remains poorly characterized. In our study, we obtained the transcriptome profile of neovascular proliferative membrane specimens from patients with PDR via high-throughput sequencing and advanced bioinformatics. more...
#> 317                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Metabolic syndrome, whose main diagnostic component is obesity, is a risk factor for lifestyle-related diseases, type 2 diabetes, and cardiovascular disease. Diet is known to affect the prevalence of metabolic syndrome. However, the effect of diet on metabolic syndrome in Japanese subjects has not been thoroughly explored. In the present study, we investigated the effect of carotenoid-rich vegetables, particularly lycopene- and lutein-rich vegetables, on the metabolic syndrome in obese Japanese men. more...
#> 318                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Autoimmune destruction of pancreatic β cells underlies type 1 diabetes (T1D). To understand T-cell mediated immune impact on human pancreatic β cells, we combine β cell specific expression of a model antigen CD19 and anti-CD19 chimeric antigen receptor T (CAR-T) cells. Co-culturing CD19-expressing -like cells and CD19 CAR-T cells results in T-cell mediated β-like cell death with release of activated T cell cytokines. more...
#> 319                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          LncRNAs are developmentally regulated and highly cell type-specific non-coding RNAs that have emerged as important regulators of cell fate commitment and maintenance. In this study, we dissected the role of lncRNAs in human pancreas development by classifying lncRNAs based on their dynamic regulation, subcellular localization, and engagement with ribosomes during the stepwise differentiation of human embryonic stem cells (hESCs) towards pancreatic fate. more...
#> 320                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Diabetic foot ulcers (DFUs) and associated impaired healing, represent a major problem, that significantly impairs the quality of life of diabetic patients, leading to prolonged hospitalization and resulting in more than 70,000 lower extremity amputations per year in the USA alone. In the present study, we prospectively followed a large group of DFU patients for 12 weeks and aimed to identify systemic and local factors that are associated with DFU healing. more...
#> 321                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Brown adipocytes (BAs) are a potential therapeutic cell source for the treatment of metabolic disease such as type 2 diabetes. In this report, human pluripotent stem cells (hPSCs) are subject to directed differentiation to brown dipocytes through a paraxial mesoderm intermediate at high-efficiency. RNA-Seq and ATAC-seq was performed to characterized hPSCs derived paraxial mesoderm and brown adipocytes generated in this study.
#> 322                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      TCF7L2 rs290487 C allele increases diabetic risk in Chinese, however the mechanism remains unclear. We herein evaluated the role of rs290487 variant in hepatic glucose homeostasis by integrating clinical and multi-omics data (ChIP-seq, ATAC-seq, RNA-seq, and metabolomics) from CRISPR/Cas9 edited PLC-PRF-5 cell lines (C/C vs. C/T). In clinical cohort, C/C genotype was associated with higher insulin resistance index and higher incidence of hepatogenous diabetes as compared to C/T heterozygote and T/T homozygote genotypes. more...
#> 323                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Excessive mitochondrial fission plays a key role in podocyte injury in diabetic kidney disease (DKD), and long noncoding RNAs (lncRNAs) are important in the development and progression of DKD. However, lncRNA regulation of mitochondrial fission in podocytes is poorly understood. Here, we want to identify how lncRNA changes in human podocytes cultured with high glucose.
#> 324                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Diabetes is characterized by hyperglycemia, loss of functional islet beta cell mass, deficiency of glucose-lowering insulin, and persistent alpha cell secretion of gluconeogenic glucagon. Still, no therapies that target these underlying processes are available. We therefore performed high-throughput screening of 300,000 compounds and extensive medicinal chemistry optimization and here report the discovery of SRI-37330, an orally bioavailable, non-toxic small molecule, which effectively rescued mice from streptozotocin- and obesity-induced (db/db) diabetes. more...
#> 325                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Interest in human brown fat as a novel therapeutic target to tackle the growing obesity and diabetes epidemic has increased dramatically in recent years. While much insight into brown fat biology has been gained from murine cell lines and models, few resources are available to study human brown fat in-vitro. In this study, we detail the derivation and characterization of a novel human ES UCP1 reporter cell line that marks UCP1 positive adipocytes in-vitro. more...
#> 326                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Common genetic traits are not well defined in hepatocellular carcinoma (HCC), because necroinflammation lasting long in prior to hepatocarcinogenesis embeds highly heterogenous genetic background in hepatocytes over the liver. We experienced a rare case with chronic hepatitis C, in which multiple liver tumors at different stages in multistep hepatocarcinogenesis were observed at the same time. Under the same genetic and etiological backgrounds, comparisons of expression profiles among dysplastic nodules (DN), well differentiated HCC (WEL), and moderately differentiated HCC (MOD) would provide critical genetic information for the initiation and progression of HCC.
#> 327                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         The aim of this study was to conduct a baseline comparison of serum-circulating miRNA in prediabetic individuals with the distinction between those who later progressed to type 2 diabetes (T2DM) and those who did not. The expression level of 798 miRNAs using NanoString technology was examined. Spearman correlation, ROC curve analysis, and logistic regression modeling were performed. Gene ontology (GO), canonical pathways analysis were used to explore the biological functions of the miRNA target genes. more...
#> 328                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Four miRNAs showed significantly different expression post-vitamin C supplementation including the down-regulation of miR-451a, and up-regulation of miR-1253, miR-1290 and miR-644a. Subsequent validation study showed only miR-451a expression was significantly different with supplementation.
#> 329                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Donor pancreata were obtained from the Beta Cell Bank of the JDRF Centre for Beta Cell Therapy in Diabetes (Brussels, Belgium), from Pancreatic Islet Processing (ECIT center) of Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute (Milan, Italy) and from the DRWF Human Islet Isolation Facility (Oxford, England). Full written consent for use of donor material for research was obtained according to Belgian, Italian and English laws. more...
#> 330                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Donor pancreata were obtained from the Beta Cell Bank of the JDRF Centre for Beta Cell Therapy in Diabetes (Brussels, Belgium), from Pancreatic Islet Processing (ECIT center) of Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute (Milan, Italy) and from the DRWF Human Islet Isolation Facility (Oxford, England). Full written consent for use of donor material for research was obtained according to Belgian, Italian and English laws. more...
#> 331                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                People living with diabetes have an increased risk of developing active tuberculosis. The effects of diabetes (HbA1c ≥6.5%) and intermediate hyperglycaemia (HbA1c 5.7-6.5%), on this transcriptomic signature were investigated by RNA-seq, to enhance understanding of immunological susceptibility in diabetes-tuberculosis comorbidity.Diabetes increased the magnitude of gene expression change in the host transcriptome in tuberculosis, characterised by an increase in innate, and decrease in adaptive immune responses. more...
#> 332                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Metformin, a biguanide agent, is the first-line treatment for type 2 diabetes mellitus due to its glucose-lowering effect. Despite its wide application in the treatment of multiple health conditions, the glycemic response to metformin is highly variable, emphasizing the need for reliable biomarkers.   We chose the RNA-Seq-based comparative transcriptomics approach to evaluate the systemic effect of metformin and highlight potential predictive biomarkers of metformin response in drug-naïve type 2 diabetes patient volunteers in vivo. more...
#> 333                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Purpose: The goal of this study is to characterize the gene expression profiles and identify genes of interest (GOI) in stenotic (AS) and regurgitant (AI) human aortic valves using RNA sequencing technology. Methods: Aortic valve leaflets were collected from non-matched transplant donor hearts (NC) and from aortic valve replacement operations (AS or AI).  Leaflets were washed in cold PBS, snap frozen, and stored at -80°C until RNA extraction. more...
#> 334                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Long noncoding RNAs (lncRNAs) is already evidently involved in a variety of biological functions and pathophysiological mechanisms underlying the diabetes. However, the role of lncRNAs in the type 2 diabetes (T2D) has not been explored clearly yet. The aim of this study was to determine the circulating lncRNA profile and confirmed the differentially expressed lncRNA between T2D patients.
#> 335                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           PURPOSE: To investigate the circulatory microRNA (miRNA) profiles of aqueous, vitreous, and plasma in order to identify biomarkers in aqueous humor or plasma that are reflecting changes in vitreous of patients with diabetes. METHODS:  Aqueous, vitreous and plasma samples were collected from a total of 27 patients - 11 controls (macular pucker or macular hole patients) and 16 patients with diabetes mellitus (DM) undergoing vitreoretinal surgery:  DM-Type I with proliferative diabetic retinopathy (PDR) (DMI-PDR), DM Type II with PDR (DMII-PDR) and DM Type II with nonproliferative DR (DMII-NPDR). more...
#> 336                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   To determine ceRNA transcribed during the PBMCs, we have employed whole genome microarray expression profiling as a discovery platform to identify ceRNA expression in PBMCs donated by T1DM (type 1 diabetes mellitus) patients and healthy volunteers.
#> 337                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   To determine miRNA transcribed during the PBMCs, we have employed whole genome microarray expression profiling as a discovery platform to identify miRNA expression in PBMCs donated by T1DM (type 1 diabetes mellitus) patients and healthy volunteers.
#> 338                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Background: Traditionally, the transcriptomic and proteomic characterisation of CD4+ T cells at the single-cell level has been performed by two largely exclusive types of technologies: single-cell RNA-sequencing (scRNA-seq) and antibody-based cytometry. Here we present a multi-omics approach allowing the simultaneous targeted quantification of mRNA and protein expression in single-cells and investigate its performance to dissect the heterogeneity of human immune cell populations. more...
#> 339                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Obesity is a major public health burden worldwide, greatly increasing the risk of diabetes, cardiovascular diseases and cancer. Obesity and associated insulin resistance are characterized by chronic low-grade inflammation driven by the cooperation of the innate immune system and dysregulated metabolism in adipose tissue and other metabolic organs. RIPK1 (Receptor-Interacting serine/threonine Protein Kinase 1) is a central regulator of inflammatory cell function that coordinates inflammation, apoptosis and necroptosis in response to inflammatory stimuli. more...
#> 340                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We collected the mid-morning urine samples, and centrifuged at 2000g for ten minutes in order to remove cells and debris, and then stored in -80 degree refrigerator. we selected 2 samples per group for the microRNA arrays in the following four groups: normal control, IGT with renal impairment, diabetes, diabetic kidney disease. In IGT renal impairment group, we have found that the expression of two microRNAs were changed. more...
#> 341                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Pathologic retinal neovascularization is a potentially blinding consequence seen in many common diseases including diabetic retinopathy, retinopathy of prematurity, and retinal vascular occlusive diseases, among others. The use of therapeutics targeting pro-angiogenesis factors such as vascular endothelial growth factor (VEGF) has proven to be highly effective, however considerable side effects exist and serial anti-VEGF treatment has been shown to decrease effectiveness over time. more...
#> 342                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The intrahepatic milieu is inhospitable to intraportal islet allografts, limiting their applicability to ameliorate Type 1 Diabetes (T1D). Islet viability in the subcutaneous space represents an unfulfilled paradigm that is crucial to ensure widespread adoption and safety of clinical islet transplantation. Herein we report that human islets transplanted subcutaneously uniformly promote long-term euglycemia when admixed with a device-free Islet Viability Matrix (IVM), through a previously unknown anti-apoptotic mechanism.
#> 343                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Patients affected by type 1 diabetes are recruited in the departments of Diabetology and Healthy Volunteers (HV) are selected based on internal records in the same hospital.  Total RNA from whole blood has been extracted following a two-step procedure. First, RNA from blood collected on PAX-Gene tubes has been extracted using Maxwell 16 LEV simplyRNA blood kit (Promega) following manufacturer recommendations and second b-globin, dominant RNA from red blood cells, has been removed using the GLOBINclear kit (Ambion) on extracted RNA. RNA sequencing has been performed from using the TruSeq Stranded mRNA preparation kit (Illumina) on 500 ng b-globin depleted RNA with a RNA Integrity Number > 8 (measured on Bioanalyzer following manufacturer recommendations), and then sequenced following a pair-end 2x75 bp protocol on NextSeq 500 or HiSeq 4000 (Illumina) at LIGAN Equipex (Lille, France).
#> 344                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Besides improving insulin sensitivity in type 2 diabetes, the thiazolidinedione family of compounds and the pharmacologic activation of their best characterized target PPARg has been proposed as a therapeutic option for cancer treatment. In the present study, we reveal a new mechanism by which the thiazolidinedione rosiglitazone contributes to tumorigenesis, which limits its therapeutic potential in cancer. more...
#> 345                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            TruCulture human whole blood ex vivo stimulation was performed on 17 healthy individuals and 17 post-onset type 1 diabetics, then gene expression was analyzed using Nanostring to characterize stimulated innate immune responses. Ex vivo whole blood stimulation revealed higher induced IFN-1 responses in type 1 diabetes as compared to healthy controls.
#> 346                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Comparative gene expression profiles of human retinal pericytes (HRMPC) and lipoaspirate derived mesenchymal stromal cells (adipose stromal cells, ASC) cultivated either in normal (1g/l) or high (4.5g/l) glucose medium to identify similarities and discrepancies and elucidate high glucose effects considering cell-based therapies in diabetic retinopathy. A hallmark of diabetic retinopathy is pericyte- dropout increased vascular permeability and progressive vascular occlusion. more...
#> 347                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Markers of biological ageing have potential utility in primary care and public health. We developed a model of age based on untargeted metabolic profiling across multiple platforms, including nuclear magnetic resonance spectroscopy and liquid chromatography-mass spectrometry in urine and serum, within a large sample (N=2,239) from the UK Airwave cohort. We validated a subset of model predictors in a Finnish cohort including repeat measurements from 2,144 individuals. more...
#> 348                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Severe obesity (SO) affects about 6% of youth in US, augmenting the risks for cardiovascular disease and Type 2 diabetes. Herein, we obtained paired omental (omVAT) and abdominal subcutaneous (SAT) adipose tissue biopsies from obese girls with SO, undergoing sleeve gastrectomy (SG), to test whether differences in cellular and transcriptomic profiles between omVAT and SAT depots affect insulin sensitivity differentially. more...
#> 349                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Cardiovascular disease (CVD) is the most common cause of death in patients with type II diabetes mellitus (T2DM). Although susceptibility to CVD is different for every patient, why some patients with T2DM develop CVD while others are protected has not yet been clarified. Patient-derived induced pluripotent stem cells (iPSCs) have been utilized to reveal the influence of genotype on phenotype and have the potential to connect a clinical phenotype to a causal gene. more...
#> 350                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We report the application of RNA-sequencing for high-throughput profiling of transcriptomes in tumor tissues from patients with breast cancer and diabetes, and in tumor tissues from breast cancer patients without diabetes.
#> 351                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Context: Context: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu and is linked to obesity and diabetes in offspring, but the mechanisms driving these effects remain largely unknown.  Alterations gene expression in amniocytes exposed to GDM in utero may identify potential mechanisms leading to metabolic dysfunction later in life. Objective: Objective: To profile changes in the transcriptome in human amniocytes exposed to GDM Methods: A nested case-control study was performed in second trimeseter amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, gestational age at birth and gestational diabetes status. more...
#> 352                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Human thermogenic adipose tissue mitigates metabolic disease, raising much interest in understanding its development and function. Here, we show that human thermogenic adipocytes specifically express a primate-specific long non-coding RNA, LINC00473 which is highly correlated with UCP1 expression and decreased in obesity and type-2 diabetes. LINC00473 is detected in progenitor cells, and increases upon differentiation and in response to cAMP. more...
#> 353                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We revealed transcriptome differences between corrected and unedited (diseased) Wolfram Syndrome patient stem cell-derived beta cells. We also identified several endocrine, pancreatic, and non-pancreatic cell types in the samples populations.
#> 354                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Human thermogenic adipose tissue mitigates metabolic disease, raising much interest in understanding its development and function. Here, we show that human thermogenic adipocytes specifically express a primate-specific long non-coding RNA, LINC00473 which is highly correlated with UCP1 expression and decreased in obesity and type-2 diabetes. LINC00473 is detected in progenitor cells, and increases upon differentiation and in response to cAMP. more...
#> 355                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Cigarette smoking is one of the largest causes of preventable death worldwide. Smoking behaviors, including age at smoking initiation (ASI), smoking dependence (SD), and smoking cessation (SC), are all complex phenotypes determined by both genetic and environmental factors as well as their interactions. To identify susceptibility loci for each smoking phenotype, numerous studies have been conducted, with approaches including genome-wide linkage scans, candidate gene-based association analysis, and genome-wide association study (GWAS). more...
#> 356                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Proinflammatory cytokines are important mediators of pancreatic beta cell dysfunction and demise in type 1 diabetes (T1D). We presently characterized human beta cell responses to IFNa by combining ATAC-seq, RNA-seq and proteomics assays. The initial beta cell response to IFNa was characterized by major chromatin remodeling, followed by marked changes in transcriptional and translational regulation. IFNa-induced changes in alternative splicing (AS) and first exon usage increased the diversity of transcripts expressed by beta cells. This, combined with changes observed on protein modification/degradation, ER stress and MHC class I, may significantly expand the peptide repertoire presented by beta cells to the immune system. On the other hand, beta cells up-regulated checkpoint proteins, such as PDL1 and HLA-E, that may protect them against the autoimmune assault. Data mining of the present multi-omics analysis led to the identification of two compound classes that revert IFNa effects on human beta cells and may be translated to clinical trials.
#> 357                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Proinflammatory cytokines are important mediators of pancreatic beta cell dysfunction and demise in type 1 diabetes (T1D). We presently characterized human beta cell responses to IFNa by combining ATAC-seq, RNA-seq and proteomics assays. The initial beta cell response to IFNa was characterized by major chromatin remodeling, followed by marked changes in transcriptional and translational regulation. IFNa-induced changes in alternative splicing (AS) and first exon usage increased the diversity of transcripts expressed by beta cells. This, combined with changes observed on protein modification/degradation, ER stress and MHC class I, may significantly expand the peptide repertoire presented by beta cells to the immune system. On the other hand, beta cells up-regulated checkpoint proteins, such as PDL1 and HLA-E, that may protect them against the autoimmune assault. Data mining of the present multi-omics analysis led to the identification of two compound classes that revert IFNa effects on human beta cells and may be translated to clinical trials.
#> 358                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Proinflammatory cytokines are important mediators of pancreatic beta cell dysfunction and demise in type 1 diabetes (T1D). We presently characterized human beta cell responses to IFNa by combining ATAC-seq, RNA-seq and proteomics assays. The initial beta cell response to IFNa was characterized by major chromatin remodeling, followed by marked changes in transcriptional and translational regulation. IFNa-induced changes in alternative splicing (AS) and first exon usage increased the diversity of transcripts expressed by beta cells. This, combined with changes observed on protein modification/degradation, ER stress and MHC class I, may significantly expand the peptide repertoire presented by beta cells to the immune system. On the other hand, beta cells up-regulated checkpoint proteins, such as PDL1 and HLA-E, that may protect them against the autoimmune assault. Data mining of the present multi-omics analysis led to the identification of two compound classes that revert IFNa effects on human beta cells and may be translated to clinical trials.
#> 359                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Insulin resistance increases patient’s risk of developing type 2 diabetes (T2D), nonalcoholic  steatohepatitis (NASH) and a host of other comorbidities including  cardiovascular disease and cancer. At the molecular level, insulin exerts its function  through the insulin receptor (IR), a transmembrane receptor tyrosine kinase. Data from  human genetic studies have shown that Grb14 functions as a negative modulator of IR  activity, and germline Grb14-knockout (KO) mice have improved insulin signaling in liver  and muscle tissues. more...
#> 360                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Cigarette smoking is one of the largest causes of preventable death worldwide. Smoking behaviors, including age at smoking initiation (ASI), smoking dependence (SD), and smoking cessation (SC), are all complex phenotypes determined by both genetic and environmental factors as well as their interactions. To identify susceptibility loci for each smoking phenotype, numerous studies have been conducted, with approaches including genome-wide linkage scans, candidate gene-based association analysis, and genome-wide association study (GWAS). more...
#> 361                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 362                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The pool of beta cell-specific CD8+ T-cells in type 1 diabetes (T1D) sustains an autoreactive potential despite having access to a constant source of antigen. To investigate the long-lived nature of these cells, we established a DNA methylation-based T cell “multipotency index” and found that beta cell-specific CD8+ T-cells retained a stem-like epigenetic multipotency score. Single cell ATAC-seq analysis confirmed the co-existence of naive and effector-associated epigenetic programs in individual beta cell-specific CD8+ T-cells. more...
#> 363                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The pool of beta cell-specific CD8+ T-cells in type 1 diabetes (T1D) sustains an autoreactive potential despite having access to a constant source of antigen. To investigate the long-lived nature of these cells, we established a DNA methylation-based T cell “multipotency index” and found that beta cell-specific CD8+ T-cells retained a stem-like epigenetic multipotency score. Single cell ATAC-seq analysis confirmed the co-existence of naive and effector-associated epigenetic programs in individual beta cell-specific CD8+ T-cells. more...
#> 364                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. more...
#> 365                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Genome wide association studies (GWAS) identified a chromosome 8 locus associated with fasting glucose (FG), insulin (FI) and lipid levels that is located near PPP1R3B (a gene which encodes the catalytic subunit of a serine/threonine protein phosphatase that promotes hepatic glycogen storage upon insulin signaling). The lead SNP rs4841132 lies in a long non-coding RNA (lncRNA) LOC157273, 175 kb away and is not in linkage disequilibrium with PPP1R3B. more...
#> 366                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Genetic factors are strongly implicated in the susceptibility to develop externalizing syndromes such as attention deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, conduct disorder, and substance use disorder (SUD). Variants in the ADGRL3 (LPHN3) gene predispose to ADHD and predict ADHD severity, disruptive behaviors comorbidity, long-term outcome, and response to treatment. In this study, we investigated whether variants within ADGRL3 are associated with SUD, a disorder that is frequently co-morbid with ADHD. more...
#> 367                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Recent studies revealed that the bromodomain and extraterminal (BET) epigenetic reader proteins resemble key regulators in the underlying pathophysiology of cancer, diabetes or cardiovascular disease. However, whether they also regulate vascular remodeling processes by direct effects on vascular cells is unknown. In this study we investigated the effects of the BET proteins on neointima formation in response to vascular injury in vivo and on human smooth muscle cell function in vitro. more...
#> 368                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Obesity and type 2 diabetes (T2D) are metabolic disorders influenced by lifestyle and genetic factors, and characterized by insulin resistance in skeletal muscle, a prominent site of glucose disposal. Numerous genetic variants have been associated with obesity and T2D, of which the majority is located in non-coding DNA regions. This suggest that most variants mediate their effect by altering the activity of gene-regulatory elements, including enhancers. more...
#> 369                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Obesity and type 2 diabetes (T2D) are metabolic disorders influenced by lifestyle and genetic factors, and characterized by insulin resistance in skeletal muscle, a prominent site of glucose disposal. Numerous genetic variants have been associated with obesity and T2D, of which the majority is located in non-coding DNA regions. This suggest that most variants mediate their effect by altering the activity of gene-regulatory elements, including enhancers. more...
#> 370                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Obesity and type 2 diabetes (T2D) are metabolic disorders influenced by lifestyle and genetic factors, and characterized by insulin resistance in skeletal muscle, a prominent site of glucose disposal. Numerous genetic variants have been associated with obesity and T2D, of which the majority is located in non-coding DNA regions. This suggest that most variants mediate their effect by altering the activity of gene-regulatory elements, including enhancers. more...
#> 371                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Pancreatic Beta-cells are essential for regulating blood glucose levels. Much of our knowledge relating to human Beta-cell development and function has depended on rodent models, which have provided a blueprint to confirm important cellular features in humans. The advent of next generation sequencing studies, however, has highlighted discrepancies in Beta-cells which exist between mice and men. The precise contribution of such differences has not yet been fully appreciated. more...
#> 372                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Adipose tissue-derived mesenchymal stem cells (ASC’s) constitute a vital population of multipotent cells capable of differentiating into end-organ tissues. However, scientific endeavors to harness the regenerative potential of ASC’s for regenerative medicine are currently limited by an incomplete understanding of the mechanisms that determine cell-lineage commitment and stemness. In the current study, we used reduced representation bisulfite sequencing (RRBS) analysis to identify epigenetic gene targets and cellular processes that are responsive to 5-azathioprine, a potent inducer of DNA methylation. more...
#> 373                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The generation of pancreatic cell types from renewable cell sources holds promise for cell replacement therapies for diabetes. Although most effort has focused on generating pancreatic beta cells, there is considerable evidence that glucagon secreting alpha cells are critically involved in disease progression and proper glucose control. Here we report on the generation of stem cell-derived human pancreatic alpha (SC-alpha) cells from pluripotent stem cells via a transient pre-alpha cell intermediate. more...
#> 374                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 The goal of the study was to identify genes whose aberrant expression can contribute to diabetic retinopathy. We determined differential response in gene expression to high glucose in lymphoblastoid cell lines derived from matched type 1 diabetic individuals with and without retinopathy. Those genes exhibiting the largest difference in glucose response between diabetic subjects with and without retinopathy were assessed for association to diabetic retinopathy utilizing genotype data from a meta-genome-wide association study. more...
#> 375                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       DNA methylation may be involved in development of type 1 diabetes (T1D), but previous epigenome-wide association studies were conducted among cases with clinically diagnosed diabetes. Using multiple pre-disease peripheral blood samples on the Illumina 450K and EPIC platforms, we investigated longitudinal methylation differences between 87 T1D cases and 87 controls from the prospective Diabetes Autoimmunity Study in the Young (DAISY) cohort. more...
#> 376                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Cell cycle progression plays an important role in mediating the transition from a differentiated state to a pluripotent stem cell. Conversely, establishing limitations in proliferative potential may be important to achieve functional maturity as well as to prevent abnormal growths after transplantation of stem cell derived products. Here we induced exit from the cell cycle in pancreatic progenitors by interfering with the progression of DNA replication and determined growth potential, differentiation and maturation to insulin producing endocrine cells. more...
#> 377                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Early-onset complex autoimmunity can arise from monogenic activating mutations in inflammatory signalling pathways or loss of function mutations of immunoregulatory molecules. We sought to define the molecular basis of severe early-onset autoimmunity, characterised by autoimmune diabetes, cytopenias, hepatitis, enteropathy and interstitial lung disease, in a child without pathogenic variants in STAT3 and FOXP3. more...
#> 378                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Combined single-cell RNAseq and electrophysiological profiling of human pancreatic islet cells (pancreas patch-seq) to link transcriptomic phenotypes of islet cells to their physiologic properties.
#> 379                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              The adult kidney replaces lost cells in-vivo via proliferation of cells functioning as committed clonal progenitors. Here we combined the generation of single cell derived clonal cultures from human adult kidney with transcriptomic analysis for molecular characterization of in-vitro clonal behavior at inception and after propagation. We discovered two types of clones; rapidly proliferating de-differentiated fibroblast-like (FL) originating from the proximal tubule and stably proliferating cuboidal epithelial-like (EL) originating from distal segments that efficiently propagate with one cell giving rise to 3.3*10(6) cells. more...
#> 380                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Maternal obesity impacts the health of offspring, increasing the risk of developing obesity and/or other metabolic dysregulation in childhood or later in life. Using a genome-wide methylation assay, we identified sex-dependent dysregulation of the methylome of CD3+ T-lymphocytes, a cell type that plays an important role in obesity and inflammatory diseases, in newborn offspring of overweight and obese mothers. more...
#> 381                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   We investigated the genome-wide DNA methylation profiles in sperm by comparing 8 individuals with T2DM and 9 non-diabetic controls using whole genome bisulfite sequencing (WGBS) method. Our study provides the first evidence that T2DM reprograms sperm DNA methylome and provides new insights into the intricate mechanisms of susceptibility to T2DM in offspring.
#> 382                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 383                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Technical replicate testing was performed to determine the measurement precision of each analyte. Peripheral blood samples were collected in tempus tubes from a healthy control subject with no family history of autoimmunity (n=1) and from subjects with Type 1 diabetes (n=4). Total RNA was isolated independently from 3 replicate aliquots of the same tempus samples and then globin-reduced. RNAseq libraries were prepared from the globin-reduced RNA.
#> 384  BACKGROUND: Long-term complications of type 2 diabetes (T2D), such as macrovascular and microvascular events, are the major causes for T2D-related disability and mortality. A clinically convenient, non-invasive approach for monitoring the development of these complications would improve the overall life quality of patients with T2D and help reduce healthcare burden through preventive interventions.  METHODS: A selective chemical labeling strategy for 5-hydroxymethylcytosines (5hmC-Seal) was used to profile genome-wide 5hmCs, an emerging class of epigenetic markers implicated in complex diseases including diabetes, in circulating cell-free DNA (cfDNA) from a collection of Chinese patients (n = 62). Differentially modified 5hmC markers between patients with T2D with and without macrovascular/microvascular complications were analyzed under a case-control design.  RESULTS: Statistically significant changes in 5hmC markers were associated with T2D-related macrovascular/microvascular complications, involving genes and pathways relevant to vascular biology and diabetes, including insulin resistance and inflammation. A 16-gene 5hmC marker panel accurately distinguished patients with vascular complications from those without (testing set: AUC = 0.85, 95%CI, 0.73-0.96), outperforming conventional clinical variables such as urinary albumin. In addition, a separate 13-gene 5hmC marker panel could distinguish patients with single complications from those with multiple complications (testing set: AUC = 0.84, 95%CI, 0.68-0.99), showing superiority over conventional clinical variables.  CONCLUSIONS: The 5hmC markers in cfDNA reflected the epigenetic changes in patients with T2D who developed macrovascular/microvascular complications. The 5hmC-Seal assay has the potential to be a clinically convenient, non-invasive approach that can be applied in the clinic to monitor the presence and severity of diabetic vascular complications.
#> 385                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     We investigated genome wide changes in gene expression in skin between patients with type 2 diabetes and non-diabetic patients using next generation sequencing. We compared the gene expression in skin samples taken from 27 patients (13 with type 2 diabetes and 14 non-diabetic).
#> 386                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   We report the RNA expression profiles of native veins used for AVF creation and of remodeled AVF samples obtained 6-15 weeks later at the time of transposition (if vein matured) or salvage procedure (if vein failed). We perfomed RNA-seq on native veins and AVFs with different maturation outcomes (matured vs. failed). The "matured" and "failed" subgroups were similar in terms of demographics (age range, sex distribution, ethnicity distribution), clinical characteristics (proportion of diabetes mellitus and coronary artery disease, previous hemodialysis access history), and time interval between first-stage and second-stage surgeries. more...
#> 387                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Severe angiopathy has been postulated as a major driver for diabetes associated secondary complications. So far the knowledge on underlying mechanisms and thereon based therapeutic options to attenuate these pathologies are limited. Here we systematically administered ABCB5+ MSCs for the treatment of chronic non-healing diabetic wounds employing db/db mice, a type II diabetes model as their number markedly declined during diabetes. more...
#> 388                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We propose that reprogramming of patient donor cells to tankyrase inhibitor-regulated naive hiPSC (N-hiPSC) improves the functionality of differentiated progenitors for subsequent regenerative therapies, and more effectively erases donor epigenetic aberrations sustained from chronic diseases such as diabetes .
#> 389                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Aim: The loss of insulin-secreting β-cells, ultimately characterizing most diabetes forms, demands the development of cell replacement therapies. The common endpoint for all ex vivo strategies is transplantation into diabetic patients. However, the effects of hyperglycemia environment on the transplanted cells were not yet properly assessed. Thus, the main goal of this study was to characterize global effect of brief and prolonged in vivo hyperglycemia exposure on the cell fate acquisition and maintenance of transplanted human pancreatic progenitors. more...
#> 390                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    DPN muscle exhibits features of degeneration with attempted regeneration.  In the most severely pathological muscle samples, regeneration appears to be stymied and our data suggest that this may be partly due to intrinsic dysfunction of the satellite cell pool in addition to extrinsic structural pathology (e.g. nerve damage).
#> 391                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Obesity, and visceral adiposity in particular, increases the risk of common metabolic diseases, including type 2 diabetes, cardiovascular disease, and several forms of cancer. However, the molecular mechanisms responsible for regional fat storage remain poorly characterized, preventing therapeutic innovation. We here applied a systematic genome-wide screen and translational approach, where human primary preadipocytes were isolated from liposuction aspirate and differentiated. more...
#> 392                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Protein Tyrosine Phosphatase Receptor Type N (PTPRN) plays an important role in diabetes and many cancers but its role in glioma remain poorly defined. Here, we firstly verified PTPRN expression was negatively correlated with overall survival of glioblastoma patients. Moreover, suppression of PTPRN expression reduced both U87 and U343 cell viability, suppressed proliferation, induced cell cycle arrest and inhibited glioma growth in vivo. more...
#> 393                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               We performed a comparison of transcriptome between monocyte-derived dendritic cells (moDC) cultured with neutrophil extracellular traps (NETs) from healthy donors or type 1 diabetes (T1D) patients. The source of moDCs is healthy donors and T1D patients
#> 394                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of histone modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find that MG132 treatment results in the spreading of the H3-trimethyl lysine 4 mark into gene bodies of a subset of induced genes in MCF-7 cells. The spreading of the H3K4me3 is concomitant with hyperacetylation (H3K27ac, K122ac and K9/14ac) of the corresponding gene TSS. more...
#> 395                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   There are the differential levels of methylation in the groups with and without complication to its control groups as non-diabetes and T2D without complication, two of which were classified into male and female, affects strictly the gene regulation to diabetic pathogenesis. To screen specific candidates for detecting classification of Type-2 Diabetes without or with retinopathy or nephropathy, the level of DNA methylation is the one of considerable factors to influence the differential gene expression was inspected involvement of chromosome modification. more...
#> 396                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Exploration of new markers that define impaired metabolic flexibility using an acute postprandial challenge test. Healthy subjects underwent a 4-week high-fat high-calorie diet. High-fat challenges were performed in these subjects before and after the diet and in subjects with the metabolic syndrome.
#> 397                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Type 1 diabetes (T1D) is characterized by immune mediated destruction of insulin producing β cells. Biomarkers capable of identifying T1D risk and dissecting disease-related heterogeneity represent an unmet clinical need. Aims: Towards the goal of informing T1D biomarker strategies, we profiled different classes of RNAs in human islet-derived exosomes and identified RNAs that were differentially expressed under cytokine stress conditions. more...
#> 398                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Several neurodevelopmental processes including neuronal survival, migration and differentiation are controlled by sphingolipid metabolism. Sphingomyelin is an abundant component of cell membranes. Sphingomyelinases generate ceramide from sphingomyelin as a second messenger in intracellular signaling pathways involved in cell proliferation, differentiation, or apoptosis. While the role of acid sphingomyelinase is well established, the role of neutral sphingomyelinases in human neurodevelopment has remained elusive. more...
#> 399                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Intervertebral disc degeneration (IDD) leads to low back pain and disability globally. Progressive loss of nucleus pulposus cells (NPCs) are associated with the onset of IDD. Cell-based therapy has been shown the promising for many diseases, including the IDD in preclinical studies. However, the limited availability of human NPCs has hurdled such application for IDD. This study aimed to define strategies to derive NPCs from human ESC/iPSC. more...
#> 400                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Long noncoding RNAs (lncRNAs) is already evidently involved in a variety of biological functions and pathophysiological mechanisms underlying the diabetes. However, the role of lncRNAs in the type 1 diabetes (T1D) has not been explored clearly yet. The aim of this study was to determine  the circulating lncRNA profile and confirmed the differentially expressed lncRNA between T1D patients and healthy control.
#> 401                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Progressive loss of nucleus pulposus cells (NPCs) is associated with the onset of intervertebral disc degeneration (IDD). Transplantation of NPCs, derived from human pluripotent stem cells including hESC/iPSCs, may offer a novel therapy for IDD. To date, effective in vitro differentiations of notochordal and NP cells remained to be demonstrated. Towards this end, we developed a three-step protocol to directly differentiate hESC/iPSC towards mesodermal, then notochordal and finally NPCs. more...
#> 402                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Transient Pax8 expression was reported in mouse islets during gestation, whereas a genome-wide linkage and admixture mapping study highlighted PAX8 as a candidate gene for diabetes mellitus (DM). We sought the significance of PAX8 expression in mouse and human islet biology. PAX8 was induced in gestating mouse islets and in human islets treated with recombinant prolactin. Global gene expression profiling of human and mouse islets overexpressing the corresponding species-specific PAX8 revealed the modulation of distinct genetic pathways that converge on cell survival. more...
#> 403                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Comparative profiling of miRNA content within CD31+EVs comparing Ctrl and T2DM patients (5 vs 5 samples with each sample prepared from the pooled plasma of 4 subjects).
#> 404                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Obesity is a leading risk factor for type-2 diabetes. Diabetes often leads to the dysregulation of angiogenesis, although, the mechanism is not fully understood. Previously, long noncoding RNAs (lncRNAs) have been found to modulate angiogenesis. In this study, we asked how the expression levels of lncRNAs change in endothelial cells in response to excessive palmitic acid treatment, an obesity-like condition. more...
#> 405                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 406                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcrips with elusive functions in metabolism. Here we report that an unexpectedly high fraction of lncRNAs, but not protein-coding mRNAs, is repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation specifically induced lncRNAs in mouse liver. Similarly, lncRNAs were lost in diabetic humans. more...
#> 407                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To identify the factors mediating the progression of di- abetic nephropathy (DN), we performed RNA sequencing of kidney biopsy samples from patients with early DN, advanced DN, and normal kidney tissue from nephrectomy samples. A set of genes that were upregulated at early but downregulated in late DN were shown to be largely renoprotective, which included genes in the retinoic acid pathway and glucagon-like peptide 1 receptor. more...
#> 408                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Myocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known, that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK-lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. more...
#> 409                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    iPS-derived monocytes and macrophages are similar with primary monocytes and macrophages compared to iPS cells from the genome-wide overview and have similar gene expression patterns.
#> 410                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The present study aimed to investigate differentially expressed genes in whole blood obtained from patients with lumbar disc prolapse and healthy volunteers. A total of 8 patients with lumbar disc prolapse and 8 healthy volunteers were recruited. An Agilent SurePrint G3 human gene expression microarray 8x60 K was used to perform the microarray analyses.
#> 411                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. more...
#> 412                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Using a discovery/validation approach we investigated associations between a panel of genes selected from a transcriptomic study and the renal function decline across time in a cohort of type 1 diabetes patients.
#> 413                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 414                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 415                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 416                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           In type 1 diabetes (T1D), the appearance of multiple islet autoantibodies indicates the onset of islet autoimmunity, often many years before clinical symptoms arise. However, the underlying molecular mechanisms in T cells that can promote aberrant activation thereby triggering autoimmune progression remain poorly understood. Here, we show that during early stages of islet autoimmunity a miRNA142-3p/Tet2 signaling axis in murine and human CD4+T cells interferes with the efficient induction of regulatory T (Treg) cells accompanied by impairments in Treg stability. more...
#> 417                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Insulin resistance (IR) is likely to induce metabolic syndrome and type 2 diabetes mellitus (T2DM). Gluconeogenesis (GNG) is a complex metabolic process that may result in glucose generation from certain non-carbohydrate substrates. Chinese herbal medicine astragalus polysaccharides and berberine have been documented to ameliorate IR, and combined use of astragalus polysaccharide (AP) and berberine (BBR) are reported to synergistically produce an even better effect. more...
#> 418                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 419                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           In type 1 diabetes (T1D), the appearance of multiple islet autoantibodies indicates the onset of islet autoimmunity, often many years before clinical symptoms arise. However, the underlying molecular mechanisms in T cells that can promote aberrant activation thereby triggering autoimmune progression remain poorly understood. Here, we show that during early stages of islet autoimmunity a miRNA142-3p/Tet2 signaling axis in murine and human CD4+T cells interferes with the efficient induction of regulatory T (Treg) cells accompanied by impairments in Treg stability. more...
#> 420                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 421                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 422                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) are small non-coding RNA molecules that have the ability to drive cell lineage decisions by regulating the expression of hundreds of genes. Although evidence indicates that miRNAs have roles in pancreas development and endocrine cell function, the role of miRNAs in pancreatic endocrine cell differentiation has not been systematically explored. To address this, we performed genome-wide small RNA sequencing analysis in pancreatic progenitor cells differentiated in vitro from human embryonic stem cells and endocrine cells isolated from whole human islets. more...
#> 423                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We provide evidence that viral miRNAs use 6mer seed toxicity to kill cells
#> 424                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Distinct characteristics of adipose tissue at different localization of human body has shown greater significance in development of metabolic disorders. Visceral adipose tissue in particular is known to be associated with obesity related metabolic complications that include type II diabetes. In this experiment, we attempt to profile transcriptome signatures of adipocyte, stromal vascular fraction (SVF) and adipose tissue from subcutaneous and visceral adipose tissue from obese individuals.
#> 425                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The complex relationship between metabolic disease risk and body fat distribution in humans involves cellular characteristics which are specific to each body fat compartment.  We applied single-cell RNA sequencing (scRNA-Seq) to identify these depot-specific differences in the stromal vascular fraction of visceral (VAT) and subcutaneous (SAT) adipose tissue of obese individuals. We characterized multiple immune cells, endothelial cells, fibroblasts, adipose and hematopoietic stem cell progenitors. more...
#> 426                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Heterogeneous populations of human bone marrow-derived stromal cells (BMSC) are among the most frequently tested cellular therapeutics for treating degenerative and immune disorders, which occur predominantly in the aging population. Currently, it is unclear whether advanced donor age and commonly associated comorbidities affect the properties of ex vivo-expanded BMSCs. Thus, we stratified cells from adult and elderly donors from our biobank (n = 10 and n = 13, mean age 38 and 72 years, respectively) and compared their phenotypic and functional performance, using multiple assays typically employed as minimal criteria for defining multipotent mesenchymal stromal cells (MSCs).We found that BMSCs from both cohorts meet the standard criteria for MSC, exhibiting similar morphology, growth kinetics, gene expression profiles, and pro-angiogenic and immunosuppressive potential and the capacity to differentiate toward adipogenic, chondrogenic, and osteogenic lineages.We found no substantial differences between cells from the adult and elderly cohorts. more...
#> 427                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      β-cell specific IFT88 knock-out mice recapitulate human diabetes with impaired insulin secretion and altered islet hormone paracrine regulation. To examine the signaling pathways regulating islet cell function, we subjected protein lysates of whole islets from control and IFT88 knockout mice to a commercial signaling-protein array analysis (Full Moon Bio, Inc). Samples were probed against 1358 antibodies with 2 replicates per antibody on 76 x 25 x 1mm glass slides.
#> 428                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    β-cell specific IFT88 knock-out mice recapitulate human diabetes with impaired insulin secretion and altered islet hormone paracrine regulation. To examine the signaling pathways regulating islet cell function, we subjected protein lysates of whole islets from control and IFT88 knockout mice to a commercial phospho-antibody array analysis (Full Moon Bio, Inc). Samples were probed against 1318 site-specific and phospho-specific antibodies with 2 replicates per antibody on 76 x 25 x 1mm glass slides.
#> 429                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Type 1 diabetes (T1D) is a chronic autoimmune disease that results from destruction of pancreatic β-cells. T1D subjects were recently shown to harbor distinct intestinal microbiome profiles. Based on these findings, the role of gut bacteria in T1D is being intensively investigated. The mechanism connecting intestinal microbial homeostasis with the development of T1D is unknown.  Specific gut bacteria such as Bacteroides dorei (BD) and Ruminococcus gnavus (RG) show markedly increased abundance prior to the development of autoimmunity. more...
#> 430                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          A slower transmethylation of one-carbon substrates in the edematous form of severe acute malnutrition (ESAM) suggests that downstream aberrations in DNA methylation could drive differences in acute pathogenesis between ESAM and non-edematous malnutrition (NESAM). Here, we integrate genome-wide assessments of DNA methylation with corresponding gene expression profiles and sequence variation to show that relative to NESAM, acute ESAM is characterized by significant hypomethylation at 99% of differentially methylated loci in two SAM cohorts, whereas recovered adults show no significant differences in methylation. more...
#> 431                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Analysis of monogenic kidney disease-causing genes, and secondary pathology resulting from systemic diseases including diabetes and hypertension, highlight the importance of the kidney’s filtering system, the renal corpuscles. To elucidate the developmental processes that establish the renal corpuscle, we employed single-nucleus droplet-based sequencing to capture single nuclei from the human fetal kidney. more...
#> 432                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Circular RNA (circRNA) microarray analysis was performed to examine the expression profiles of circRNAs in diabetic foot ulcers (DFU) and in human excisional skin wounds 7 days after injury.
#> 433                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Hsa_circ_0084443 expression level is down-regulated during normal skin wound healing and higher level of hsa_circ_0084443 was found in chronic non-healing diabetic foot ulcers compared to normal wounds. However, the biological function of hsa_circ_0084443 in epidermal keratinocytes during wound repair has not been studied. To study the genes regulated by hsa_circ_0084443, we transfected siRNA targeting hsa_circ_0084443 diagnostic junction into human primary epidermal keratinocytes to knockdown hsa_circ_0084443 expression. more...
#> 434                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Hepatocellular adenomas (HCA) are rare benign tumors mainly developed in women after 2 years of oral contraceptive use (Rooks et al., 1979). HCA are also related to other risk factors (obesity, vascular diseases, androgen and alcohol intake) or to different genetic diseases (Mac Cune Albright syndrome, glycogen storage diseases type 1a and MODY3 diabetes caused by HNF1A germline mutation) (Calderaro et al., 2013; Nault et al., 2013a). more...
#> 435                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            In humans, a subset of placental cytotrophoblasts (CTBs) invades the uterus and its vasculature, anchoring the pregnancy and ensuring adequate blood flow to the fetus. Appropriate depth is critical. Shallow invasion increases the risk of pregnancy complications, e.g., severe preeclampsia. Overly deep invasion, the hallmark of placenta accreta spectrum (PAS), increases the risk of pre-term delivery, hemorrhage and death. more...
#> 436                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Fishoil or n-3 PUFA supplementation has shown some beneficial effects in patients with NASH. It is known that n-3 PUFA can influence hepatic gene expression. However, the effect of n-3 PUFA supplementation on hepatic gene expression has not been examined in patients with NASH. Aim of this pilot study was to examine the effect of n-3 PUFA supplementation on liver n-3 PUFA levels, hepatic gene expression and liver histology in patients with NASH. more...
#> 437                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       This project was aimed to study the transciptomic profiles of cholangiocarcinoma cells cultured in different concentration of glucose. The established human cholangiocarcinoma cell line; KKU-213, and highly metastatic subline; KKU-213L5, were used. KKU-213 were cultured in either Dulbecco Modified Eagle's Medium (DMEM) with normal (5.6 mM) or high glucose (25 mM) and labeled as KKU-213NG or KKU-213HG according to thier cuture medium and KKU-213L5 was cultured in high glucose DMEM medium. more...
#> 438                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              We did the transcriptome analysis of peripheral blood mononuclear cells of LADA patients and healthy controls
#> 439                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a marked plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...
#> 440                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...
#> 441                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...
#> 442                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. more...
#> 443                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    PCOS is a widespread disease that primarily caused in-pregnancy in pregnant-age women. Normoandrogen (NA) and Hyperandrogen (HA) PCOS are distinguished under distinct level of testosterone, while markers and expression patterns for both subtypes were not adequately studied. Text-mining analysis stated the correlation for PCOS with granusola cells and thus we performed microarray analysis on granusola cells from HA PCOS, NA PCOS and normal tissue from individuals, and afterwards downloaded RNA-seq and microarray data from NCBI GEO database on granusola cells from PCOS and normal ovary. more...
#> 444                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Background: Macrophage-based immune dysregulation plays a critical role in development of delayed gastric emptying in animal models of diabetes. Human studies have also revealed loss of anti-inflammatory macrophages and increased expression of genes associated with pro-inflammatory macrophages in full thickness gastric biopsies from gastroparesis patients.  Aim: We aimed to determine broader protein expression (proteomics) and protein-based signaling pathways in full thickness gastric biopsies of diabetic (DG) and idiopathic gastroparesis (IG) patients. more...
#> 445                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Metformin is a commonly used antihyperglycaemic agent for the treatment of type 2 diabetes. Nevertheless, the exact mechanisms of action, underlying the various therapeutic effects of metformin, remain elusive. The goal of this study was to evaluate the alterations in longitudinal whole-blood transcriptome profiles of healthy individuals after a one-week metformin intervention in order to identify the novel molecular targets and further prompt the discovery of predictive biomarkers of metformin response. more...
#> 446                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We report the early transcriptional changes in human diabetic nephropathy by single nucleus RNA sequencing
#> 447                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Multiple studies endorsed the positive effect of regular exercising on mental and physical health. However, the molecular mechanisms underlying training-induced fitness in combination with personal life-style remain largely unexplored. Circulating biomarkers such as microRNAs (miRNAs) offer themselves for studying systemic and cellular changes since they can be collected from the bloodstream in a low-invasive manner. more...
#> 448                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       One of the most common congenital disorders of male infertility is Klinefelter syndrome. Because of its extreme heterogeneity in clinical and genetic presentation, the relationship between transcriptome and the clinical phenotype and the associated co-morbidities seen in KS has not been fully clarified yet. We reported here a 47 XXY karyotype Chinese male (KS) with infertility and analyzed the differences in gene expression patterns of peripheral blood mononuclear cells (PBMCs) from a Chinese male and a female control with normal karyotype by single-cell sequencing. more...
#> 449                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Diabetes and breast cancer are common diseases with a major impact on the health sector in Mexico and worldwide. Epidemiological and experimental works support the link between type 2 diabetes and breast cancer; these data support that insulin resistance, hyperglycemia, hyperinsulinemia, and elevated levels of IGF-1 in patients with type II diabetes mellitus promote growth and invasiveness of tumor cells. more...
#> 450                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Here we investigated the degree by which epigenetic signatures in children from mothers with obesity or gestational diabetes mellitus are influenced by environmental factors.   We profiled the DNA methylation signature of whole blood from lean, obese and gestational diabetes mellitus mothers and their respective newborns.  DNA methylation profiles of mothers showed high similarity across groups, while on the contrary, newborns from GDM mothers showed a marked distinct epigenetic profile compared to newborns of both lean and obese mothers. more...
#> 451                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Diabetic Nephropathy (DN) is a chronic complication of diabetes and the primary cause of end stage renal disease. DN can be differentially diagnosed only through histological investigation. Therefore, there is need for molecular biomarkers, such as miRNAs, to discriminate among different histological lesions in diabetics. Aim of this study was to identify a pattern of differentially expressed miRNAs in kidney biopsies of DN patients and to assess their potential as differential diagnostic biomarkers. more...
#> 452                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Stem cell-derived β (SC-β) cells are an emerging regenerative therapy to compensate for loss of functional β cell mass in diabetes. Glucose-stimulated insulin secretion in SC-β cells is variable in vitro but stabilizes after transplantation and maturation under the kidney capsule of mice. We identified mechanisms correlated with functional maturation using RNA-sequencing and co-expression network analysis. more...
#> 453                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Aim: To improve risk stratification in patients with stable coronary artery disease (CAD), we aimed to identify genes in monocytes predictive of new ischemic events in patients with CAD and determine to what extent expression of these transcripts resembles expression in acute myocardial infarction (AMI). Results: COX10 and ZNF484 distinguished between AMI and the whole group of stable CAD patients with an accuracy of 90%. more...
#> 454                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        In type 2 diabetes, pancreatic beta-cells fail to compensate for the presence of insulin resistance in target tissues and represent a central player in the disease development. Identifying and studying innovative molecular mechanisms that lead to beta-cell failure in diabetes represent an interesting line of research and are necessary. N6-Methyladenosine (m6A) is the most abundant modification in mRNA and is found virtually in all mammals. more...
#> 455                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      β-cell specific Mettl14 knock-out mice display reduced N6-methyladenosine (m6A) levels and recapitulate human Type II diabetes (T2D) islet phenotype with early diabetes onset and mortality secondary to decreased β-cell proliferation and insulin degranulation. To gain insights into the role of m6A in regulating the IGF1/insulin -> AKT - > PDX1 pathway and to dissect the signaling networks modulating AKT phosphorylation,  we subjected freshly isolated islets from control and Mettl14 knock-out mice to phospho-antibody microarrays.
#> 456                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        In type 2 diabetes, pancreatic beta-cells fail to compensate for the presence of insulin resistance in target tissues and represent a central player in the disease development. Identifying and studying innovative molecular mechanisms that lead to beta-cell failure in diabetes represent an interesting line of research and are necessary. N6-Methyladenosine (m6A) is the most abundant modification in mRNA and is found virtually in all mammals. more...
#> 457                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Diabetic foot ulcers (DFUs) are characterized by a chronic inflammation state which prevents cutaneous wound healing, andDFUs eventually lead to infection and leg amputation. Macrophages located in DFUs are locked in an pro-inflammatory phenotype. In this study, the effect of hyperglycemia and hypoxia on the macrophage phenotype was analyzed. For this purpose, a microarray was performed to study the gene expression profile of macrophages cultivated in a high glucose concentration. more...
#> 458                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Phenotypic flexibility is used as a measure for health and can be studied during nutritional challenge tests. Changes in gene expression are early markers and give insight into mechanisms. Energy restriction (ER) has a variety of beneficial health effects and can be used to investigate different health states to study postprandial changes during challenge tests. Objective: We aimed to determine the postprandial effects of a 20% ER diet on whole genome expression profiles of peripheral blood mononuclear cells (PBMCs). more...
#> 459                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Type 2 diabetes is associated with obesity, and is characterized by insulin resistance in target tissues of the hormone combined with insufficient systemic insulin. Insulin resistance apparently begins in subcutaneous adipocytes that fail to further accumulate triacylglycerol. To understand the pathogenesis of transition from lean to obesity and to diabetes, we performed transcriptome profiling by RNA-sequencing of isolated primary human adipocytes. more...
#> 460                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
#> 461                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
#> 462                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. more...
#> 463                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Metformin, the most widely administered diabetes drug, has been proposed as a candidate for host directed therapy for tuberculosis although very little is known about its effects on human host responses to Mycobacterium tuberculosis. When added in vitro to PBMCs isolated from healthy non-diabetic volunteers, metformin increased glycolysis, inhibited the mTOR targets, strongly reduced M. tuberculosis induced production of TNF-alpha (-58%), IFN-gamma (-47%) and IL-beta (-20%), while increasing phagocytosis. more...
#> 464                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Metformin, the most widely administered diabetes drug, has been proposed as a candidate for host directed therapy for tuberculosis although very little is known about its effects on human host responses to Mycobacterium tuberculosis. When added in vitro to PBMCs isolated from healthy non-diabetic volunteers, metformin increased glycolysis, inhibited the mTOR targets, strongly reduced M. tuberculosis induced production of TNF-α (-58%), IFN-gamma (-47%) and IL-1β (-20%), while increasing phagocytosis. more...
#> 465                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We identified a rare subset of autoreactive lymphocytes with a hybrid phenotype of T and B cells including coexpression of TCR and BCR and key lineage markers of both cell types (hereafter referred to as dual expressers or DEs).  To investigate the dual phenotype of DEs at single cell resolution, we examined their transcriptomes using single cell RNA sequencing (scRNA-seq). We sorted individual DEs, Bcon and Tcon cells from PBMCs of one type I diabetes patient and analyzed the transcriptomes  of 34 DEs,  20 Bcon , and 23 Tcon  using the plate-based SMART-seq2 protocol (Tirosh and Suva, 2018; Tirosh et al., 2016). more...
#> 466                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Defining cellular and molecular identities within the kidney is necessary to understand its organization and function in health and disease. Here we demonstrate a reproducible method with minimal artifacts for single-nucleus Droplet-based RNA sequencing (snDrop-Seq) that we use to resolve thirty distinct cell populations in human adult kidney. We define molecular transition states along more than ten nephron segments spanning two major kidney regions. more...
#> 467                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       A 6-year-old boy, second son of healthy parents affected with epileptic encephalopathy of neonatal onset. Pregnancy with gestational diabetes controlled with diet. Delivery was uneventful. Since 48 hours of life, he presented episodes of cyanosis, generalized hypertonia, and tonic asymmetric postures followed by apnea. Video-EEG at 5 days of life showed bilateral and asynchronous spike-and-wave. Seizures were refractory to phenobarbital but were controlled with phenytoin. more...
#> 468                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Background: Clinical data identified an association between the use of HMG-CoA reductase inhibitors (statins) and incident diabetes in patients with underlying diabetes risk factors such as obesity, hypertension and dyslipidemia. The molecular mechanisms however are unknown. Methods: An observational cross-sectional study included 910 severely obese patients, mean (SD) body mass index 46.7 (8.7), treated with or without statins (ABOS cohort: a biological atlas of severe obesity). more...
#> 469                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               In vitro differentiation of human stem cells can produce pancreatic beta cells, the insulin-secreting cell type whose loss underlies Type 1 Diabetes. As a step towards mastery of this process, we report on transcriptional profiling of >100,000 individual cells sampled during in vitro beta cell differentiation and describe the cells that emerge. We resolve populations corresponding to beta cells, alpha-like poly-hormonal cells, non-endocrine cells that resemble pancreatic exocrine cells and a previously unreported population resembling enterochromaffin cells. more...
#> 470                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Adipocyte progenitor cells (APCs) provide the reservoir of regenerative cells to produce new adipocytes, although their identity in humans remains elusive. Using FACS analysis, gene expression profiling and metabolic and proteomic analyses, we identified three APCs subtypes in human white adipose tissues. The APC subtypes are molecularly distinct but possess similar proliferative and adipogenic capacities. more...
#> 471                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   This is a study of 114 newborns aimed at identifying associations of cord blood methylation profiles with measures of newborn adiposity. Neonatal adiposity is a risk factor for childhood obesity. Investigating contributors to neonata adiposity is important for understanding early life obesity risk. Epigenetic changes of metabolic genes in cord blood may contribute to excessive neonatal adiposity and subsequent childhood obesity. more...
#> 472                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Obesity underpins the development of numerous chronic diseases such as type II diabetes mellitus. It is well established that obesity negatively alters immune cell frequencies and functions. Mucosal Associated Invariant T (MAIT) cells are a population of innate T cells, which we have previously reported are dysregulated in obesity, with altered circulating and adipose tissue frequencies and a reduction in their IFN-gamma production, which is a critical effector function of MAIT cells in host defence. more...
#> 473                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Using influenza infection as a disease model, we used a systems biology approach to analyse host response and to identify immune pathways that might contribute to disease progression. We recruited influenza patients with varying severity of infection (n=154) and collected peripheral blood samples within 24 hours of their presentation to hospitals. Gene-expression arrays of these samples were analysed using weighted gene co-expression network analysis to detect disease-driving modules. more...
#> 474                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) is a lipid raft enzyme that regulates plasma membrane (PM) fluidity. Here we report that SMPDL3b excess, as observed in podocytes in diabetic kidney disease (DKD), impairs insulin receptor isoform B-dependent pro-survival insulin signaling by interfering with insulin receptor isoforms binding to caveolin-1 in PM. SMPDL3b excess affects the production of active sphingolipids resulting in decreased ceramide-1-phosphate (C1P) content as observed in human podocytes in vitro and in kidney cortexes of diabetic db/db mice in vivo. more...
#> 475                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Mutations in HNF1A cause Maturity Onset Diabetes of the Young type 3, the second most frequent form of diabetes caused by single gene mutation. We generated human pancreatic stem cell-derived endocrine cells with mutations in HNF1A and show that HNF1A deficiency impairs scβ-cell fate, insulin granule maturation and the secretion of insulin in a glucose responsive manner. Single-cell RNA sequencing reveals that HNF1A orchestrates a network of genes involved in glucose metabolism, zinc transport, calcium ion binding and hormone exocytosis. more...
#> 476                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Fish contains high quality proteins and essential nutrients including vitamin D (VitD3). Fish peptide consumption can lower cardiovascular disease (CVD) risk factors and studies showed an association between VitD3 deficiency, CVD and CVD risk factors such as diabetes. This study investigated acute effects of a single dose of VitD3, bonito fish peptide hydrolysate (BPH), or a combination of both on CVD risk factors and whole blood gene expression levels. more...
#> 477                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Mitochondrial DNA (mtDNA) 3243A>G tRNALeu(UUR) heteroplasmic mutation (m.3243A>G) exhibits clinically heterogeneous phenotypes. While the high mtDNA heteroplasmy exceeding a critical threshold causes mitochondrial encephalomyopathy, lactic acidosis with stroke-like episodes (MELAS) syndrome, the low mtDNA heteroplasmy causes maternally inherited diabetes with or without deafness (MIDD) syndrome. How quantitative differences in mtDNA heteroplasmy produces distinct pathological states has remained elusive. more...
#> 478                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We have studied the impact of T2D on open chromatin in human pancreatic islets. We used assay for transposase-accessible chromatin using sequencing (ATAC-seq) to profile open chromatin in islets from T2D and non-diabetic  donors. We identified ATAC-seq peaks representing open chromatin regions  in islets of non-diabetic and diabetic donors. The majority of ATAC-seq peaks mapped near transcription start sites. more...
#> 479                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               White adipose tissue (WAT) is a central factor in the development of type 2 diabetes. Despite the epidemiological importance of WAT there is a paucity of translational models to study long term changes in mature adipocytes. Here, we describe a novel method for the culture of mature white adipocytes under a permeable membrane. Compared to existing culture methods such as adipose tissue explants and adipocyte ceiling culture, Membrane mature Adipocyte Aggregate Cultures (MAAC) are superior at maintaining adipogenic gene expression through 2 weeks of culture, do not dedifferentiate, and are under reduced hypoxic stress relative to adipose tissue explants. more...
#> 480                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Despite substantial declines in mortality following myocardial infarction (MI), subsequent left ventricular remodelling (LVRm) remains a significant long-term complication. Extracellular small non-coding RNAs (exRNAs) have been associated with cardiac inflammation and fibrosis and we hypothesized that they are associated with post-MI LVRm phenotypes. RNA sequencing of exRNAs was performed on plasma samples from patients with “beneficial” (decrease LVESVI ≥20%, n=11) and “adverse” (increase LVESVI ≥15%, n=11) LVRm. more...
#> 481                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 482                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We generated expression profiles of TH1 and TREG cells from T1D and healthy subjects by RNA-Seq. By integrating RNA-Seq dta with other data sets, we predicted and validated serveral T1D risk SNPs.
#> 483                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Most type 1 diabets (T1D) associated SNPs are located in non-coding regions, making it hard to understand their functional impact. We performed epigenomic profiling of two enhancer marks, H3K4me1 and H3K27ac, using primary TH1 and TREG cells from healthy  and T1D subjects. By integrating enhancers predicted using these ChIP-Seq data, T1D associated SNPs and additional supporting data, we found and validated several novel risk SNPs for T1D.
#> 484                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                We conducted a genome-wide placental transcriptome study aiming at the identification of functional pathways representing the molecular link between maternal pre-pregnancy BMI and fetal growth. We used RNA microarray (Agilent 8 X 60 K), medical records, and questionnaire data from 183 mother-newborn pairs from the ENVIRONAGE birth cohort study (Flanders, Belgium). We applied a weighted gene co-expression network analysis (WGCNA) and identified genes modules and hub genes that were associated with maternal BMI as well as newborn birth weight. more...
#> 485                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Mutations in HNF1A cause Maturity Onset Diabetes of the Young type 3, the second most frequent form of diabetes caused by single gene mutation. We generated human pancreatic stem cell-derived endocrine cells with mutations in HNF1A and show that HNF1A deficiency impairs scβ-cell fate, insulin granule maturation and the secretion of insulin in a glucose responsive manner. Single-cell RNA sequencing reveals that HNF1A orchestrates a network of genes involved in glucose metabolism, zinc transport, calcium ion binding and hormone exocytosis. more...
#> 486                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 487                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...
#> 488                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Type 1 diabetes (T1D) is caused by autoimmune destruction of pancreatic β cells. Mounting evidence supports a central role for β-cell alterations in triggering the activation of self-reactive T-cells in T1D. However, the early deleterious events that occur in β cells, underpinning islet autoimmunity are not known. We hypothesized that epigenetic modifications induced in β cells by inflammatory mediators play a key role in initiating the autoimmune response. more...
#> 489                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    The study was aimed to identify novel autoantibody(AAB) biomarkers for Type 1 diabetes.
#> 490                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            RAD21 ChIA-PET in human MSiPS cells  For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
#> 491                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           RAD21 ChIA-PET in human MSFIB cells (fibroblast from skin from donor Michael Snyder)  For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
#> 492                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        RAD21 ChIA-PET in human MSLCL cells (B-cell-derived lymphoblastoid cell line from donor Michael Snyder)  For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
#> 493                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Peripheral blood samples were collected from control-arm subjects enrolled in 6 clinical trials conducted by the Immune Tolerance Network and Type 1 Diabetes TrialNet. The included trials evaluated immune-modifying therapy in new-onset T1D, with similar trial timecourses, primary outcomes, and data and sample collection. Total RNA was isolated from whole blood samples and then globin-reduced. RNAseq libraries were prepared from the globin-reduced RNA.
#> 494                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Peripheral blood samples were collected from subjects enrolled in the TrialNet study TN-09. This was a phase II study of the effects of the T cell costimulation inhibitor CTLA4-Ig (abatacept) in new-onset T1D. Total RNA was isolated from whole blood samples and then globin-reduced. RNAseq libraries were prepared from the globin-reduced RNA.
#> 495                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Introduction: In human placenta, alteration in trophoblast differentiation has a major impact on placental maintenance and integrity. Moreover, abnormal syncytial fusion seems to be implicated in the development of many complications including pre-eclampsia and intra-uterine growth restriction (IUGR). However, little is known about the mechanisms that control cytotrophoblast fusion into syncytiotrophoblast. more...
#> 496                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Age-related macular degeneration (AMD) is a complex multifactorial disease with at least 34 loci contributing to genetic susceptibility.  To gain functional understanding of AMD genetics, we generated transcriptional profiles of retina from 453 individuals including both controls and cases at distinct stages of AMD.  We integrated retinal transcriptomes, covering 13,662 protein-coding and 1,462 noncoding genes, with genotypes at over 9 million common single nucleotide polymorphisms (SNPs) for expression quantitative trait loci (eQTL) analysis of a tissue not included in Genotype-Tissue Expression (GTEx) and other large datasets. more...
#> 497                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Prenatal development is a critical period for programming of neurological disease. Preeclampsia, a pregnancy complication involving oxidative stress in the placenta, has been associated with long-term health implications for the child, including an increased risk of developing schizophrenia and autism spectrum disorders in later life. We have shown previously, in a rodent model of placental oxidative stress, that culture medium conditioned by the placenta alters neuronal characteristics when applied to primary cortical cultures in vitro and mimics many of the neurodevelopmental changes observed in the offspring brain. more...
#> 498                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 OBJECTIVE Diet intervention in obese adults is the first strategy to induce weight loss and to improve insulin sensitivity. We hypothesized that improvements in insulin sensitivity after weight loss from a short-term dietary intervention tracks with alterations in expression of metabolic genes and abundance of specific lipid species. RESEARCH DESIGN AND METHODS Eight obese, insulin resistant, non-diabetic adults were recruited to participate in a three-week low calorie diet intervention study (1000 kcal/day). more...
#> 499                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Metformin is a well tolerated and often prescribed treatment for type 2 diabetes. However, the effect of metformin on gene expression in endothelial cells remains unknown. We used RNA-seq to profile gene expression in primary human aortic endothelial cells stimulated with metformin in normoglycaemic and hyperglycaemic conditions. We identified novel pathways in hyperglycaemic endothelial cells that may be involved in the development of endothelial dysfunction. more...
#> 500                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Intrauterine growth restriction (IUGR) is associated with increased susceptibility to obesity, metabolic syndrome and type 2 diabetes. Although the mechanisms underlying the fetal origin of metabolic disease are poorly understood, evidence suggests epigenomic alterations play a critical role. We sought to identify changes in DNA methylation patterns that define IUGR in CD3+ T-cells purified from umbilical cord blood obtained from appropriate for gestational age (Control) and IUGR male newborns using a genome-wide assay. more...
#> 501                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Animal studies have linked disturbed adipose tissue clock gene rhythms to the pathophysiology of the metabolic syndrome. However, data on molecular clock rhythms in human patients are limited. Therefore, in a standardized real life setting, we compared diurnal gene expression profiles in subcutaneous adipose tissue between obese patients with type 2 diabetes and age-matched healthy lean control subjects, using RNA sequencing. more...
#> 502                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    This is a transcriptomics analysis contributing to a bigger project that tries to shed light on the role of type 2 diabetes mellitus (T2DM) as a risk factor for colon cancer (CC). Here we present a gene expression screening of 7 colon tumor xenograft samples, 2 with diabetic mice and 5 with normal blood glucose levels. For xenograft model details see: Prieto I, et al. (2017) Colon cancer modulation by a diabetic environment: A single institutional experience. more...
#> 503                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            This is a transcriptomics analysis contributing to a bigger project that tries to shed light on the role of type 2 diabetes mellitus (T2DM) as a risk factor for colon cancer (CC). Here we present a gene expression screening of paired tumor and normal colon mucosa samples in a cohort of 42 CC patients, 23 of them with T2DM. Using gene set enrichment, we identified an unexpected overlap of pathways over-represented in diabetics compared to non-diabetics, both in tumor and normal mucosa, including diabetes-related metabolic and signaling processes. more...
#> 504                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Thiazolidinedione drugs (TZDs) target the transcriptional activity of PPARg to reverse insulin resistance in type 2 diabetes, but side effects limit their clinical use. Here, using human adipose stem cell-derived adipocytes, we demonstrate that single-nucleotide polymorphisms (SNPs) were enriched at sites of patient-specific PPARg binding, which correlated with the individual-specific effects of TZD rosiglitazone (rosi) on gene expression. more...
#> 505                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            MicroRNAs (miRNAs) are noncoding RNAs representing an important class of gene expression modulators. Extracellular circulating miRNAs are both candidate biomarkers for disease pathogenesis and mediators of cell-to-cell communication. We examined the miRNA expression profile of total serum and serum derived exosome-enriched extracellular vesicles in people with normal glucose tolerance or type 2 diabetes. more...
#> 506                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           EndoC-βH1 is emerging as a critical human β cell model to study the genetic and environmental etiologies of β cell (dys)function and diabetes. Comprehensive knowledge of its molecular landscape is lacking, yet required, for effective use of this model. Here, we report chromosomal (spectral karyotyping), genetic (genotyping), epigenomic (ChIP-seq and ATAC-seq), chromatin interaction (Hi-C and Pol2 ChIA-PET), and transcriptomic (RNA-seq and miRNA-seq) maps of EndoC-βH1. more...
#> 507                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Identification of filamin-A as a target for insulin and IGF1 action. Insulin analogues have been developed to achieve further improvement in the therapy of diabetes. However, modifications introduced into the insulin molecule might enhance their affinity to the insulin-like growth factor-1 receptor (IGF1R). Most tumors, including endometrial cancers, express high levels of IGF1R. The present study was aimed at identifying the entire set of genes that are differentially activated by insulin glargine or detemir, in comparison to regular insulin and IGF1, in Type 1 and Type 2 endometrial cancer cell lines (ECC-1 and USPC-1, respectively). more...
#> 508                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      We report that the effect of GDM on gene expression differs between feto-placental endothelial cells of male vs female progeny, i.e. after pregnancy with a male or female offspring.
#> 509                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 510                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Amyotrophic lateral sclerosis (ALS) is an incurable and fatal neurodegenerative disease. Increasing the chances of success for future clinical strategies requires more in-depth knowledge of the molecular basis underlying disease heterogeneity. We recently laid the foundation for a molecular taxonomy of ALS by whole transcriptome expression profiling of motor cortex from sporadic ALS (SALS) patients. more...
#> 511                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We have identified molecular-level alternations in different adipose depots (thigh, visceral and subcutaneous) of Asian Indians (both male and female) suffering from type-2 diabetes as compared to age and BMI matched normal glucose tolerant subjects by functional analysis of differentially expressed genes, and correlation of gene expression estimates with measured intermediate traits associated with T2D and its related co-morbidities (Hb1Ac, HOMA-B, HOMA-R, NEFA, Triglyceride, Total Cholesterol, HDL, LDL, VLDL, Leptin, Adiponectin, TNF-α,  Serum- Creatinine,  IL-6, High sensitivity - serum-creatinine (hs-CRP) and also size of adipocytes). more...
#> 512                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Sirtuin deacetylases and forkhead box class O (FOXO) transcription factors are central regulators of cell survival, cell cycle and cellular resistance to stress in response to signals from hormones, growth factors and oxidative stress. FOXO activity is modulated by the sirtuins, which function in a NAD+-dependent manner. Sirtuin activity, on the other hand is subject to inhibition by a natural compound nicotinamide (NAM). more...
#> 513                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Sirtuin deacetylases and forkhead box class O (FOXO) transcription factors are central regulators of cell survival, cell cycle and cellular resistance to stress in response to signals from hormones, growth factors and oxidative stress. FOXO activity is modulated by the sirtuins, which function in a NAD+-dependent manner. Sirtuin activity, on the other hand is subject to inhibition by a natural compound nicotinamide (NAM). more...
#> 514                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           The liver is a major site for synthesis, storage and redistribution of carbohydrates, proteins and lipids. In addition, it is well-known that maternal obesity (MO) increases risk of offspring cardiovascular disease (CVD), diabetes and obesity. However, the mechanisms by which the MO intrauterine environment predisposes offspring to CVD and metabolic dysregulation are unknown. The goal of this study was to assess the impact of MO on primate fetal liver and identify underlying molecular mechanisms by which MO increases disease risk. more...
#> 515                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Accumulation of visceral fat around internal organs, is a strong risk predictor for cardiometabolic disease. Although fat deposition at distinct anatomical sites is influenced by genetic factors their functional mechanism remains poorly understood. Here, we show ENPP6 as a neural determinant of selectively visceral adiposity. Through dual-energy X-ray absorptiometry (DXA) body composition analysis in 1,301 individuals from the isolated population of Orkney, we identified low-frequency variants at 4q35.1 associated with a reduction of DXA fat distribution (rs144607341/rs17583822, P = 2.7 x 10-10/ 2.0 x 10-9). more...
#> 516                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Human embryonic stem cells (hESCs) are a potential unlimited source of insulin-producing β-cells for diabetes treatment. A greater understanding of how β-cells form during embryonic development will improve current hESC differentiation protocols. As β-cells are formed from NEUROG3-expressing endocrine progenitors, this study focused on characterizing the single-cell transcriptomes of mouse and hESC-derived endocrine progenitors. more...
#> 517                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Natural and stable cell identity switches, where terminally-differentiated cells convert into different cell-types when stressed, represent a widespread regenerative strategy in animals, yet they are poorly documented in mammals. In mice, some glucagon-producing pancreatic α-cells become insulin expressers upon ablation of insulin-secreting β-cells, promoting diabetes recovery. Whether human islets also display this plasticity for reconstituting β-like cells, especially in diabetic conditions, remains unknown. more...
#> 518                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Purpose: Pancreatic islet transplantation is an effective cell therapy for type 1 diabetes (T1D), but its clinical application is limited by the shortage of donor pancreata. Among the potential alternatives, the differentiation of human embryonic stem cells (hESc) into insulin-producing β-cells has taken an early lead. However, while the proportion of β-cells obtained through current methods is relatively high, a significant percentage of undefined non-endocrine cell types are still generated. more...
#> 519                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Natural and stable cell identity switches, where terminally-differentiated cells convert into different cell-types when stressed, represent a widespread regenerative strategy in animals, yet they are poorly documented in mammals. In mice, some glucagon-producing pancreatic α-cells become insulin expressers upon ablation of insulin-secreting β-cells, promoting diabetes recovery. Whether human islets also display this plasticity for reconstituting β-like cells, especially in diabetic conditions, remains unknown. more...
#> 520                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Understanding the molecular mechanisms regulating the maintenance and destruction of intervertebral disc may lead to the development of new therapies for intervertebral disc degeneration (IDD). Here we present evidence from miRNA microarray analyses of clinical data sets along with in vitro and in vivo experiments that miR-141 is a key regulator of IDD. Gain- and loss-of-function studies show that miR-141 drives IDD by inducing nucleus pulposus (NP) apoptosis. more...
#> 521                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Peripheral blood samples were collected from subjects enrolled in the TrialNet study TN-05. This was a phase II study of the effects of the anti-CD20 monoclonal antibody rituximab in new-onset T1D. Total RNA was isolated from whole blood samples and then globin-reduced. RNAseq libraries were prepared from the globin-reduced RNA.
#> 522                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Background: Imprinted genes are defined by their preferential expression from one of the two parental alleles. This unique mode of gene expression is dependent on allele-specific DNA methylation profiles established at regulatory sequences called imprinting control regions. These loci are frequently used as biosensors to study how environmental exposures affect methylation and transcription. However, a critical unanswered question is whether they are more, less or equally sensitive to environmental stressors as the rest of the genome. more...
#> 523                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Insulin gene mutations are a leading cause of neonatal diabetes. They can lead to proinsulin misfolding and its retention in endoplasmic reticulum (ER). This results in increased ER-stress suggested to trigger beta-cell apoptosis. In humans, the mechanisms underlying beta-cell failure remain unclear. Here we show that misfolded proinsulin impairs developing beta-cell proliferation without increasing apoptosis. more...
#> 524                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Intrahepatic cholangiocarcioma has two molecular classification of intrahepatic CCA with distinct clinical, pathological, biological and prognostic differences
#> 525                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Analysis of neutrophils purified from peripheral blood of patients with symptomatic and pre-symptomatic type 1 diabetes (T1D), at risk of T1D, and healthy controls.
#> 526                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Cellular senescence, an irreversible proliferative arrest, functions in tissue remodeling during development and is implicated in multiple aging-associated diseases. While senescent cells often manifest an array of senescence-associated phenotypes, such as cell cycle arrest, altered heterochromatin architecture, reprogrammed metabolism and senescence-associated secretory phenotype(SASP), the identification of senescence cells has been hindered by lack of specific and universal biomarkers. more...
#> 527                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Diabetes is prevalent worldwide and associated with severe health complications, including blood vessel damage that leads to cardiovascular disease and death. Here we report the development of a 3D blood vessel organoid culture system from human pluripotent stem cells. These human blood vessel organoids contain endothelial cells and pericytes that self-assemble into interconnected capillary networks enveloped by a basement membrane. more...
#> 528                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 529                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Background: Here, the role of α-ketoglutarate (αKG) in the epi-metabolic control of DNA demethylation has been investigated in therapeutically relevant cardiac mesenchymal cells (CMSCs) isolated from controls and type 2 diabetes donors. Methods & results: Quantitative global analysis, methylated and hydroxymethylated DNA sequencing and gene specific GC methylation detection revealed an accumulation of 5mC, 5hmC and 5fC in the genomic DNA of human CMSCs isolated from diabetic (D) donors (D-CMSCs). more...
#> 530                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Type 2 diabetes mellitus is a chronic age-associated degenerative metabolic disease that reflects relative insulin deficiency and resistance. Extracellular vesicles (EVs; exosomes, microvesicles and apoptotic bodies) are small (50-400 nM) lipid-bound vesicles capable of shuttling functional proteins, nucleic acids, and lipids as part of intercellular communication systems. Recent studies in mouse models and in cell culture suggest that EVs may modulate insulin signaling. more...
#> 531                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The common gamma chain (γc) is required for productive signaling by interleukin (IL)-15, IL-21 and IL-2, which are critically involved in immune activation and regulation. IL-21 and IL-15 are implicated in the pathogenesis of type-1 diabetes, graft-versus-host disease, and celiac disease (CeD), a gluten-mediated autoimmune-like enteropathy. Attempts to treat type-1 diabetes and graft-versus-host disease with biologics targeting one particular cytokine have failed. more...
#> 532                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Using an integrated approach to characterize the pancreatic tissue and isolated islets from a 33-year-old with 17 years of type 1 diabetes (T1D), we found donor islets contained β cells without insulitis and lacked glucose-stimulated insulin secretion despite a normal insulin response to cAMP-evoked stimulation. With these unexpected findings for T1D, we sequenced the donor DNA and found a pathogenic heterozygous variant in hepatocyte nuclear factor 1 alpha (HNF1A). more...
#> 533                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Pancreatic endocrine cells orchestrate the precise control of blood glucose levels, but the contribution of each cell type to diabetes or obesity remains elusive. Here we used a massively parallel single-cell RNA-seq technology (Drop-Seq) to analyze the transcriptome of 26,677 pancreatic islets cells from both healthy and type II diabetic (T2D) donors. We have analyzed cell type-specific gene signatures, and detected several rare α or β cell subpopulations with high sensitivity. more...
#> 534                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Identification of cell surface markers specific to human pancreatic β-cells would allow in vivo analysis and imaging. Here we introduce a biomarker – ectonucleoside triphosphate diphosphohydrolase-3 (NTPDase3) – that is expressed on the cell surface of essentially all adult human β-cells, including those from individuals with type 1 or type 2 diabetes (T1D, T2D). NTPDase3 is expressed dynamically during postnatal human pancreas development, appearing first in acinar cells at birth, but several months later its expression declines in acinar cells while concurrently emerges in islet β-cells. more...
#> 535                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Background: Long-term exposure to elevated levels of free fatty acids (FFAs) is deleterious for beta-cell function and may contribute to development of type 2 diabetes mellitus (T2DM). Whereas mechanisms of impaired glucose-stimulated insulin secretion (GSIS) in FFA-treated beta-cells have been intensively studied, biological events preceding the secretory failure, when GSIS is accentuated, are poorly investigated. more...
#> 536                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The aim of this study was to understand if gene expression in atherosclerotic plaque macrophages is altered by diabetes. Laser capture microdissection (LCM) was used to specifically isolate macrophage enriched regions from human carotid atherosclerotic plaque samples. RNA isolated was then sent for sequencing using the Illumina bead array system. Gene expression data revealed that 106 genes from diabetic macrophages are differentially expressed (FDR<0.2) and provide mechanistic evidence for the involvement of Runt-related transcription factor 1 (RUNX1) in the development of diabetic atherosclerosis.
#> 537                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Circadian misalignment, such as in shift work, has been associated with obesity and type 2 diabetes, however, direct effects of circadian misalignment on skeletal muscle insulin sensitivity and muscle molecular circadian clock have never been investigated in humans. Here we investigated insulin sensitivity and muscle metabolism in fourteen healthy young lean men (age 22.4 ± 2.8 years; BMI 22.3 ± 2.1 kg/m2 [mean ± SD]) after a 3-day control protocol and a 3.5-day misalignment protocol induced by a 12-h rapid shift of the behavioral cycle. more...
#> 538                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Recent genome-wide association studies (GWAS) have identified gene variants associated with coronary artery disease including ADAMTS7, PHACTR1, KIAA1462/JCAD (Junctional Protein Associated with Coronary Artery Disease) and many others. JCAD has been identified as a novel component of endothelial cell-cell junctions (Akashi et al., 2011, BBRC) and regulates angiogenesis (Hara et al, ATVB, 2017). In our study, we observed that JCAD is a 148-KDa protein identified by mass spectrometry, but display a band shift to around 180-200 KDa, suggesting that JCAD is subject to multiple post-translatinonal modification. more...
#> 539                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Human CD8+ T cells are the final mediators of autoimmune β-cell destruction in type 1 diabetes. However, their target epitopes have not been demonstrated to be naturally processed and presented by β cells. We therefore performed an epitope discovery study combining HLA Class I peptidomics and transcriptomics strategies. Inflammatory cytokines increased β-cell peptide presentation in vitro, paralleling upregulation of HLA Class I expression. more...
#> 540                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. more...
#> 541                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. more...
#> 542                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Diabetes is prevalent worldwide and associated with severe health complications, including blood vessel damage that leads to cardiovascular disease and death. We report the development of 3D blood vessel organoids from human embryonic and induced pluripotent stem cells. These human blood vessel organoids contain endothelium, perivascular pericytes, and basal membranes, and self-assemble into lumenized interconnected capillary networks. more...
#> 543                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Transcriptome comparison of glomeruli from kidneys with diabetic nephropathy (DN) and glomeruli from the unaffected portion of tumor nephrectomies. Transcritomics profile of glomeruli in DN patients explored SRGAP2 was strongly associated with proteinuria and involved in podocyte cytoskeleton organization
#> 544                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Our current understanding of the pathogenesis of T1D arose in large part from studies using the non-obese diabetic (NOD) mouse model of type 1 diabetes (T1D). Of concern, therapeutic interventions shown to significantly dampen or even reverse disease in mouse models have not successfully translated into interventions in human T1D. The present study addresses this disconnect in research translation by directly analyzing human donor islets from individuals with T1D, aiming to provide insight into disease mechanisms and identify potential target pathways for therapeutic intervention. more...
#> 545                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            New measures are needed to predict type 1 diabetes disease trajectory.  We have developed a sensitive array-based bioassay whereby patient plasma is used to induce transcription in healthy “reporter” leukocytes.  Here we report a refined gene ontology-based inflammatory index (I.I.359) that is based upon expression levels of 359 transcripts identified in cross-sectional studies of new onset Type 1 diabetes patients and controls, where higher scores reflect greater inflammatory bias. more...
#> 546                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 547                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Diabetes is a complex metabolic syndrome characterized by prolonged high blood glucose levels. It is known that diabetes is associated with an elevated risk of cancer, however, the underlying molecular mechanisms are largely unknown. In particular, it remains unclear as to how hyperglycemia may affect epigenetic checkpoints and tumor suppressor pathways, thus enabling oncogenic transformation. Here we show that long-term hyperglycemic conditions adversely impact the anti-tumor epigenetic mark DNA 5-hydroxymethylcytosine (5hmC) through direct regulation of the tumor suppressor and DNA 5mC hydroxymethylase, TET2. more...
#> 548                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Role of circRNAs in active tuberculosis (TB) remains unknown. The present study was aimed to determine plasma circRNA expression profile in active TB patients to identify potential biomarker by circRNA microarrays.
#> 549                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            We investigated whether variants fine-mapped for Rheumatoid Arthritis (RA) and Type 1 Diabetes overlap with open chromatin regions specifically after stimulation. We show that rs117701653, a potentially causal variant for RA near CD28, overlaps open chromatin regions only after stimulation. We futhermore observe a small increase in enhancer activity for this variant under stimulatory conditions using a luciferase assay. more...
#> 550                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            There is a temporal window from the time diabetes is diagnosed to the appearance of overt kidney disease during which time the disease progresses quietly without detection.  Currently, there is no way to detect early diabetic nephropathy (EDN). Here we performed an unbiased assessment of gene-expression analysis of postmortem human kidneys using microarrays to identify candidate genes that may contribute to EDN.
#> 551                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             To delineate the effects of BCL11A (a type 2 diabetes risk gene) in human beta cell function we knockdown BCL11A in primary human beta cells and generated and sequenced RNA-seq libraries from 4 human donors
#> 552                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 553                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         This paper describes the first time a high-content environmental chemicals screen using pancreatic β-like cells derived from human pluripotent stem cells (hPSCs), and discovered that a commonly used pesticide, propargite, induces pancreatic β-cell DNA damage and necrosis. More interestingly, we found out the genetic background of β-like cells affects their response to propargite-induced toxicity, based on isogenic hPSC platform, including for variants GWAS identified associated with T1D, since isogenic GSTT1-/- and PTPN2-/- pancreatic β-like cells are hypersensitive to propargite-induced β-cell death both in vitro and in vivo. more...
#> 554                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         This paper describes the first time a high-content environmental chemicals screen using pancreatic β-like cells derived from human pluripotent stem cells (hPSCs), and discovered that a commonly used pesticide, propargite, induces pancreatic β-cell DNA damage and necrosis. More interestingly, we found out the genetic background of β-like cells affects their response to propargite-induced toxicity, based on isogenic hPSC platform, including for variants GWAS identified associated with T1D, since isogenic GSTT1-/- and PTPN2-/- pancreatic β-like cells are hypersensitive to propargite-induced β-cell death both in vitro and in vivo. more...
#> 555                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           In our study, we generated and sequenced small RNA libraries from commercially available brain total RNA or human blood plasma samples.  These samples were generated with MAD-DASH, a method we developed employing CRISPR/Cas9 ribonucleoprotein targeting specific overabundant sequences such as adapter dimer or miRNAs to reduce these sequences from final libraries. We sequenced treated and untreated samples to demonstrate specificity, efficacy, and reproducibility of our MAD-DASH small-RNA sequencing protocol.
#> 556                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      TaqMan®Array  Human  MicroRNA  Cards  were used to profile the differential expression of human microRNAs in patients with CKD versus heathy controls
#> 557                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       In the past few decades, the prevalence of overweight and obesity has sharply increased in children and adolescents. Childhood obesity life are associated with increased risk of cardiovascular disease (CVD), diabetes mellitus, metabolic syndrome, sleep disturbances and certain cancers in adulthood. Childhood obesity has become a serious global public health challenge. Long noncoding RNAs (lncRNAs) have an important role in adipose tissue function and energy metabolism homeostasis, and abnormalities may lead to obesity. more...
#> 558                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Myometrial biopsies were collected from 20 women undergoing primary cesarean sections in well-characterized clinical scenarios: 1) term labor of spontaneous onset (TL, n=5); 2) term non-labor (TNL, n=5); 3) spontaneous PTB in the setting of chorioamnionitis (PTB-HCA) and 4) indicated preterm birth (PTB) non-labor (PTB-NL, n=5).  RNAs were profiled using 2nd-generation RNA sequencing.
#> 559                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Type 2 Diabetes (T2D) is a complex metabolic disorder due to a progressive insulin secretory defect on the background of insulin resistance. We found a muscle specific lncRNA we named TDNC1(T2D down-regulated non-coding RNA 1) whose expression is reduced in T2D patients as well as young individuals with family history of T2D. We used Microarray to assess for global gene expression pattern following ectopic expression of this lncRNA.
#> 560                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Recent study has revealed that long non-coding RNAs (lncRNAs) perform as important regulators of cellular physiology and pathology, which makes them promising therapeutic and diagnostic entities. We found lncRNA WAKMAR1 is significantly down-regulated in wound-edge keratinocytes from venous ulcer and diabetic foot ulcer compared to the normal wounds. To study the genes regulated by WAKMAR1, we transfected lncRNA GapmeRs into human primary epidermal keratinocytes to inhibit its expression. more...
#> 561                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Through development and use of a minimal component protocol for derivation of late stage pancreatic progenitors and beta-like cells, we compared WT and GLIS3-/- pancreatic cells at different stages and discovered that GLIS3-/- cells show an ectopic activation of TGF-beta signaling.
#> 562                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Cystic fibrosis (CF)-related diabetes (CFRD) is an increasingly common and devastating comorbidity of CF, affecting ~35% of adults with CF. However, the underlying causes of CFRD are unclear. Here, we examined cystic fibrosis transmembrane conductance regulator (CFTR) islet expression and whether the CFTR participates in islet endocrine cell function using murine models of b cell CFTR deletion, and normal and CF human pancreas and islets. more...
#> 563                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Introduction: There is increasing evidence that consumption of cocoa products have a beneficial effect on cardio-metabolic health, but the underlying mechanisms remain unclear. Cocoa contains a complex mixture of flavan-3-ols. Epicatechin, a major monomeric flavan-3-ol, is considered to contribute to the cardio-protective effects of cocoa. We investigated effects of pure epicatechin supplementation on whole genome gene expression profiles of circulating immune cells. more...
#> 564                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           We investigate whether lower weight gain with insulin detemir is due to a decrease in energy intake or an increase in energy output and whether any change in energy balance is accompanied by changes in hormones, lipid metabolism and muscle gene expression.
#> 565                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The goal of this study was to analyse the effect of a 12 weeks treatment with rosiglitazone on insulin sensitivity in the muscle of type 2 diabetic patients.  Ten diabetic patients were submitted to a 3 hours euglycemic-hyperinsulinemic clamp. Skeletal muscle biopsies were taken before and after the clamp. Samples from the same patients (obtained before and after the clamp) were hybridized on the same microarray. more...
#> 566                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Obesity has emerged as a formidable health crisis due to its association with metabolic risk factors such as diabetes, dyslipidaemia and hypertension. Recent work has demonstrated the multifaceted roles of lncRNAs in regulating mouse adipose development, but its implication in human adipocytes remain largely unknown at least partially due to the lack of a comprehensive lncRNA catalog, particularly those specifically expressed in brown adipose tissue (BAT). more...
#> 567                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Factors predicting body weight gain and associated disturbed glucose metabolism remain to be established. Here we assessed the role of subcutaneous adipocyte lipid mobilization (lipolysis) in spontaneous long-term (>10 years) body weight changes. In two independent clinical cohorts we found that low stimulated lipolysis at baseline correlated inversely with body mass index changes over time. Disturbed lipolysis gave odds ratios of ≥4.6 for weight gain and ≥3.2 for development of insulin resistance and impaired fasting glucose/type 2 diabetes. more...
#> 568                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              In traditional Chinese medicine (TCM), blood stasis syndrome (BSS) is mainly manifested by the increase of blood viscosity, platelet adhesion rate and aggregation, and the change of microcirculation, resulting in vascular endothelial injury. It is an important factor in the development of diabetes mellitus (DM). The aim of this study was to screen out the potential candidate microRNAs (miRNAs) in DM patients with BSS by high-throughput sequencing (HTS) and bioinformatics analysis. more...
#> 569                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            In traditional Chinese medicine (TCM), blood stasis syndrome (BSS) is mainly manifested by the increase of blood viscosity, platelet adhesion rate and aggregation, and the change of microcirculation, resulting in vascular endothelial injury. It is an important factor in the development of diabetes mellitus (DM). According to the differences in the internal and external environment of the individual disease, BSS were divided into qi-deficiency and blood stasis syndrome (QDBS), qi-stagnation and blood stasis syndrome (QSBS), cold-coagulation and blood stasis syndrome (CCBS), heat-accumulation and blood stasis syndrome (HABS). more...
#> 570                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       This study compared the transcriptome profiling (RNA-seq) of CD3+ T cells from nondiabetic (ND) individuals and patients with type 1 diabetes (T1D).
#> 571                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Preeclampsia (PE) is a complex, heterogeneous disorder of pregnancy, demonstrating considerable variability in observed maternal symptoms and fetal outcomes. We recently identified five clusters of placentas within a large gene expression microarray dataset (N=330, GSE75010), of which four contained a substantial number of PE samples. However, while transcriptional analysis of placentas can subtype patients, we hypothesized that the addition of epigenetic information should reveal gene regulatory mechanisms behind the distinct PE pathologies. more...
#> 572                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Objective: Homozygous loss-of-function mutations in the gene coding for the homeobox transcription factor (TF) PDX1 leads to pancreatic agenesis, whereas heterozygous mutations can cause Maturity-Onset Diabetes of the Young 4 (MODY4). Although the function of Pdx1 is well studied in pre-clinical models during insulin-producing β-cell development and homeostasis, it remains elusive how this TF controls human pancreas development by regulating a downstream transcriptional program. more...
#> 573                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              We sequenced the transcriptomes of seven samples of hypothalamic neurons dervied from pluripotent stem cells taken from healthy patients; five samples of hypothalamic neurons derived from pluripotent stem cells of constitutionally obese donors; five samples of sectioned hypothalami from post-mortem dissection of brains, and two samples for motor neurons derived from pluripotent stem cells of healthy donors in order to assess the similarity of our iPSC-derived cells against those of sectioned brains and to identify possible transcriptional disfunction which might underlie extreme, inherited obesity.
#> 574                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The p.R482W hotspot mutation in A-type nuclear lamins causes familial partial lipodystrophy of Dunnigantype (FPLD2), a lipodystrophic syndrome complicated by early-onset atherosclerosis. Molecular mechanisms underlying endothelial cell dysfunction conferred by the lamin A mutation remain elusive. However, lamin A regulates epigenetic developmental pathways and mutations could perturb these functions. more...
#> 575                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We aimed to determine the association between extracellular miRs and HIV infection, and have demonstrated unique expression profile of 29 miRs in HIV+ subjects and 34 miRs in elite controllers as compared to HIV- subjects. Elite HIV+ subjects are those  who are HIV+, not on antiretroviral therapy, and with HIV viral load <200 copies/mL.
#> 576                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       This data represents whole transcriptome total RNA gene expression profiles of peripheral blood mononuclear cells collected from 29 advanced heart failure patients on the day before undergoing mechanical circulatory support surgery. Keywords = Advanced Heart Failure. Keywords =  Mechanical Circulatory Support. Keywords = Biological Age. Keywords = PBMC. Keywords = Immune Response. Keywords = Peripheral Blood. more...
#> 577                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Progressive failure of insulin-producing beta cells is the central event leading to diabetes, yet the signalling networks controlling beta cell fate remain poorly understood. Here we show that SRp55, a splicing factor regulated by the diabetes susceptibility gene GLIS3, has a major role in maintaining function and survival of human beta cells. RNA-seq analysis revealed that SRp55 regulates the splicing of genes involved in cell survival and death, insulin secretion and JNK signalling. more...
#> 578                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Human ß cell dedifferentiation as a potent mechanism of diabetes is gaining prominence. Several data suggest an upregulation of the transcription factor SOX9, a progenitor and duct cell marker during ß cell dedifferentiation. However, its targets in such cells need more understanding. Here, we overexpressed SOX9 and a constitutively active mutant (VP16-SOX9∆TAD) in Human pancreatic beta EndoC-ßH1 cells in order to understand its targets.
#> 579                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic β cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than β cell death, suggesting loss of β cell identity. more...
#> 580                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     There is already strong evidence indicating that different types of non-coding RNAs, including microRNAs (miRNAs) and long non-coding RNAs, are key players in the regulation of β-cell functions and in the development of diabetes. However, the role of the newly discovered class of circular RNAs remains to be elucidated. We therefore analysed circular RNA expression in human islet samples.
#> 581                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             BACKGROUND & AIMS: Metabolic syndrome is a newly identified risk factor for hepatocellular carcinoma (HCC), however the molecular mechanisms still remain unclear. To elucidate this issue, cross-species analysis was performed to compare gene expression patterns of HCC from human patients and melanocortin 4 receptor-knockout (MC4R-KO) mice, developing HCC with obesity, insulin resistance and dyslipidemia. more...
#> 582                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             BACKGROUND & AIMS: Metabolic syndrome is a newly identified risk factor for hepatocellular carcinoma (HCC), however the molecular mechanisms still remain unclear. To elucidate this issue, cross-species analysis was performed to compare gene expression patterns of HCC from human patients and melanocortin 4 receptor-knockout (MC4R-KO) mice, developing HCC with obesity, insulin resistance and dyslipidemia. more...
#> 583                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      summary : Tubulointerstitial transcriptome from ERCB subjects with chronic kidney disease and living donor biopsies. Samples included in this analysis have been previously analyzed using older CDF definitions and are included under previous GEO submissions - GSE47184 (chronic kidney disease samples), and GSE32591 (IgA nephropathy samples).
#> 584                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              summary : Glomerular Transcriptome from European Renal cDNA Bank subjects and living donors. Samples included in this analysis have been previously analyzed using older CDF definitions and are included under previous GEO submissions - GSE47183 (chronic kidney disease samples), and GSE32591 (IgA nephropathy samples).
#> 585                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Explaining the genetics of many diseases is challenging because most associations localize to regulatory regions. We present a novel computational method for discovering disease-driving mechanisms acting across multiple disease-associated, non-coding genomic regions. Application to a matrix of 213 phenotypes and 1,544 transcription factor (TF) binding datasets identifies 2,264 significant associations for hundreds of TFs in 92 phenotypes, including prostate and breast cancers. more...
#> 586                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            49 human patient mRNA profiles was generated using HG-U133 Plus 2.0 microarrays. Procesed in Affymetrix Expression console using Plier normalization method and later processed in Partek Genomics Suite. The clustering figure was generated using HCE clustering software. We sought to determine the mechanisms underlying failure of muscle regeneration that is observed in dystrophic muscle through hypothesis generation using muscle profiling data (human dystrophy and murine regeneration). more...
#> 587                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Diabetes is a multifactorial disorder and epigenetics changes are increasingly appreciated to influence the development of diabetic complications. Chromatin remodeling and histone acetylation are implicated in activation of the inflammatory response. Recently, histone deacetylase (HDAC) inhibitors (HDACi) have proved to reduce the severity of inflammatory diseases. We have previously shown that chromatin alterations regulated by HDACi in HepG2 cells stimulated by hyperglycemia reduced hepatic glucose production. more...
#> 588                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            The prevalence of type 2 diabetes mellitus (T2D) is increasing constantly and various risk factors such as obesity, aging, nutritional states and physical inactivity, in addition to genetic pre-dispositions in different populations has been identified. The consequences of high blood glucose include damaged blood vessels, leading to arteriosclerosis and chronic diabetic microangiopathies. These changes lead to occlusive angiopathy, altered vascular permeability, or tissue hypoxia, resulting in complications such as heart disease, strokes, kidney disease, blindness, impaired wound healing, chronic skin ulcers, or amputations. more...
#> 589                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Total RNA was isolated from WBCs. For the analysis of genome-wide expression differences in small non-coding RNAs (sncRNAs) and long-coding and non-coding RNAs (mRNAs and lncRNAs), NGT and GDM pregnant women were selected. Twenty-nine GDM-associated mature micro-RNAs (miRNAs) with increased expression and one hundred sixty-three mRNAs with reduced expression associated with GDM were found (P<0.05 and FDR<0.1).
#> 590                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Diabetic foot ulcers (DFUs) are the leading cause of lower leg amputations in diabetic population. To better understand molecular pathophysiology of DFUs we used patients’ specimens and genomic profiling. We identified 3900 genes specifically regulated in DFUs. Moreover, we compared DFU to human skin acute wound (AW) profiles and found DNA repair mechanisms and regulation of gene expression among the processes specifically suppressed in DFUs, whereas essential wound healing-related processes, inflammatory/immune response or cell migration, were not activated properly. more...
#> 591                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Many patients with type 1 diabetes (T1D) have residual beta cells producing small amounts of C-peptide long after disease onset, but develop an inadequate glucagon response to hypoglycemia following T1D diagnosis. The features of these residual beta cells and alpha cells persisting in the islet endocrine compartment are largely unknown due to difficulty of comprehensive investigation. By studying the T1D pancreas and isolated islets, we show that remnant beta cells appeared to maintain several aspects of regulated insulin secretion. more...
#> 592                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 593                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Pancreatic islet beta cell failure causes type 2 diabetes (T2D). The IMIDIA consortium has used a strategy entailing a stringent comparative transcriptomics analysis of islets isolated enzymatically or by laser microdissection from two large cohorts of non-diabetic (ND) and T2D organ donors (OD) or partially pancreatectomized patients (PPP). This work led to the identification of a signature of genes that were differentially expressed between T2D and ND regardless of the sample type (OD or PPP). more...
#> 594                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Pancreatic islet beta cell failure causes type 2 diabetes (T2D). The IMIDIA consortium has used a strategy entailing a stringent comparative transcriptomics analysis of islets isolated enzymatically or by laser microdissection from two large cohorts of non-diabetic (ND) and T2D organ donors (OD) or partially pancreatectomized patients (PPP). This work led to the identification of a signature of genes that were differentially expressed between T2D and ND regardless of the sample type (OD or PPP). more...
#> 595                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       While histone deacetylase (HDAC) inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. While histone hyperacetylation has long been considered the paradigmatic mechanism of action, recent genome-wide profiles indicate more complex interactions with the epigenome. In particular, HDAC inhibitors also induce histone deacetylation at the promoters of highly active genes, resulting in gene suppression. more...
#> 596                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      In this study, we explored transcriptional differences in human neutrophils from patients with intracranial aneurysms and a demographic and comorbidity paired population of controls
#> 597                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                In summary, we discovered (1) that glucose dose-dependently inhibits cardiac maturation in vitro and in vivo, (2) that the maturation-inhibitory effect is dependent on nucleotide biosynthesis via the PPP, (3) that the developing heart accomplishes glucose deprivation condition by limiting the glucose uptake at late gestational stages during normal embryogenesis, and (4) that perturbation of the glucose deprivation in gestational diabetes affects natural cardiomyocyte maturation and potentially contributes to congenital heart disease.
#> 598                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Metabolic alterations relevant to postprandial dyslipidemia were previously identified in the intestine of obese subjects with systemic insulin resistance. These dysregulations were closely associated with an amplification of intestinal lipogenesis and lipoprotein output, which was triggered by insulin resistance likely sustained by oxidative stress and inflammation. The aim of the study was to identify the genes deregulated by the presence of systemic insulin resistance in the intestine of severely obese subjects. more...
#> 599                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 600                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Our goal was to measure molecular phenotypes associated with coronary atherosclerosis severity in a geriatric cohort.
#> 601                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Our goal was to measure molecular phenotypes associated with coronary atherosclerosis severity in a geriatric cohort.
#> 602                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Friedreich’s ataxia (FRDA; OMIM 229300), an autosomal recessive neurodegenerative mitochondrial disease, is the most prevalent hereditary ataxia. In addition, FRDA patients showed additional non-neurological features such as scoliosis, diabetes and cardiac complications. Hypertrophic cardiomyopathy, which is found in two thirds of patients at the time of diagnosis, is the primary cause of death in these patients. more...
#> 603                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      As organisms age, cells accumulate genetic and epigenetic changes that eventually lead to impaired organ function or catastrophic failure such as cancer. Here we describe a single-cell transcriptome analysis of 2544 human pancreas cells from donors, spanning six decades of life. We find that islet cells from older donors have increased levels of disorder as measured both by noise in the transcriptome and by the number of cells which display inappropriate hormone expression, revealing a transcriptional instability associated with aging. more...
#> 604                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Oral squamous cell carcinoma (OSCC) is the sixth most common cause of cancer mortality worldwide, and the five-year survival rate remains low in patients with advanced OSCC. Many studies indicate that microRNAs (miRNAs) may paly critical roles in OSCC carcinogenesis, but the dynamic composition and functions of miRNAs-mRNAs regulatory networks in OSCC pathogenesis remain largely unknown. Thus, detailed investigations of OSCC-associated miRNAs and their regulated networks may provide insights into mechanistic understanding of OSCC progression and development of new strategies of OSCC management. more...
#> 605                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Circulating ex-RNAs altered in plasma after acute exercise target pathways involved in inflammation, including miR-181b-5p.
#> 606                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            There is growing evidence that transplantation of cadaveric human islets is an effective therapy for type 1 diabetes. However, gauging the suitability of islet samples for clinical use remains a challenge. We hypothesized that islet quality is reflected in the expression of specific genes. Therefore, gene expression in 59 human islet preparations was analyzed and correlated with diabetes reversal after transplantation in diabetic mice. more...
#> 607                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           There is increasing evidence that metabolic diseases originate in early life, and epigenetic changes have been implicated as key drivers of this early life programming. This led to the hypothesis that epigenetic marks present at birth may predict an individual’s future risk of obesity and type 2 diabetes. In this study, we assessed whether epigenetic marks in blood of newborn children were associated with BMI and insulin sensitivity later in childhood. more...
#> 608                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Type 1 diabetes mellitus (T1DM) results from an autoimmune attack against the insulin-producing ß cells which leads to chronic hyperglycemia. Exosomes are lipid vesicles derived from cellular multivesicular bodies that are enriched in specific miRNAs, potentially providing a disease-specific diagnostic signature. To assess the value of exosome miRNAs as biomarkers for T1DM, miRNA expression in plasma-derived exosomes was measured. more...
#> 609                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The epigenome is often deregulated in cancer and treatment with inhibitors of bromodomain and extra-terminal proteins, the readers of epigenetic acetylation marks, represents a novel therapeutic approach. Here, we have characterized the anti-tumour activity of the novel bromodomain and extra-terminal (BET) inhibitor BAY 1238097 in preclinical lymphoma mod- els. BAY 1238097 showed anti-proliferative activity in a large panel of lym- phoma-derived cell lines, with a median 50% inhibitory concentration between 70 and 208 nmol/l. more...
#> 610                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        In the study, patients with type 2 diabetes with obesity and hyperlipidemia were treated by traditional Chinese medicine Jiangtang Tiaozhi Prescription of 24 weeks, we chosed 6 effective cases, 6 invalid cases and 6 health people  as control to analysis the molecular mechanism of TCM treatment. According to the research of LncRNA microarray, GO analysis, Pathway analysis, we found out the target LncRNAs, as well as their associated mRNAs were contribute to the good outcome of Jiangtang Tiaozhi Formula. more...
#> 611                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Human embryonic stem cells (hESCs) potentially offer new routes to study, on the basis of the Developmental Origins of Health and Disease (DOHaD) concept, how the maternal environment during pregnancy influences the offspring health and can predispose to chronic disease in later life. Reactive Oxygen Species (ROS), antioxidant defences, and cellular redox status state play an important role in the regulation of gene expression and are involved in diabetes and metabolic syndromes as in aging. more...
#> 612                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Novel strategies are needed to modulate β-cell differentiation and function as potential β-cell replacement or restorative therapies for diabetes. We previously demonstrated that small molecules based on the isoxazole scaffold drive neuroendocrine phenotypes. The nature of the effects of isoxazole compounds on β cells was incompletely defined.  We find that isoxazole largely induced genes that support neuroendocrine and β-cell phenotypes, and suppressed a set of genes important for proliferation. more...
#> 613                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Insulin resistance is considered to be a pathogenetic mechanism in several and diverse diseases (e.g. type 2 diabetes, atherosclerosis) often antedating them in apparently healthy subjects. The aim of this study was to investigate whether IR per se is characterized by a specific pattern of gene expression.  We analyzed the transcriptomic profile of peripheral blood mononuclear cells in two groups (10 subjects each) of healthy individuals, with extreme insulin resistance or sensitivity, matched for BMI, age and gender, selected within the MultiKnowledge Study cohort (n=148). more...
#> 614                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 615                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Accumulating evidence suggests that dysregulation of hypoxia-regulated transcriptional mechanisms is involved in development of chronic kidney diseases (CKD). However, it remains unclear how hypoxia-induced transcription factors (HIFs) and subsequent biological processes contribute to CKD development and progression. In our study, genome-wide expression profiles of more than 200 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium. more...
#> 616                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Accumulating evidence suggests that dysregulation of hypoxia-regulated transcriptional mechanisms is involved in development of chronic kidney diseases (CKD). However, it remains unclear how hypoxia-induced transcription factors (HIFs) and subsequent biological processes contribute to CKD development and progression. In our study, genome-wide expression profiles of more than 200 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium. more...
#> 617                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Impaired skeletal muscle function is a central feature in the pathophysiology of type 2 diabetes (T2DM). The disease phenotype could be due to immature muscle cell development, which in turn may occur as the result of disturbed microRNA-mediated regulation of muscle differentiation in T2DM. To address this hypothesis, we assessed global miRNA expression during in vitro differentiation of muscle stem cells derived from T2DM patients and healthy controls. more...
#> 618                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Single-cell RNA-seq (scRNA-seq) of pancreatic islets have reported on α- and β-cell gene expression in mice and subjects of predominantly European ancestry. We aimed to assess these findings in East-Asian islet-cells. 448 islet-cells were captured from three East-Asian non-diabetic subjects for scRNA-seq. Hierarchical clustering using pancreatic cell lineage genes was used to assign cells into cell-types. more...
#> 619                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Intrauterine exposure to hyperglycemic environment is reported to confer increased metabolic risk in later life, supporting the “developmental origins of health and disease” hypothesis. Epigenetic alterations are suggested as one of the possible underlying mechanisms. We measured DNA methylation using Infinium HumanMethylation450 BeadChip in siblings discordant for maternal gestational diabetes mellitus (GDM), which may allow possible genetic and environmental confounding effects to be reduced. more...
#> 620                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Background:  Stress cardiomyopathy (SCM) is a unique form of LV dysfunction that more often occurs in women.  Patients with SCM have a higher Troponin I/B-type natriuretic peptide ratio than AMI, but little is known about other circulating proteins.  The goals of this study were to compare plasma proteins in SCM and AMI to learn about the pathophysiology of SCM and also to identify putative biomarkers of SCM. more...
#> 621                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The incidence of pre-diabetes (PD) and Type-2 Diabetes Mellitus (T2D) is a worldwide epidemic. African American (AA) individuals are disproportionately more likely to become diabetic than other ethnic groups. Over the long-term, metabolic complications related to diabetes result in significant alterations in growth hormone (GH) and insulin-like growth factor-1 (IGF-1). Considering the limited exercise-related studies in the area of gene expression changes with disease progression, the objective of this study was to examine differences in exercise-induced gene expression related to the GH and IGF-1 pathways in peripheral blood mononuclear cells (PBMCs) of healthy (CON) and PD AA individuals. more...
#> 622                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Age-related alterations in immunity have been linked to increased incidence of infections and decreased responses to vaccines in the aging population. Human peripheral blood monocytes are known to promote antigen presentation and antiviral activities; however, the impact of aging on monocyte functions remains an open question. We present an in-depth global analysis examining the impact of aging on classical (CD14+CD16-), intermediate (CD14+CD16+), and non-classical (CD14dimCD16+) monocytes. more...
#> 623                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Age-related alterations in immunity have been linked to increased incidence of infections and decreased responses to vaccines in the aging population. Human peripheral blood monocytes are known to promote antigen presentation and antiviral activities; however, the impact of aging on monocyte functions remains an open question. We present an in-depth global analysis examining the impact of aging on classical (CD14+CD16-), intermediate (CD14+CD16+), and non-classical (CD14dimCD16+) monocytes. more...
#> 624                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Circadian rhythms are essential for temporal (~24 h) regulation of molecular processes in diverse species. Dysregulation of circadian gene expression has been implicated in the pathogenesis of various disorders, including hypertension, diabetes, depression, and cancer. Recently, microRNAs (miRNAs) have been identified as critical modulators of gene expression post-transcriptionally, and perhaps involved in circadian clock architecture or their output functions. more...
#> 625                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Hyperglycemia is an essential factor leading to micro- and macrovascular diabetic complications. Macrophages are key innate immune regulators of inflammation that undergo 2 major directions of functional polarization: classically (M1) and alternatively (M2) activated macrophages. The aim of the study was to examine the effect of hyperglycemia on transcriptional activation of M0, M1 and M2 human macrophages.
#> 626                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of histological findings, from simple steatosis to steatohepatitis (NASH), the latter presenting a higher risk of cardiovascular and kidney diseases, type 2 diabetes and end-stage liver disease. NAFLD is seen as the hepatic manifestation of the metabolic syndrome and affects up to 70-80% of obese patients. There are currently no approved pharmacological therapies for NASH, thus the only option is lifestyle intervention or bariatric surgery in order to lose weight and to improve insulin resistance. more...
#> 627                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Natural killer (NK) cells contribute to the development of obesity-associated insulin resistance. We demonstrate that in mice obesity promotes the expansion of interleukin-6 receptor (IL6Ra)-expressing NK cells, which also express a number of other myeloid lineage genes such as the colony-stimulating-factor 1 receptor (Csf1r). Selective ablation of Csf1r- expressing NK cells prevents obesity and insulin resistance. more...
#> 628                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Metabolic diseases, including type 2 diabetes and obesity are relevant negative prognostic factor in patients with breast cancer (BC). We have investigated the mechanisms through which elevated glucose levels affect tamoxifen sensitivity of estrogen receptor positive (ER+) BC cells. We found that MCF7 BC cell sensitivity to tamoxifen was 2-fold reduced in 25mM glucose (HG), a concentration mimicking hyperglycaemia, compared to 5.5 mM glucose (LG), resembling normal fasting glucose levels in humans. more...
#> 629                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     We report the RNA expression of insulin-GFP+ cells derived from CDKAL1-/- hESCs and CDKAL1-/-hESCs overexpressing MT1E
#> 630                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 The presence of a coding variant affecting plasma high density lipoprotein cholesterol (HDLC) levels was evaluated in subjects with elevated or normal plasma levels of HDLC. Carriers of the variant were further analyzed phenotypically
#> 631                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Here, we show that histone deacetylase Sirt6 protects against podocyte injury through epigenetic regulation of Notch signaling. Sirt6 is downregulated in renal biopsies from patients with podocytopathies and its expression negatively correlates withglomerular filtration rate. more...
#> 632                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The dataset comprises of circulating miRNAs in human subjects with various types of liver impairments. In our study, we analyzed a total 48 serum samples from a group of 42 subjects that included  subjects with accidental acetaminophen overdose (APAP), hepatitis B infection (HBV), liver cirrhosis (LC) and type 2 diabetes mellitus (T2DM) subjects with alanine amino transference (ALT) elevation. As a control 16 sex and age matched healthy controls from subjects with no evidence of liver disease were analyzed. more...
#> 633                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 634                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Islet-reactive T cells found in peripheral blood of type 1 diabetes (T1D) subjects are thought to be involved in disease pathogenesis, but full understanding of their role is complicated by their presence also in blood of in healthy subjects. To elucidate their role in T1D, we have combined flow cytometry and single cell RNA sequencing (RNA-seq) techniques to link prior antigen exposure, inferred from expanded TCR clonotypes, and functional capacities of islet antigen-reactive CD4+ memory T cells. more...
#> 635                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Islet-reactive T cells found in peripheral blood of type 1 diabetes (T1D) subjects are thought to be involved in disease pathogenesis, but full understanding of their role is complicated by their presence also in blood of in healthy subjects. To elucidate their role in T1D, we have combined flow cytometry and single cell RNA sequencing (RNA-seq) techniques to link prior antigen exposure, inferred from expanded TCR clonotypes, and functional capacities of islet antigen-reactive CD4+ memory T cells. more...
#> 636                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Islet-reactive T cells found in peripheral blood of type 1 diabetes (T1D) subjects are thought to be involved in disease pathogenesis, but full understanding of their role is complicated by their presence also in blood of in healthy subjects. To elucidate their role in T1D, we have combined flow cytometry and single cell RNA sequencing (RNA-seq) techniques to link prior antigen exposure, inferred from expanded TCR clonotypes, and functional capacities of islet antigen-reactive CD4+ memory T cells. more...
#> 637                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Islet-reactive T cells found in peripheral blood of type 1 diabetes (T1D) subjects are thought to be involved in disease pathogenesis, but full understanding of their role is complicated by their presence also in blood of in healthy subjects. To elucidate their role in T1D, we have combined flow cytometry and single cell RNA sequencing (RNA-seq) techniques to link prior antigen exposure, inferred from expanded TCR clonotypes, and functional capacities of islet antigen-reactive CD4+ memory T cells. more...
#> 638                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Although a large set of data is available concerning organogenesis in animal models, information remains scarce on human organogenesis. In this work, we performed temporal mapping of human fetal pancreatic organogenesis using cell surface markers. We demonstrate that in the human fetal pancreas at 7 weeks of development, the glycoprotein 2 (GP2) marks a multipotent cell population that will differentiate either into the acinar, ductal and endocrine lineages. more...
#> 639                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with limited effective treatment options. PDAC tumors frequently harbor the constitutively activated form of KRAS which drives proliferative signaling, but directly targeting KRAS has so far been unsuccessful. To overcome this limitation, combinatorial treatment strategies have been developed to inhibit upstream activators and downstream effectors of KRAS signaling. more...
#> 640                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Genome-scale DNA methylation profiling using the Infinium DNA methylation BeadChip platform and samples from normal human eye and five ocular- related diseases
#> 641                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Dysregulated expression of long noncoding RNAs (lncRNAs) has been demonstrated as being implicated in a variety of human diseases. In the study we aimed to determine lncRNA profile in CD8+ T cells response to active tuberculosis (TB).
#> 642                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Prenatal environmental conditions may influence disease risk in later life. We previously found a gene-environment interaction between the paraoxonase 1 (PON1) Q192R genotype and prenatal pesticide exposure leading to a cardio-metabolic risk profile at school age. However, the molecular mechanisms involved have not yet been resolved. It has been hypothesized that epigenetics might be involved. The aim of the present study was to investigate whether DNA methylation patterns in blood cells were related to prenatal pesticide exposure level, PON1 Q192R genotype, and associated metabolic effects observed in the children. more...
#> 643                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Atrial fibrillation (AF), the most common cardiac rhythm disorder, is a major cause of cardiovascular morbidity and mortality. AF is characterized by the rapid and irregular activation of the atrium with diverse abnormalities, including electrical, structural, metabolic, neurohormonal, or molecular alterations.3 Although the pathophysiology of AF is complex, it has traditionally been treated with antiarrhythmic drugs that control the rhythm by altering cardiac electrical properties, principally by modulating ion channel function. more...
#> 644                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We compared the plasma miRNA expression profiles between healthy and GDM women by microarray analysis.Our study offers new insights into circulating biomarkers of GDM and thus provides a valuable resource for future investigations.
#> 645                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Skeletal muscle is one of the primary tissues involved in the development of type 2 diabetes (T2D). Obesity is tightly associated with T2D, making it challenging to isolate specific effects attributed to the disease alone. By using an in vitro myocyte model system we were able to isolate the inherent properties retained in myocytes originating from donor muscle precursor cells, without being confounded by varying extracellular factors present in the in vivo environment of the donor. more...
#> 646                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Purpose: Identification of RUNX1 via next-generation sequencing (NGS) of fibrovascular membranes in patients with proliferative diabetic retinopathy. Methods: Transcriptomic analysis with Illumina HiSeq2000 of fibrovascular membrane and control retina CD31+ samples. The sequence reads were analyzed with ANOVA (ANOVA) and targets with significance (fold change > +/-1.5 and p-value < 0.05) were selected for with Cufflinks, DeSeq2, Partek E/M, and EdgeR. more...
#> 647                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Background: Intrauterine exposure to gestational diabetes mellitus (GDM) confers a lifelong increased risk for metabolic and other complex disorders to the offspring. GDM-induced epigenetic modifications modulating gene regulation and persisting into later life are generally assumed to mediate these increased disease risks. To identify candidate genes for fetal programming, we compared genome-wide methylation patterns of fetal cord bloods (FCBs) from GDM and control pregnancies. more...
#> 648                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The molecular transducers of benefits from different exercise modalities remain incompletely defined. Here we report that 12 weeks of high-intensity aerobic interval (HIIT), resistance (RT), and combined exercise training enhanced insulin sensitivity and lean mass, but only HIIT and combined training improved aerobic capacity and skeletal muscle mitochondrial respiration. HIIT revealed a more robust increase in gene transcripts than other exercise modalities, particularly in older adults, although little overlap with corresponding individual protein abundance was noted. more...
#> 649                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 650                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Obesity-induced white adipose tissue (WAT) fibrosis is believed to accelerate WAT dysfunction. Two progenitor populations could be distinguished in omental white adipose tissue (oWAT) of morbidly obese individuals based on CD9 expression. In addition, the frequency of CD9high progenitors in oWAT correlates with oWAT fibrosis level, insulin-resistance severity and type 2 diabetes. To further gain insight into the functional differences between the CD9high and CD9low progenitor subsets, we performed transcriptomic profiling of FACS-sorted progenitor populations isolated from oWAT of obese individuals. more...
#> 651                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     The NEET proteins mitoNEET (mNT) and nutrient-deprivation autophagy factor-1 (NAF-1) are required for cancer cell proliferation and resistance to oxidative stress. MitoNEET and NAF-1 are also implicated in a number of other human pathologies including diabetes, neurodegeneration and heart disease, as well as in development, differentiation and aging. Previous studies suggested that mNT and NAF-1 could function in the same pathway in cancer cells, preventing the over-accumulation of iron and reactive oxygen species (ROS) in mitochondria. more...
#> 652                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Open chromatin provides access to DNA binding proteins for the correct spatiotemporal regulation of gene expression. Mapping chromatin accessibility has been widely used to identify the location of cis regulatory elements (CREs) including promoters and enhancers. CREs show tissue- and cell-type specificity and disease-associated variants are often enriched for CREs in the tissues and cells that pertain to a given disease. more...
#> 653                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      ACTH-dependent hypercortisolism caused by a pituitary adenoma [Cushing’s disease (CD)] is the most common cause of endogenous Cushing’s syndrome. CD is often associated with several morbidities, including hypertension, diabetes, osteoporosis/bone fractures, secondary infections, and increased cardiovascular mortality. While the majority (≈80%) of the corticotrophinomas visible on pituitary magnetic resonance imaging are microadenomas (MICs, <10 mm of diameter), some tumors are macroadenomas (MACs, ≥10 mm) with increased growth potential and invasiveness, exceptionally exhibiting malignant demeanor. more...
#> 654                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). It is not diagnosed or managed properly in the majority of patients, because its pathogenesis remains controversial. In this study, using microarray-based genome-wide expression analyses, we sought to identify both common and distinct mechanisms underlying the pathogenesis of DM and DPN. The results demonstrated that down-regulation of the neurotrophin-MAPK signaling pathway may be the major mechanism of DPN pathogenesis, thus providing a potential approach for DPN treatment.
#> 655                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Context: Compared with European Americans, African Americans (AAs) are more insulin resistant, have a higher insulin secretion response to glucose, and develop type 2 diabetes more often. Molecular processes and/or genetic variations contributing to altered glucose homeostasis in high-risk AAs remain uncharacterized. Objective: Adipose and muscle transcript expression profiling and genotyping were performed in 260 AAs to identify genetic regulatory mechanisms associated with insulin sensitivity (SI). more...
#> 656                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Context: Compared with European Americans, African Americans (AAs) are more insulin resistant, have a higher insulin secretion response to glucose, and develop type 2 diabetes more often. Molecular processes and/or genetic variations contributing to altered glucose homeostasis in high-risk AAs remain uncharacterized. Objective: Adipose and muscle transcript expression profiling and genotyping were performed in 260 AAs to identify genetic regulatory mechanisms associated with insulin sensitivity (SI). more...
#> 657                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Epigenetic drift, an aging-associated change of the epigenome is one of the factors that can influence the rate and course of aging. In fact, even subtle changes of the miRnome can affect cellular functions. Therefore, changes of aging-associated miRNA expression in peripheral blood mononuclear cells (PBMC) of long-lived humans (n=24, mean age 94.8±3.9 years) and healthy, young individuals (n=24, 28.0±4.0 years) was evaluated using next generation sequencing. more...
#> 658                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Inappropriate activation or inadequate regulation of CD4+ and CD8+ T cells may contribute to the initiation and progression of multiple autoimmune and inflammatory diseases. Studies on disease-associated genetic polymorphisms have highlighted the importance of biological context for many regulatory variants, which is particularly relevant in understanding the genetic regulation of the immune system and its cellular phenotypes. more...
#> 659                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              To evaluate whether serum micoRNAs can be biomarkers for diagnosis of type 1 diabetes mellitus, we analyzed the serum microRNA expression profiles in 6 patients with new-onset type 1 diabetes mellitus and 6 age- and gender-matched healthy controls. A difference was observed in 31 miRNAs between the patients and controls (fold change ≥ 2, P < 0.05)
#> 660                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        We profiled gene expression in peripheral blood cells from 17 obese patients by microarray analysis and revealed that visceral fat adiposity impact on gene expression profile in peripheral blood cells compared to subcutaneous fat accumulation.
#> 661                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Background: Moderate weight loss can ameliorate adverse health effects associated with obesity, reflected by an improved adipose tissue (AT) gene expression profile. However, the effect of rate of weight loss on the AT transcriptome is unknown.  Objective: We investigated the global AT gene expression profile before and after two different rates of weight loss that resulted in similar total weight loss, and after a subsequent weight stabilization period. more...
#> 662                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Role of lncRNAs in human adaptive immune response to active tuberculosis (TB) infection is largely unexplored. The objective of this study was to characterize lncRNA expression profile in primary human B cell response to active TB infection using mcroarray assay.
#> 663                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Type 1 diabetes is characterized by the destruction of pancreatic beta cells, and generating new insulin-producing cells from other cell types is a major aim of regenerative medicine. One promising approach is transdifferentiation of developmentally related pancreatic cell types including glucagon-producing alpha cells. In a genetic model, overexpression of the master regulatory transcription factor Pax4 or loss of its counterplayer Arx are sufficient to induce the conversion of alpha cells to functional beta-like cells. more...
#> 664                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   In this study, we examined the association of DNA methylation with metabolic traits in humans using adipose tissue samples from the Metabolic Syndrome in Men (METSIM) cohort. The METSIM cohort has been thoroughly characterized for longitudinal clinical data of metabolic traits including a 3-point oral glucose tolerance test, cardiovascular disorders, diabetes complications, drug and diet questionnaire, as well as high density genotyping, and genome-wide expression in adipose. more...
#> 665                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     The objective of this study was the identification of serum microRNAs that can differentiate osteoporotic fracture patients with and without type-2 diabetes from healthy control subjects. For that purpose circulating microRNAs were profiled by real-time quantitative PCR using a custom 384-well panel in 200 µl serum samples. Univariate and multivariate statistical tools were used in order to identify single as well as combinations of circulating microRNas that were characteristic of patients with prevalent osteoporotic fractures: a qRT-PCR-based classifier consisting of miR-550a-5p, miR-96-5p, miR-32-3p and miR-486-5p can distinguish T2D women with (DMFx) and without fragility fractures (DM) with high specifitiy and sensitivity (AUC = 0.93). more...
#> 666                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Islet transplantation has the potential to benefit patients with type I diabetes, but this cellular therapy is limited by a shortage of islets, which necessitates the collection or production of islets from alternative sources. If islets produced from stem cells are to be used for transplant therapy they should precisely replicate beta-cell function. Characterization of the unique molecular mechanisms underlying the beta-cell’s response to glucose stimulation will allow a better understanding of critical elements that the alternative cells must possess. more...
#> 667                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                BACKGROUND & AIMS: Although patients infected by genotype 1b hepatitis C virus (HCV) with Q(70) and/or M(91)core gene mutations have an almost five-fold increased risk of developing hepatocellular carcinoma (HCC) and increased insulin resistance, the absence of a suitable experimental system has precluded direct experimentation on the effects of these mutations on cellular gene expression. METHODS: HuH7 cells were treated long-term with human serum to induce differentiation and to produce a model system for testing high-risk and control HCV. more...
#> 668                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Differences in gene regulation between healthy glucocorticoid receptor N363S single nucleotide polymorphism carriers and noncarrier controls may underlie the emergence of metabolic syndrome, Type 2 diabetes and cardiovascular disease associated with the N363S polymorphism.
#> 669                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Biologic agents active in other autoimmune settings have had variable effectiveness in newly diagnosed type 1 diabetes (T1D) where treatment across therapeutic targets is accompanied by transient stabilization of C-peptide levels in some patients, followed by progression at the same rate as in control groups. Why disparate treatments lead to similar clinical courses is currently unknown. Here, we use integrated systems biology and flow cytometry approaches to elucidate immunologic mechanisms associated with C-peptide stabilization in T1D subjects treated with the anti-CD3 monoclonal antibody, teplizumab. more...
#> 670                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Biologic agents active in other autoimmune settings have had variable effectiveness in newly diagnosed type 1 diabetes (T1D) where treatment across therapeutic targets is accompanied by transient stabilization of C-peptide levels in some patients, followed by progression at the same rate as in control groups. Why disparate treatments lead to similar clinical courses is currently unknown. Here, we use integrated systems biology and flow cytometry approaches to elucidate immunologic mechanisms associated with C-peptide stabilization in T1D subjects treated with the anti-CD3 monoclonal antibody, teplizumab.
#> 671                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Background. Novel and targetable mutations are needed for improved understanding and treatment of lung cancer in never-smokers. Methods. Twenty-seven lung adenocarcinomas from never-smokers were sequenced by both exome and mRNA-seq with respective normal tissues. Somatic mutations were detected and compared with pathway deregulation, tumor phenotypes and clinical outcomes. Results. Although somatic mutations in DNA or mRNA ranged from hundreds to thousands in each tumor, the overlap mutations between the two were only a few to a couple of hundreds. more...
#> 672                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 673                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Biologic agents active in other autoimmune settings have had variable effectiveness in newly diagnosed type 1 diabetes (T1D) where treatment across therapeutic targets is accompanied by transient stabilization of C-peptide levels in some patients, followed by progression at the same rate as in control groups. Why disparate treatments lead to similar clinical courses is currently unknown. Here, we use integrated systems biology and flow cytometry approaches to elucidate immunologic mechanisms associated with C-peptide stabilization in T1D subjects treated with the anti-CD3 monoclonal antibody, teplizumab. more...
#> 674                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Biologic agents active in other autoimmune settings have had variable effectiveness in newly diagnosed type 1 diabetes (T1D) where treatment across therapeutic targets is accompanied by transient stabilization of C-peptide levels in some patients, followed by progression at the same rate as in control groups. Why disparate treatments lead to similar clinical courses is currently unknown. Here, we use integrated systems biology and flow cytometry approaches to elucidate immunologic mechanisms associated with C-peptide stabilization in T1D subjects treated with the anti-CD3 monoclonal antibody, teplizumab. more...
#> 675                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 This study was performed to measure gene expression in peripheral whole blood RNA samples of established Type 1 diabetics.
#> 676                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         This SuperSeries is composed of the SubSeries listed below.  Grant ID: Award No. W81XWH-16-1-0130 Grant title: Peer Reviewed Medical Research Program Funding Source: Assistant Secretary of Defense for Health Affairs Affiliation: Jackson Laboratory for Genomic Medicine, Farmington, CT Name: Michael Stitzel
#> 677                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Blood glucose levels are tightly controlled by the coordinated action of at least five cell types constituting pancreatic islets. Changes in the proportion and/or function of these cells are associated with genetic and molecular pathophysiology of monogenic, type 1, and type 2 diabetes (T2D). Cellular heterogeneity impedes precise understanding of the molecular components of each islet cell type that govern islet dysfunction, particularly the less abundant delta and gamma/pancreatic polypeptide (PP) cells. more...
#> 678                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Blood glucose levels are tightly controlled by the coordinated action of at least five cell types constituting pancreatic islets. Changes in the proportion and/or function of these cells are associated with genetic and molecular pathophysiology of monogenic, type 1, and type 2 diabetes (T2D). Cellular heterogeneity impedes precise understanding of the molecular components of each islet cell type that govern islet dysfunction, particularly the less abundant delta and gamma/pancreatic polypeptide (PP) cells. more...
#> 679                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       In nonalcoholic fatty liver disease (NAFLD), hepatic gene expression and fatty acid (FA) composition have been reported independently but a comprehensive gene expression profiling in relation to FA composition is lacking. The aim was to assess this relationship. In a cross-sectional study, hepatic gene expression (Illumina Microarray) was first compared among 20 patients with simple steatosis (SS), 19 with nonalcoholic steatohepatitis (NASH), and 24 healthy controls (HC). more...
#> 680                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Epidemiologically related traits may share genetic risk factors, and pleiotropic analysis could identify individual loci associated with these traits. Because of their shared epidemiological associations, we conducted pleiotropic analysis of genome-wide association studies of lung cancer (12 160 lung cancer case patients and 16 838 control subjects) and cardiovascular disease risk factors (blood lipids from 188 577 subjects, type 2 diabetes from 148 821 subjects, body mass index from 123 865 subjects, and smoking phenotypes from 74 053 subjects). more...
#> 681                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Here, we report a key role for the transcription factor Pax6 in the maintenance of adult beta-cell identity and function. Pax6 is down regulated in beta-cells of diabetic db/db mice and in wild type mice treated with an insulin receptor antagonist, revealing metabolic control of expression. Deletion of Pax6 in beta-cells of adult mice leads to lethal hyperglycemia and ketosis, due to loss of beta-cell function and expansion of alpha-cells. more...
#> 682                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Caloric restriction (CR) is considered to increase lifespan and to prevent various age-related diseases in different non-human organisms. Only a limited number of CR studies have been performed in humans, and results put CR as a beneficial tool to decrease risk factors in several age-related diseases. The question remains at what age CR should be implemented to be most effective with respect to healthy aging. more...
#> 683                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Background and Aims: Hepatocyte nuclear factor 1 (HNF1) transcription factors direct tissue specific gene regulation in liver, pancreas and kidney and are associated with diabetes. Here we investigate the transcriptional network governed by HNF1 in an intestinal epithelial cell line.  Methods: Chromatin immunoprecipitation followed by direct sequencing (ChIP-seq) was used to identify HNF1 binding sites genome-wide. more...
#> 684                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           DNA methylation plays an important role in development of disease and the process of aging. In this study we examine DNA methylation at 476,366 sites throughout the genome of white blood cells from a population cohort (N = 421) ranging in age from 14 to 94 years old. Age affects DNA methylation at almost one third (29%) of the sites (Bonferroni adjusted P-value <0.05), of which 60.5% becomes hypomethylated and 39.5% hypermethylated with increasing age. more...
#> 685                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  To understand organ function it is important to have an inventory of the cell types present in the tissue and of the corresponding markers that identify them. This is a particularly challenging task for human tissues like the pancreas, since reliable markers are limited.  Transcriptome-wide studies are typically done on pooled islets of Langerhans, which obscures contributions from rare cell types and/or potential subpopulations. more...
#> 686                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Obesity is a critical health concern, and identifying new biomarkers has become essential for better understanding the progression to disease such as type 2 diabetes. DNA methylation has become a useful epigenetic biomarker in part due to its susceptibility to disease influence. Detecting methylation changes in blood is important as it is an easily accessible, compared to the insulin responsive tissue skeletal muscle. more...
#> 687                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Diabetic foot ulcers (DFUs) are one of the major complications of diabetes. Its molecular pathology remains poorly understood, impeding the development of effective treatments. Although it has been established that multiple cell types, including fibroblasts, keratinocytes, macrophages and endothelial cells, all contribute to inhibition of healing, less is known regarding individual contributions of each cell type. more...
#> 688                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                While the function of the mammalian pancreas hinges on complex interactions of distinct cell types, gene expression profiles have primarily been described with bulk mixtures of cells. Here, we invoked inDrop, a droplet-based single-cell RNA-Seq method, to determine the transcriptomes of over 12,000 individual pancreatic cells from four human donors and two strains of mice. Cells could be divided into 15 clusters that matched previously characterized cell types: all endocrine cell types, including rare ghrelin-expressing epsilon-cells, exocrine cell types, vascular cells, Schwann cells, quiescent and activated pancreatic stellate cells, and four types of immune cells. more...
#> 689                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         The prevalence of metabolic syndrome comprising obesity, type 2 diabetes mellitus and cardiovascular disease has been on the rise world-wide in recent years. As non-communicable diseases such as type 2 diabetes mellitus have their roots in prenatal development and conditions such as maternal gestational diabetes (GDM), we aimed to test this hypothesis in primary cells derived from the offspring of GDM mothers compared to control subjects. more...
#> 690                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      IL-6 is a proinflammatory cytokine implicated in multiple autoimmune diseases. Here we show that IL-6 induced STAT3 and STAT1 phosphorylation is enhanced in CD4 and CD8 T cells from patients with T1D compared to healthy controls. Enhanced IL-6/pSTAT3 is associated with increased surface IL-6R and early clinical disease. The transcriptome of IL-6 treated CD4 T cells from T1D patients reveals upregulation of genes involved in T cell migration. more...
#> 691                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               We performed RNA sequencing (RNAseq) on peripheral blood mononuclear cells (PBMCs) to identify differentially expressed gene transcripts (DEGs) after kidney transplantation and after the start of immunosuppressive drugs. RNAseq is superior to microarray to determine DEGs because it’s not limited to available probes, has increased sensitivity, and detects alternative and previously unknown transcripts. more...
#> 692                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Comparison of gene expression in pancreatic islets of BTBR-ob/ob mouse model of obesity-induced type 2 diabetes, and in non-diabetic control mice, B6-ob/ob identified Asf1b as an important gene candidate predictive of diabetic outcome. Asf1B expression was suppressed in response to age in both B6 and BTBR islets, induced by obesity only in B6 islets. This is consistent with other studies reporting a decline in -cell proliferation with age. more...
#> 693                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Squamous cell carcinoma (SCC) is the second most common cancer worldwide and accounts for approximately 30% of all keratinocyte cancers.  The vast majority of cutaneous SCCs of the head and neck (cSCCHN) are readily curable with surgery and/or radiotherapy unless high-risk features are present.  Perineural invasion (PNI) is recognized as one of these high-risk features.  The molecular changes during clinical PNI in cSCCHN have not been previously investigated. more...
#> 694                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Pancreatic islet cells are critical for maintaining normal blood glucose levels and their malfunction underlies diabetes development and progression. We used single-cell RNA sequencing to determine the transcriptomes of 1,492 human pancreatic α-, β-, δ- and PP cells from non-diabetic and type 2 diabetes organ donors. We identified cell type specific genes and pathways as well as 245 genes with disturbed expression in type 2 diabetes. more...
#> 695                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     CD4 T cell responses are characterized based on a limited number of molecular markers selected from exisiting knowledge. The goal of the experiment was to assess antigenic-peptide specific T-cell responses in vitro without bias using microarrays.
#> 696                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     CD4 T cell responses are characterized based on a limited number of molecular markers selected from exisiting knowledge. The goal of the experiment was to assess antigenic-peptide specific T-cell responses in vitro without bias using microarrays.
#> 697                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Circular RNA expression profiling of human nucleus pulposus derived from patients with IDD in comparison with those derived from cadaveric disc as normal control. We have identified the expression profiles of miRNAs (GSE63492), lncRNAs, mRNAs (GSE56081) in IDD using 5 normal discs as control and 5 IDD discs. Accumulating evidence indicates that circRNAs are key regulators of gene expression by interacting with miRNAs. more...
#> 698                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Validation of predicted gene expression of human mesangial cells after 24h Tacrolimus stimulus Objective: To evaluate tacrolimus as therapeutic option for diabetic nephropathy (DN) based on molecular profile and network-based molecular model comparisons. Materials and Methods: We generated molecular models representing pathophysiological mechanisms of DN and tacrolimus mechanism of action (MoA) based on literature derived data and transcriptomics datasets. more...
#> 699                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Impaired ability of insulin to stimulate cellular glucose uptake and regulate metabolism, that is insulin resistance (IR), links adiposity to metabolic disorders such as type 2 diabetes (T2D), dyslipidemia and cardiovascular disease (Langenberg, 2012). Both genetic and epigenetic factors are implicated in development of systemic IR (Vaag, 2001). IR is characterized by elevated levels of fasting insulin in the general circulation. more...
#> 700                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Impaired ability of insulin to stimulate cellular glucose uptake and regulate metabolism, that is insulin resistance (IR), links adiposity to metabolic disorders such as type 2 diabetes (T2D), dyslipidemia and cardiovascular disease (Langenberg, 2012). Both genetic and epigenetic factors are implicated in development of systemic IR (Vaag, 2001). IR is characterized by elevated levels of fasting insulin in the general circulation. more...
#> 701                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Impaired ability of insulin to stimulate cellular glucose uptake and regulate metabolism, that is insulin resistance (IR), links adiposity to metabolic disorders such as type 2 diabetes (T2D), dyslipidemia and cardiovascular disease (Langenberg, 2012). Both genetic and epigenetic factors are implicated in development of systemic IR (Vaag, 2001). IR is characterized by elevated levels of fasting insulin in the general circulation. more...
#> 702                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Endodermal stem/progenitor cells have diverse potential applications in research and regenerative medicine, so a readily available source could have widespread uses. Here we describe derivation of human induced endodermal progenitor cells (hiEndoPCs) from gastrointestinal epithelial cells using a cocktail of defined small molecules along with support from tissue-specific mesenchymal feeders. The hiEndoPCs show clonal expansion in culture and give rise to hepatocytes, pancreatic endocrine cells, and intestinal epithelial cells when treated with defined soluble molecules directing differentiation. more...
#> 703                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Endodermal stem/progenitor cells have diverse potential applications in research and regenerative medicine, so a readily available source could have widespread uses. Here we describe derivation of human induced endodermal progenitor cells (hiEndoPCs) from gastrointestinal epithelial cells using a cocktail of defined small molecules along with support from tissue-specific mesenchymal feeders. The hiEndoPCs show clonal expansion in culture and give rise to hepatocytes, pancreatic endocrine cells, and intestinal epithelial cells when treated with defined soluble molecules directing differentiation. more...
#> 704                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Endodermal stem/progenitor cells have diverse potential applications in research and regenerative medicine, so a readily available source could have widespread uses. Here we describe derivation of human induced endodermal progenitor cells (hiEndoPCs) from gastrointestinal epithelial cells using a cocktail of defined small molecules along with support from tissue-specific mesenchymal feeders. The hiEndoPCs show clonal expansion in culture and give rise to hepatocytes, pancreatic endocrine cells, and intestinal epithelial cells when treated with defined soluble molecules directing differentiation. more...
#> 705                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Periodontitis affects 47.1% of adult population in the U.S. Porphyromonas gingivalis is an opportunistic oral pathogen that colonizes the oral mucosa, invades myeloid dendritic cells and accesses the bloodstream, brain, placenta and other organs in human with periodontitis. Periodontitis also sustains a chronic long-term pro-inflammatory immune disorder, potentially contributing to other systemic conditions such as cardiovascular disease, type 2 diabetes mellitus, adverse pregnancy outcomes, and osteoporosis. more...
#> 706                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            A robust system using disease relevant cells to systematically evaluate the role in diabetes for loci identified through genome wide association studies (GWAS) is urgently needed. Toward this goal, we created isogenic mutant human embryonic stem cell (hESC) lines in GWAS-identified candidate diabetes genes including CDKAL1, KCNQ1 and KCNJ11, and used directed differentiation to evaluate the function of derivative human beta-like cells. more...
#> 707                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We successfully sequenced and annotated more than 400 cells from child, adult control, type 1 diabetes and type 2 diabetes donors. We detect donor-type specific transcript variation. We also report that cells from child donors have less defined gene signature. Cells from type 2 diabetes donors resemble juvenile cells in gene expression.
#> 708                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Genome-wide profiling of placental DNA methylation in relation to arsenic exposure. The Illumina 450k methylation array was used to profile 343 samples for which 3 different measurements of arsenic exposure were available during gestation. These samples have been collected from the New Hampshire Birth Cohort Study (NHBCS).
#> 709                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         MicroRNA expression profiling of human nucleus pulposus derived from patients with IDD in comparison with those derived from cadaveric disc as normal control. We have identified the expression profiles of miRNAs in IDD using scoliotic nucleus pulposus as controls (GSE19943). It is noteworthy that scoliotic discs are not strictly normal discs. Therefore, the microRNA expression profiles were revisited using normal discs as control.
#> 710                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            substantial number of people at risk to develop type 2 diabetes could not improve insulin sensitivity by physical training intervention. We studied the mechanisms of this impaired exercise response in 20 middle-aged individuals who performed a controlled eight weeks cycling and walking training at 80 % individual VO2max. Participants identified as non-responders in insulin sensitivity (based on Matsuda index) did not differ in pre-intervention parameters compared to high responders. more...
#> 711                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        To understand organ (dys)function it is important to have a complete inventory of its cell types and the corresponding markers that unambiguously identify these cell types. This is a challenging task, in particular in human tissues, because unique cell-type markers are typically unavailable, necessitating the analysis of complex cell type mixtures. Transcriptome-wide studies on pancreatic tissue are typically done on pooled islet material. more...
#> 712                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 713                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     RNA-seq profiling was conducted on clinically-annotated human pancreatic adenocarcinoma cancer tissues
#> 714                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Genome-wide profiling of placental DNA methylation in relation to neurobehavioral development. The Illumina 450k methylation array was used to profile 335 samples. These samples have been collected from the Rhode Island Child Health Study (RICHS).
#> 715                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Hyperglycemia is a hallmark in prediabetes and type 2 diabetes mellitus (T2DM) which increases risk of micro and macrovascular complications such as diabetic retinopathy, diabetic nephropathy (microvascular complications), and peripheral vascular disease, cerebrovascular disease and cardiovascular diseases (macrovascular complications). Endothelial cells are affected in both cases. In this study, we investigated the miRNA expression changes in HUVECs during different glucose treatment (5mM, 10mM, 25mM and 40mM glucose) at various time intervals (6, 12, 24 and 48hrs). more...
#> 716                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Autoreactive CD8+ T-cells recognizing autoantigens expressed by pancreatic islets lead to the destruction of insulin-producing β-cells in type 1 diabetes, but these T-cell also occur in healthy subjects. We tested the hypothesis that uncontrolled expansion of diabetogenic T-cells in patients occurs, resulting from failure to activate apoptosis. We compared function, transcriptome and epigenetic regulation thereof in relation with fate upon repeated exposure to islet-autoantigen of islet autoreactive T-cells from healthy and type 1 diabetic donors with identical islet epitope specificity and HLA-A2 restriction. more...
#> 717                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             DNA-methylation profiling of Whole blood genomic DNAs collected at EDIC baseline and monocytes at EDIC years 16/17 years from participants of Diabetes Control and Complications Trial/ Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study This SuperSeries is composed of the SubSeries listed below.
#> 718                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Study the association of DNA-methylation and metabolic memory by examing DNA-methylation alternation  between cases (received conventional therapy in DCCT  and showing retinopathy or albuminuria progression at EDIC year-10)  and Controls(in DCCT intensive treatment group  and did not have retinopathy or nephropathy progression during EDIC]
#> 719                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Study the association of DNA-methylation and metabolic memory by examing DNA-methylation alternation between cases (received conventional therapy in DCCT  and showing retinopathy or albuminuria progression at EDIC year-10)  and Controls (in DCCT intensive treatment group  and did not have retinopathy or nephropathy progression during EDIC).
#> 720                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 721                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We describe Nfib as an important regulator of chromatin accessibility in Small cell lung cancer (SCLC).
#> 722                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Preeclampsia and gestational diabetes mellitus (GDM) are two of the most common clinical conditions during pregnancy that could result in adverse utero environments of the fetus. Fetal exposure to poor environments in uterus also raises the risk of future adulthood disorders known as fetal origins of adult disease (FOAD). Epigenetic modifications like cytosine methylation and histone modification have been proposed to be involved in FOAD. more...
#> 723                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     The study of epigenetic mechanisms of gene regulation and the role of these mechanisms in developmental reprogramming of the genome and disease susceptibility has increased in recent years. Molecular epigenetic mechanisms regulating gene expression include DNA methylation, histone modifications, and small non-coding RNAs (e.g., microRNAs). MicroRNAs (miRNAs) are short, single-stranded RNA that regulate post-transcriptional control of the translation of mRNA. more...
#> 724                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Intensive efforts are focused on identifying regulators of human pancreatic islet cell growth and maturation to accelerate development of therapies for diabetes. After birth, islet cell growth and function are dynamically regulated; however, establishing these age-dependent changes in humans has been challenging. Here we describe a multimodal strategy for isolating pancreatic endocrine and exocrine cells from children and adults to identify age-dependent gene expression and chromatin changes on a genomic scale. more...
#> 725                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         We report a mechanism through which the transcription machinery directly controls topoisomerase 1 (TOP1) activity to adjust DNA topology throughout the transcription cycle. By comparing TOP1 occupancy using ChIP-Seq, versus TOP1 activity using TOP1-Seq, a method reported here to map catalytically engaged TOP1, TOP1 bound at promoters was discovered to become fully active only after pause-release. This transition coupled the phosphorylation of the carboxyl-terminal-domain (CTD) of RNA polymerase II (RNAPII) with stimulation of TOP1 above its basal rate, enhancing its processivity. more...
#> 726                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Current therapy has turned HIV infection into a chronic condition. Clinically, some patients suffer prematurely from ailments associated with advanced age; however, the relationship between HIV and aging is unclear. Here we have collected a large cohort of HAART treated HIV+ subjects with both recent and chronic infection and recapitulated the shared phenotype of HIV and age. To further understand this signal, we applied validated models of DNA methylation-based biological age to establish a clear link between HIV infection and molecular age advancement. more...
#> 727                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We recently reported the scalable in vitro production of functional stem cell-derived β cells.  Here we extend this approach to generate SC-β cells from Type 1 diabetic patients (T1D), a cell type that is destroyed during disease progression and has not been possible to extensively study.  These cells express β cell markers, respond to glucose both in vitro and in vivo, prevent alloxan-induced diabetes in mice, and respond to anti-diabetic drugs. more...
#> 728                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Type 2 diabetes is a complex disease associated with many underlying pathomechanisms. Epigenetic regulation of gene expression by DNA methylation has become increasingly recognized as an important component in the etiology of type 2 diabetes. We performed genome-wide methylome and transcriptome analysis in liver from severely obese patients with or without type 2 diabetes to discover aberrant pathways underlying the development of insulin resistance. more...
#> 729                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Type 2 diabetes is a complex disease associated with many underlying pathomechanisms. Epigenetic regulation of gene expression by DNA methylation has become increasingly recognized as an important component in the etiology of type 2 diabetes. We performed genome-wide methylome and transcriptome analysis in liver from severely obese patients with or without type 2 diabetes to discover aberrant pathways underlying the development of insulin resistance. more...
#> 730                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Insulin resistance is central to diabetes and metabolic syndrome. To define the consequences of genetic insulin resistance distinct from those secondary to cellular differentiation or in vivo regulation, we generated induced pluripotent stem cells (iPSCs) from individuals with insulin receptor mutations and age-appropriate control subjects and studied insulin signaling and gene expression compared with the fibroblasts from which they were derived. more...
#> 731                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 732                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Background: In vitro models are an essential tool towards understanding the molecular characteristics of colorectal cancer (CRC) and the testing of therapies for CRC. To this end we established 21 novel CRC cell lines of which six were derived from liver metastases. Extensive genetic, genomic, transcriptomic and methylomic profiling was performed in order to characterize these new cell lines and all data is made publically available. more...
#> 733                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Background: In vitro models are an essential tool towards understanding the molecular characteristics of colorectal cancer (CRC) and the testing of therapies for CRC. To this end we established 21 novel CRC cell lines of which six were derived from liver metastases. Extensive genetic, genomic, transcriptomic and methylomic profiling was performed in order to characterize these new cell lines and all data is made publically available. more...
#> 734                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Application of Systems Genetics analysis for systematic evaluation of candidate causal genes associated with risk of Type 1 Diabetes along with follow-up bioinformatics pathway analysis.
#> 735                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Mitochondrial defects are associated with a spectrum of human disorders, ranging from rare, inborn errors of metabolism to common, age-associated diseases such as diabetes and neurodegeneration. In lower organisms, genetic “retrograde” signaling programs have been identified that promote cellular and organism survival in the face of mitochondrial dysfunction. Here, we characterized the transcriptional component of the human mitochondrial retrograde response in an inducible model of mitochondrial dysfunction. more...
#> 736                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Background: The bile acid-activated farnesoid X receptor (FXR) is a nuclear receptor regulating bile acid, glucose and cholesterol homeostasis. Obeticholic acid (OCA; also known as INT-747 or 6α-ethyl-chenodeoxycholic acid), a promising drug for the treatment of non-alcoholic steatohepatitis (NASH) and type 2 diabetes, activates FXR. Mouse studies demonstrated that FXR activation by OCA (INT-747) alters hepatic expression of many genes. more...
#> 737                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Diabetic retinopathy (DR) is the leading cause of blindness in working-age people. Pericyte loss is one of the pathologic cellular events in DR, which weakens the retinal microvessels. Damages to the microvascular networks are irreversible and permanent, thus further progression of DR is inevitable. In this study, we hypothesize that multipotent perivascular progenitor cells derived from human ESCs (hESC-PVPCs) improve the damaged retinal vasculature in the streptozotocin (STZ)-induced diabetic rodent models. more...
#> 738                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Atrial fibrillation (AF) is currently the most prevalent arrhythmia worldwide.Recent clinical data implicate the additional contribution of non-coding RNAs in the pathogenesis of AF,which include microRNAs(miRNAs), endogenous small interfering RNAs, PIWIinteracting RNAs, and lncRNA. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with AF has not been reported. more...
#> 739                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Analysis of umbilical cord tissue in newborns of type 1 diabetic mothers at gene expression level. The hypothesis tested in the present study was that intrauterine diabetic milieu may effect of fetal umbilical cord gene expression, and via umbilical cord, the alterations may be produced in other fetal tissues as well. Results provide an information of the differentially expressed genes and enriched pathways, such as the dowregulated genes on the pathway on blood vessel development in umbilical cords from diabetic pregnancies.
#> 740                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          DNA microarray analysis was performed to investigate the expression of genes in HGF stimulated with palmitate Type 2 diabetes (T2D) is characterized by decreased insulin sensitivity and higher concentrations of free fatty acids (FFAs) in plasma. Among FFAs, saturated fatty acids (SFAs), such as palmitate, have been proposed to promote inflammatory responses. Although many epidemiological studies have shown a link between periodontitis and T2D, little is known about the clinical significance of SFAs in periodontitis. more...
#> 741                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 742                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  MicroRNAs (miRNAs) contribute to chronic kidney disease progression via negatively regulating mRNA abundance. However, their association with clinical outcome remains poorly understood. We performed large-scale miRNA and mRNA expression profiling on cryo-cut renal biopsy sections from a discovery (n=43) and a validation (n=29) cohort. In the discovery cohort (GEO Series accession number GSE45980), miRNAs differentiating stable and progressive cases were determined, and putative target mRNAs showing inversely correlated expression profiles were identified. more...
#> 743                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    MicroRNAs (miRNAs) significantly contribute to chronic kidney disease (CKD) progression via regulating mRNA expression and abundance. However, their association with clinical outcome remains poorly understood. We performed large scale miRNA and mRNA expression profiling on cryo-cut renal biopsy sections from n=43 subjects. miRNAs differentiating stable and progressive cases were determined, and putative target mRNAs showing inversely correlated expression profiles were identified and further characterized. more...
#> 744                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic insulin-producing β cells. CD4+ T cells are integral to the pathogenesis of T1D, but biomarkers that define their pathogenic status in T1D are lacking. miRNAs have essential functions in a wide range of tissues/organs, including the immune system. We reasoned that CD4+ T cells from individuals at high risk for T1D (pre-T1D) might be distinguished by an miRNA signature. more...
#> 745                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Objective: Although glucagon-secreting α-cells and insulin-secreting β-cells have opposing functions in regulating plasma glucose levels, the two cell types share a common developmental origin and have overlaps in their transcriptome and epigenome profiles. Notably, destruction of one of these cell populations can stimulate repopulation via transdifferentiation of the other cell type, at least in mice, suggesting plasticity between these cell fates. more...
#> 746                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Diabetes mellitus is a complex and heterogeneous disease that has β cell dysfunction at its core. Glucose toxicity affects pancreatic islets where it leads to β cell apoptosis. However, the role of JNK/β-catenin signaling pathway in glucotoxic β-cell apoptosis is poorly understood. To identify the potential genes whose expression changed in response to high glucose, we performed microarray analysis of gene expression in the RNAKT-15 cells for 48 h. more...
#> 747                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The presence of a coding variant affecting plasma high density lipoprotein cholesterol (HDLC) levels  was evaluated in subjects with elevated plasma levels of HDLC.
#> 748                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The obese people with abnormal BMI are predisposed to insulin resistance and diabetes. At the same time, human subjects with obesity and high BMI that are otherwise insulin sensitive are an interesting group to study the underlying gene expression patterns which provide them with such protective phenotype. Objective: Insulin resistance (IR) is one of the earliest predictors of type 2 diabetes. However, diagnosis of IR is limited. more...
#> 749                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     We identified EGF as the top candidates predicting kidney function through an intrarenal transcriptome-driven approach, and demonstrated it is an independent risk predictor of CKD progression and can significantly improve prediction of renal outcome by established clinical parameters in diverse populations with CKD from a wide spectrum of causes and stages
#> 750                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 751                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Gene expression of tumor sample of mexican patients with breast cancer. Samples obtained from the Hospital San Jose Tec de Monterrey.
#> 752                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    miRNAs expression of tumor sample of mexican patients with breast cancer. Samples obtained from the Hospital San Jose Tec de Monterrey.
#> 753                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Genome-wide association studies have been tremendously successful in identifying genetic variants associated with complex diseases. The majority of association signals are intergenic and evidence is accumulating that a high proportion of signals lie in enhancer regions.We use Capture Hi-C to investigate, for the first time, the interactions between associated variants for four autoimmune diseases and their functional targets in B- and T-cell lines. more...
#> 754                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        In a prospective case-control study, we identified novel transcriptional classifiers for TB among US patients and systematically compared their accuracy to other classifiers in published studies.
#> 755                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Individual differences in peripheral blood transcriptomes in older adults as a function of demographic, socio-economic, psychological, and health history characteristics.
#> 756                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Analysis of gene expression associated with exercise response. The hypothesis tested was that individuals with Type 2 Diabetes that failed to demonstrate exercise-induced metabolic improvements would also reflect this lack of response in their skeletal muscle transcriptional profile at baseline. Of 186 genes identified by microarray analysis, 70% were upregulated in Responders and downregulated in Non-responders. more...
#> 757                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 758                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The molecular clock is a transcriptional oscillator present in brain and peripheral cells that coordinates behavior and physiology with the solar cycle. Here we reveal that the clock gates insulin secretion through genome-wide transcriptional control of the pancreatic exocyst across species. Clock transcription factors bind to unique enhancer sites in cycling genes in beta cells that diverge from those in liver, revealing the dynamics of inter-tissue clock control of genomic and physiologic processes important in glucose homeostasis.
#> 759                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Chronic inflammation leading to pro-inflammatory macrophage infiltration contributes to the pathogenesis of type 2 diabetes and subsequently the development of diabetic nephropathy. Mesenchymal stem cells (MSCs) possess unique immunomodulatory and cytoprotective properties making them an ideal candidate for therapeutic intervention We used microarrays to detail changes in the gene expression profile of monocytes isolated from type 2 diabetic patients with end-stage renal disease and non-diabetic control subjects following co-culture with MSCs.
#> 760                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Analysis of expression profile of peripheral blood from pancreatic ductal adenocarcinoma patients RNA expression profile of peripheral blood from pancreatic ductal adenocarcinoma patients
#> 761                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           The microRNA profiles in the vitreous of proliferative vitreoretinal disease (PVD) such as proliferative diabetic retinopathy with fibrovascular membrane and macular hole (MH) patients were studied by RT-PCR.
#> 762                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                These experiments were performed to identify differentially expressed genes in the pancreas of healthy humans, auto-antibody positive and type 1 diabetic patients. All samples were obtained from the network of pancreatic organ donors with diabetes (nPOD).  ID numbers are specified.  Patient information can be obtained at http://www.jdrfnpod.org/
#> 763                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Diabetes and Arteriosclerosis progression are frequently observed in borderline Type 2 diabetes cases. Onset of complications (arteriosclerosis and renal damage) due to Type 2 diabetes is well documented; it is extremely important to prevent or delay their progression. Type 2 diabetes onset and progression has been controlled through dietary habits and exercise, although these remain insufficient. Chlorella ingestion improves blood glucose and cholesterol concentrations in mice and humans, although no reports have evaluated Chlorella effects in borderline diabetics. more...
#> 764                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  ChIP-seq of H3K27ac was performed in regulatory T cells (resting and activated) and conventional T cells (naïve, effector, memory) in mouse and human.  A small number of regulatory elements were lineage specific in both mouse and human and represented the 'core' lineage specification program.  Regulatory element acetylation levels were associated with genetic variation in humans and lineage-specific loci were enriched for autoimmune risk-alleles (especially type 1 diabetes) identified in classic and fine-resolution genome-wide association studies.
#> 765                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 766                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that canakinumab, a monoclonal antibody to IL-1B, improves beta-cell function in patients with new-onset T1D. more...
#> 767                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Background: Blocking the action of the pro-inflammatory cytokine interleukin-1 (IL-1) reduces beta-cell secretory dysfunction and apoptosis in vitro, diabetes incidence in animal models of Type 1 diabetes mellitus (T1D), and glycaemia via improved beta-cell function in patients with T2D. We hypothesised that anakinra, a recombinant human IL-1 receptor antagonist, improves beta-cell function in patients with new-onset T1D. more...
#> 768                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We investigated the short and long term effects of electrically induced exercise on mRNA expression of human paralyzed muscle. We developed an exercise dose that activated the muscle for 0.6% of the day. The short term effects were assessed 3 hours after a single dose of exercise, while the long term effects were assessed after training 5 days per week for at least one year (adherence 81%). A single dose of electrical stimulation increased the mRNA expression of transcriptional, translational, and enzyme regulators of metabolism important to shift muscle toward an oxidative phenotype (PGC-1a, NR4A3, IFRD1, ABRA, PDK4). more...
#> 769                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Gene expression analyses of fibroblasts obtained from healthy controls, Medalist -C patients and Medalist +C patients. Type 1diabetes (T1D) is associated with late complications, mechanisms underscoring which are poorly understood. We report the derivation of induced pluripotent stem cells (iPSCs) from patients with longstanding T1D (disease duration ≥ 50years) with severe (designated Medalist +C) or absent to mild complications (designated Medalist -C). more...
#> 770                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 771                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. more...
#> 772                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. more...
#> 773                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        We carried out a high throughput analysis of insulin-induced kinase signaling pathways in primary fibroblasts from 35 unrelated individuals.  We found that extensive individual variation exists in induction of various signaling pathways.  ERK signaling displayed the greatest variation, which led to extensive variation in expression of downstream target genes. Our results suggest that phenotypic variation in kinase signaling mediates variation in downstream processes of insulin response. more...
#> 774                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Adipose tissues play an important role in the pathophysiology of obesity-related disease including type 2 diabetes. To describe gene expression patterns and functional pathways in obesity-related type 2 diabetes, we performed global transcript profiling of omental adipose tissue in morbidly obese individuals with or without diabetes.
#> 775                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               In-vitro expansion of functional adult human β-cells is an attractive approach for generating insulin-producing cells for transplantation. However, human islet cell expansion in culture results in loss of β-cell phenotype and epithelial-mesenchymal transition (EMT). This process activates expression of ZEB1 and ZEB2, two members of the zinc-finger homeobox family of E-cadherin repressors, which play key roles in EMT. more...
#> 776                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The project is directed to the development of selective glucocorticoid receptor agonists for anticancer therapy. Glucocorticoids (GC) are widely used in treatment of many types of cancer due to its ability to induce apoptosis in malignant cells (in blood cancer therapy) and to prevent nausea and emesis (in the chemotherapy of solid tumors). However, severe dose-limiting side effects occur, including osteoporosis, muscle wasting, diabetes and other metabolic complications. more...
#> 777                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The project is directed to the development of selective glucocorticoid receptor agonists for anticancer therapy. Glucocorticoids (GC) are widely used in treatment of many types of cancer due to its ability to induce apoptosis in malignant cells (in blood cancer therapy) and to prevent nausea and emesis (in the chemotherapy of solid tumors). However, severe dose-limiting side effects occur, including osteoporosis, muscle wasting, diabetes and other metabolic complications. more...
#> 778                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             We present a novel method, termed BisPCR2, for targeted bisulfite sequencing and apply it in the setting of validating type 2 diabetes CpG susceptibility loci
#> 779                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Genes related to sleep and wakefulness were evaluated by RNA microarray in patients, including CKD,HD patients and control subjects.
#> 780                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The host response in critically ill patients with sepsis, septic shock remains poorly defined. Considerable research has been conducted to accurately distinguish patients with sepsis from those with non-infectious causes of disease. Technological innovations have positioned systems biology at the forefront of biomarker discovery. Analysis of the whole-blood leukocyte transcriptome enables the assessment of thousands of molecular signals beyond simply measuring several proteins in plasma, which for use as biomarkers is important since combinations of biomarkers likely provide more diagnostic accuracy than the measurement of single ones or a few. more...
#> 781                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Background: The prevalence of type 2 diabetes has increased dramatically in recent decades. Increasing brown adipose tissue (BAT) mass and activity has recently emerged as an interesting approach to not only increase energy expenditure, but also improve glucose homeostasis. BAT can be recruited by prolonged cold exposure in lean, healthy humans. Here, we tested whether cold acclimation could have therapeutic value for patients with type 2 diabetes by improving insulin sensitivity. more...
#> 782                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      We performed gene expression microarray analysis of skeletal muscle biopsies from normal glucose tolerant subjects and type 2 diabetes subjects obtained during a 60 min bicycle ergometer exercise and the 180 min of recovery phase
#> 783                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Coronary artery disease (CAD) is the leading cause of human morbidity and mortality worldwide, underscoring the need to improve diagnostic strategies. Platelets play a major role, not only in the process of acute thrombosis during plaque rupture, but also in the formation of atherosclerosis itself. MicroRNAs are endogenous small non-coding RNAs that control gene expression and are expressed in a tissue and disease-specific manner. more...
#> 784                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Circulating miRNAs constitute a novel class of disease biomarkers, which are altered in diabetes but the effect of diabetes associated inflammation as seen in chronic wounds is unknown. We here compared the miRNA pattern in diabetic patients in presence or absence of chronic wound with PAD.
#> 785                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Understanding distinct gene expression patterns of normal adult and developing fetal human pancreatic a and b cells is crucial for developing stem cell therapies, islet regeneration strategies, and therapies designed to increase b cell function in patients with diabetes (type 1 or 2). Toward that end, we have developed methods to highly purify a, b, and d cells from human fetal and adult pancreata by intracellular staining for the cell-specific hormone content, sorting the sub-populations by flow cytometry and, using next generation RNA sequencing, we report on the detailed transcriptomes of fetal and adult a and b cells. more...
#> 786                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Melioidosis, caused by Gram negative bacteria Burkholderia pseudomallei, is a major type of community-acquired septicemia in Southeast Asia and Northern Australia with high mortality and morbidity rate. More accurate and rapid diagnosis is needed for improving the management of septicemic melioidosis. We previously identified 37-gene candidate signature to distinguish septicemic melioidosis from sepsis due to other pathogens. more...
#> 787                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Differencies between groups between pre and post haematopoietic stem cell transplantation children Immune reactions are among the most serious complications observed after hematopoietic stem cell transplantation (HSCT) in children. Microarray technique allows for simultaneous assessment of expression of nearly all human genes. The objective of the study was to compare the whole genome expression in children before and after HSCT. more...
#> 788                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      A previous study from this laboratory demonstrated that up-regulating HNF4a could reverse the malignant phenotypes of HCC by inducing redifferentiation of HCC cells to hepatocytes. To study the mechanisms of the hepatic differentiation effect by HNF4α, we used the cDNA microarray to detect differential gene expression profiles of Hep3B infected with AdHNF4α and AdGFP. Expression profile analysis revealed that HNF4α positively regulated 1218 mRNAs and negatively regulated 1411 mRNAs for more than 2 times. more...
#> 789                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Background/aims: Serum concentrations of the hepatokine fibroblast growth factor (FGF) 21 are elevated in obesity, type‐2 diabetes, and the metabolic syndrome. We asked whether FGF21 levels differ between subjects with metabolically healthy vs. unhealthy obesity (MHO vs. MUHO) opening the possibility that FGF21 is a cross‐talker between liver and adipose tissue in MUHO. Furthermore, we studied the effects of chronic FGF21 treatment on adipocyte differentiation, lipid storage, and adipokine secretion. more...
#> 790                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Skeletal muscle adapts to exercise training of various modes, intensities and durations with a programmed gene expression response. This study dissects the independent and combined effects of exercise mode, intensity and duration to identify which exercise has the most positive effects on skeletal muscle health. Full details on exercise groups can be found in: Kraus et al Med Sci Sports Exerc. 2001 Oct;33(10):1774-84 and Bateman et al Am J Cardiol. more...
#> 791                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Histopathology is insufficient to predict disease progression and clinical outcome in lung adenocarcinoma. Here we show that gene-expression profiles based on microarray analysis can be used to predict patient survival in early-stage lung adenocarcinomas. Genes most related to survival were identified with univariate Cox analysis. Using either two equivalent but independent training and testing sets, or 'leave-one-out' cross-validation analysis with all tumors, a risk index based on the top 50 genes identified low-risk and high-risk stage I lung adenocarcinomas, which differed significantly with respect to survival. more...
#> 792                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes.  While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal.  In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. more...
#> 793                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 794                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. more...
#> 795                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. more...
#> 796                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Diabetes Mellitus (DM) is a chronic, severe disease rapidly increasing in incidence and prevalence and is associated with numerous complications. Patients with DM are at high risk of developing diabetic foot ulcers (DFU) that often lead to lower limb amputations, long term disability, and a shortened lifespan. Despite this, the effects of DM on human foot skin biology are largely unknown. Thus, the focus of this study was to determine whether DM changes foot skin biology predisposing it for healing impairment and development of DFU. more...
#> 797                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 798                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of unmedicated newly diagnosed human pre-diabetics and type 2 diabetics.
#> 799                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Objective: to compare changes in gene expression by microarray from subcutaneous adipose tissue from HIV treatment naïve patients treated with efavirenz based regimens containing abacavir (ABC), tenofavir (TDF) or zidovidine (AZT). There were significant divergence between ABC and the other two groups 6 months after treatment in genes controlling cell adhesion and environmental information processin, with some convergence at 18 months. more...
#> 800                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          We have performed gene expression microarray analysis to profile transcriptomic signatures between insulin resistance high risk subjects and insulin resistance low risk subjects
#> 801                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Skeletal myocytes are metabolically active and susceptible to insulin resistance, thus implicated in type 2 diabetes (T2D). This complex disease involves systemic metabolic changes and their elucidation at the systems level requires genome-wide data and biological networks. Genome-scale metabolic models (GEMs) provide a network-context to integrate high-throughput data. We generated myocyte-specific RNA-seq data and investigated their correlation with proteome data. more...
#> 802                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Myotonic Dystrophy Type-2 (DM2) is an autosomal dominant disease caused by the expansion of a CCTG tetraplet repeat. It is a multisystemic disorder, affecting skeletal muscles, the heart, the eye, the central nervous system and the endocrine system. Whole mRNAs expression was measured in the muscle of DM2 patients and compared it to controls.We identified distinct genes modulated in DM2 patients compared to controls.
#> 803                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     This SuperSeries is composed of the SubSeries listed below.  Each of the SubSeries contained in this SuperSeries represents identical RNA samples used for hybridization to different array platforms.
#> 804                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Diabetic Retinopathy (DR) is a progressive disease affecting the structure and cellular composition of the microvasculature. Several factors like genetic, environmental and biochemical are involved in the development of DR. However, the inheritance pattern of this disease is multi factorial resulting from the interaction of one or more genes but the exact mechanism is not completely understood. Over the decade there has been alot of molecular genetics work done in nuclear genome for DR in different ethnic groups and  identified several candidate genes involved in disease pathogenesis but the role of these genes in the development of disease is not yet clearly understood. more...
#> 805                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Age-related changes in DNA methylation occurring in blood leukocytes during early childhood may reflect epigenetic maturation. We hypothesized that some of these changes involve gene networks of critical relevance in leukocyte biology and conducted a prospective study to elucidate the dynamics of DNA methylation. Serial blood samples were collected at 3, 6, 12, 24, 36, 48 and 60 months after birth in 10 healthy girls born in Finland and participating in the Type 1 Diabetes Prediction and Prevention Study. more...
#> 806                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Type 1 diabetes (T1D) is a polygenic autoimmune disorder caused by autoreactive T cells that recognize pancreatic islet antigens and subsequently destroy insulin-producing β-cells. Pancreatic lymph nodes (PLN) are an essential site for the development of T1D, where tolerance to pancreatic self-antigens is first broken and the autoimmune responses are amplified. The purpose of this study was to identify candidate genes and pathways in the PLN that may contribute to the pathogenesis of T1D.
#> 807                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Despite the significant reduction in the overall burden of cardiovascular disease (CVD) over the past decade, CVD still accounts for a third of all deaths in the United States and worldwide each year. While efforts to identify and reduce risk factors for atherosclerotic heart disease (i.e. hypertension, dyslipidemia, diabetes mellitus, cigarette smoking, inactivity) remain the focus of primary prevention, the inability to accurately and temporally predict acute myocardial infarction (AMI) impairs our ability to further improve patient outcomes. more...
#> 808                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Due to an increasingly aging population, the incidence of dementias such as Alzheimer’s disease are steadily rising, with recent estimates predicting >115million dementia sufferers by 2050.   The ability to identify early markers in blood, which appear before the onset of clinical symptoms is of considerable interest to allow early intervention, particularly in “high risk” groups such as those with Type 2 Diabetes (T2D). more...
#> 809                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Despite some success in identifying CNVs responsible for metabolic phenotypes including obesity and diabetes mellitus, there are as yet no data available to suggest whether or not CNVs might be involved in the etiology of the NAFLD spectrum. This report is a comprehensive analysis of copy number in Malaysian patients with NAFLD.
#> 810                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               To investigate the umbilical cord lncRNA profiles in gestational diabetes-induced  macrosomia, the umbilical cord vein blood from normal and gestational diabetes-induced macrosomia was hybridized to a microarray containing probes representing 33,000 lncRNA genes. Quantitative real-time polymerase chain reaction (qPCR) was used to validate selected differentially expressed lncRNAs. The gene ontology (GO), pathway and network analysis were performed. more...
#> 811                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         The objective of this study was to examine relationships between weight loss through changes in lifestyle and peripheral blood gene expression profiles. Substantial weight loss (-15.2+3.8%) in lifestyle participants was associated with improvement in selected cardiovascular risk factors and significant changes in peripheral blood gene expression from pre- to post-intervention: 132 unique genes showed significant expression changes related to immune function and inflammatory responses involving endothelial activation. more...
#> 812                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 813                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      We performed global microRNA expression profiling of a cohort of primary melanoma patient samples linked to a well-annotated clinical database. The goal of this study was to identify microRNA that are associated to or correlated with various clinical parameters and patient outcomes. Candidate microRNA were identified for building prognostic models and functional testing.
#> 814                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Obesity is associated with insulin resistance and increased intrahepatic triglyceride (IHTG) content, which are key risk factors for diabetes and cardiovascular disease. However, a subset of obese people does not develop these metabolic complications. We tested the hypothesis that MNO, but not MAO, people are protected from the adverse metabolic effects of weight gain. To this end, global transcriptional profile in adipose tissue before and after weight gain was evaluated by microarray analyses.
#> 815                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Using a functional approach to investigate the epigenetics of Type 2 Diabetes (T2D), we combine three lines of evidence – diet-induced epigenetic dysregulation in mouse, epigenetic conservation in humans, and T2D clinical risk evidence – to identify genes implicated in T2D pathogenesis through epigenetic mechanisms related to obesity. Beginning with dietary manipulation of genetically homogeneous mice, we identify differentially DNA-methylated genomic regions. more...
#> 816                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  This study compared whole transcriptome signatures of 6 immune cell subsets and whole blood from patients with an array of immune-associated diseases. Fresh blood samples were collected from healthy subjects and subjects diagnosed type 1 diabetes, amyotrophic lateral sclerosis, and sepsis, as well as multiple sclerosis patients before and 24 hours after the first treatment with IFN-beta. At the time of blood draw, an aliquot of whole blood was collected into a Tempus tube (Invitrogen), while the remainder of the primary fresh blood sample was processed to highly pure populations of neutrophils, monocytes, B cells, CD4 T cells, CD8 T cells, and natural killer cells. more...
#> 817                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    The pathogenesis of IDD is still unclear, and microRNA has been reported playing an important role in occurrence and development of many diseases. But to date, the research about the role of microRNA in IDD is rare.
#> 818                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Genes dysregulated in cystic fibrosis (CF) and primary pulmonary arterial hypertension (PAH) at a late stage of pulmonary failure are still largely unknown. Blood samples taken in the frame of the French cohort of lung transplantation COLT offers the opportunity to identify in blood specific gene signatures of each disease and a common gene signature for both pathologies. A microarray analysis was performed with homogeneous groups of CF patients (n=23), PAH (n=13) patients and healthy volunteers (n=28). more...
#> 819                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Peripheral blood samples of patients with acute myocardial infarction were matched with those of control patients to identify possible differences in corresponding gene expression profiles. The controls were matched to cases based on gender, age, status of diabetes mellitus and smoking status. Six months cardiovascular survival status of the cases was used to identify two distinct subgroups among the cases. more...
#> 820                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Skeletal muscle is the key site of peripheral insulin resistance in type 2 diabetes. Insulin-stimulated glucose uptake is decreased in differentiated diabetic myotubes in keeping with a retained genetic/epigenetic defect of insulin action. Microarray analysis was used to investigate differences in gene expression with differentiation in diabetic cultures compared to controls.
#> 821                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Analysis of microRNA expression in vastus lateralis muscle biopsies from 11 genetically identical twin pairs discordant for type 2 diabetes. This eliminates the influence of genotype and leads to the identification of microRNAs that are exclusively influenced by environmental (non-genetic) factors.
#> 822                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          In addition to the well-known short noncoding RNAs as miRNAs, increasing evidence suggests that long noncoding RNAs (lncRNAs) act as key regulators in a wide aspect of biologic processes. Dysregulated expression of lncRNAs has been demonstrated being implicated in a variety of human diseases. However, there is relative paucity of information regarding the role of lncRNAs in intervertebral disc degeneration (IDD) hitherto. more...
#> 823                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              The rising incidence of obesity and related disorders such as diabetes and heart disease has  focused considerable attention on the discovery of novel therapeutics. One promising  approach has been to increase the number or activity of brown-like adipocytes in white  adipose depots, as this has been shown to prevent diet-induced obesity and reduce the  incidence and severity of type 2 diabetes. Thus, the conversion of fat-storing cells into  metabolically active thermogenic cells has become an appealing therapeutic strategy to  combat obesity. more...
#> 824                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            FUS-CHOP and EWS-CHOP balanced translocations characterize myxoid liposarcoma which encompasses myxoid (ML) and round cell (RC) variants initially believed to be distinct diseases. Currently, myxoid and RC liposarcoma are regarded to represent the well differentiated and the poorly differentiated ends, respectively, within spectrum of myxoid liposarcoma where the fusion proteins blocking lipogenic differentiation play a role in tumor initiation while molecular determinants associated to progression to RC remain poorly understood. more...
#> 825                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            FUS-CHOP and EWS-CHOP balanced translocations characterize myxoid liposarcoma which encompasses myxoid (ML) and round cell (RC) variants initially believed to be distinct diseases. Currently, myxoid and RC liposarcoma are regarded to represent the well differentiated and the poorly differentiated ends, respectively, within spectrum of myxoid liposarcoma where the fusion proteins blocking lipogenic differentiation play a role in tumor initiation while molecular determinants associated to progression to RC remain poorly understood. more...
#> 826                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Chemotherapy-related endothelial damage contributes to the early development of cardiovascular morbidity in testicular cancer patients. We aimed to identify relevant mechanisms of and search for candidate biomarkers for this endothelial damage. Human micro-vascular endothelial cells (HMEC-1) were exposed to bleomycin or cisplatin with untreated samples as control. 18k cDNA microarrays were used. Gene expression differences were analysed at single gene level and in gene sets clustered in biological pathways and validated by qRT-PCR. more...
#> 827                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1. However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, sug- gesting that this complex plays a dichotomous and poorly understood role in cancer2,3. Here we provide genomic, cellular, and mouse mod- elling data demonstrating that the polycomb group gene SUZ12 func- tions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1. more...
#> 828                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1. However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, suggesting that this complex plays a dichotomous and poorly understood role in cancer2,3. Here we provide genomic, cellular, and mouse mod- elling data demonstrating that the polycomb group gene SUZ12 func- tions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1. more...
#> 829                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Human induced pluripotent stem cells changed the face of stem cell biology as they represent a renewable source of stem cells with the potential to differentiated into multiple lineages in a manner akin to embryonic stem cells that can be collected without the need for the destruction of an embryo. The potential of these cells as research tools is vast as they can be pushed to generate different cell types depending on research interest. more...
#> 830                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    The generation of insulin-producing pancreatic cells from stem cells in vitro would provide an unprecedented cell source for drug discovery and cell transplantation therapy in diabetes. However, insulin-producing cells previously generated from human pluripotent stem cells (hPSC) lack many functional characteristics of bona fide β cells. Here we report a scalable differentiation protocol that can generate hundreds of millions of glucose-responsive β cells from hPSC in vitro. more...
#> 831                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Pancreatic tumors with small size can cause type3C Diabetes Mellitus (PCA-DM) but the mechanism is unknown. In this study we aimed at revealing the mRNA and long noncoding RNA (LncRNA) expression patterns of pancreatic tumors that triggered PCA-DM. Four pancreatic tumors from patients with PCA-DM (A1-A4), four pancreatic tumors from patients without PCA-DM (B1-B4), and four pancreatic tissues from patients with pancreatitis were individually profiled with Agilent microarrays(Arraystar Human LncRNA Array v3.0).
#> 832                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Aspirin-exacerbated respiratory disease (AERD) is one phenotype of asthma, often in the form of a severe and sudden attack. Due to time consuming and laborious oral aspirin challenge (OAC) for diagnosis of AERD, non-invasive biomarkers have been searched. Therefore, we scrutinize AERD-associated exonic SNPs and examine the diagnostic potential of combination of these candidate SNPs to predict AERD
#> 833                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 834                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Given the possible critical importance of placental gene imprinting and random monoallelic expression on fetal and infant health, most of those genes must be identified, in order to understand the risks that the baby might meet during pregnancy and after birth. Therefore, the aim of the current study was to introduce a workflow and tools for analyzing imprinted and random monoallelic gene expression in human placenta, by applying whole-transcriptome (WT) RNA sequencing of placental tissue and genotyping of coding DNA variants in family trios. more...
#> 835                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            In vitro expansion of adult human islet β cells is an attractive solution for the shortage of tissue for cell replacement therapy of type 1 diabetes. Using a lineage tracing approach, we have demonstrated that β-cell-derived (BCD) cells rapidly dedifferentiate in culture and can proliferate for up to 16 population doublings. Dedifferentiation is associated with changes resembling epithelial-mesenchymal transition (EMT). more...
#> 836                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      By restraining T cell activation and promoting regulatory T cell (Treg) expansion, myeloid-derived suppressor cells (MDSC) and tolerogenic dendritic cells (DC) (tDC) can control self-reactive and anti-graft effector T cells in autoimmunity and transplantation. Their therapeutic use and characterization, however, is limited by their scarce availability in the peripheral blood of tumor-free donors. In the present study we describe and characterize a novel population of myeloid suppressor cells, named fibrocytic MDSC (f-MDSC), that are differentiated from umbilical cord blood (UCB) precursors by a 4 day culture with FDA approved cytokines (rh-GM-CSF and rh-G-CSF). more...
#> 837                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Ras-related associated with diabetes (RRAD) is a small Ras-related GTPase that is frequently inactivated by DNA methylation of the CpG island in its promoter region in cancer tissues. However, the role of the methylation-induced RRAD inactivation in tumorigenesis remains unclear. In this study, the Ras regulated-transcriptome and epigenome were profiled by comparing T29H (a RasV12-transformed human ovarian epithelial cell line) with T29 (an immortalized but non-transformed cell line) through Reduced representation bisulfite sequencing (RRBS-seq) and Digital gene expression (DGE) . more...
#> 838                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Ras-related associated with diabetes (RRAD) is a small Ras-related GTPase that is frequently inactivated by DNA methylation of the CpG island in its promoter region in cancer tissues. However, the role of the methylation-induced RRAD inactivation in tumorigenesis remains unclear. In this study, the Ras regulated-transcriptome and epigenome were profiled by comparing T29H (a RasV12-transformed human ovarian epithelial cell line) with T29 (an immortalized but non-transformed cell line) through Reduced representation bisulfite sequencing (RRBS-seq) and Digital gene expression (DGE) . more...
#> 839                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Glucocorticoid excess is linked to central obesity, adipose tissue insulin resistance and type 2 diabetes mellitus. The aim of our study was to investigate the effects of dexamethasone on gene expression in human subcutaneous and omental adipose tissue, in order to identify potential novel mechanisms and biomarkers for glucocorticoid-induced insulin resistance in adipose tissue. Dexamethasone changed the expression of 527 genes in both subcutaneous and omental adipose tissue. more...
#> 840                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Proliferative diabetic retinopathy (PDR) is a vision-threatening disorder characterized by the formation of cicatricial fibrovascular membranes leading to traction retinal detachment. Despite the recent advance in the treatment of PDR such as vitreoretinal surgery with use of anti-vascular endothelial growth factor (VEGF) drug as an adjunct, it still remains vision-threatening disease. In order to identify genes associated with the pathogenesis of PDR, we performed gene expression analyses in fibrovascular membrane in patients with PDR using DNA microarray technology.
#> 841                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 842                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Type 1 diabetes mellitus (T1D) is a common autoimmune disease mediated by autoimmune attack against pancreatic b cells. It has been reported that dys-regulation of microRNAs (miRNAs) may contribute to the pathogenesis of autoimmune diseases, including T1D. This study sought to identify T1D associated miRNAs in the peripheral blood mononuclear cell (PBMC).
#> 843                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Type 1 diabetes mellitus (T1D) is a common autoimmune disease mediated by autoimmune attack against pancreatic b  cells.Dys-regualtion of the component of peripheral blood mononuclear cells (PBMCs), including T-cells and B-cells, and smaller amounts of NK cells and dendritic cells, have all been implicated in this process This study sought to identify T1D associated differently expressed  genes in the peripheral blood mononuclear cell (PBMC).
#> 844                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Type 1 diabetes mellitus (T1DM) results from immune mediated destruction of pancreatic beta cells. However, clinical and immunologic phenotypes of T1DM are variable. Several auto-antibodies including GADA, IA-2A, and ZnT8A, were identified in T1DM, but the prevalence of these auto-antibodies varied for a broad spectrum of T1DM. Here, we systemically profiled auto-antibodies from serum samples of 16 T1DM, 16 type 2 diabetes (T2DM) patients, and 27 healthy controls with normal glucose tolerance (NGT) using protein microarrays containing 9,480 proteins. more...
#> 845                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Here we harnessed the potential of expression arrays in 89 human pancreatic islet donors (different levels of blood glucose (HbA1c)) to identify genes regulated in this relevant tissue for type 2 diabetes (T2D).
#> 846                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Mi(cro)RNAs are small non-coding RNAs of 18-25 nucleotides in length that modulate gene expression at the post-transcriptional level. These RNAs have been shown to be involved in a several biological processes, human diseases and metabolic disorders. Proanthocyanidins, which are the most abundant polyphenol class in the human diet, have positive heath effects on a variety of metabolic disorders such as inflammation, obesity, diabetes and insulin resistance. more...
#> 847                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Mucormycosis is an increasingly common, life-threatening fungal infection caused by fungi belonging to the subphylum Mucormycotina, order Mucorales. The major risk factors for mucormycosis include uncontrolled diabetes mellitus, treatment with corticosteroids, organ or bone marrow transplantation, neutropenia, trauma and burns, malignant hematological disorders, and deferoxamine-therapy in patients receiving hemodialysis. more...
#> 848                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The developmental origins of adult disease are now recognized to reflect intrauterine conditions during embryonic and fetal life. Cell-cell communication between the maternal endometrium and the pre-implantation embryo can occur by several means. Here, we show that maternal miRNAs are secreted by the endometrial epithelium to the endometrial fluid. Microarray assessments revealed the presence of specific miRNAs that are associated with the window of implantation and therefore in direct contact with the human preimplantation embryo. more...
#> 849                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 850                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. more...
#> 851                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 852                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The type and the amount of dietary fat have a significant influence on the metabolic pathways involved in the development of obesity, metabolic syndrome, diabetes type 2 and cardiovascular diseases. However, it is unknown to what extent this modulation is achieved through DNA methylation. We assessed the effects of cholesterol intake, the proportion of energy intake derived from fat, the ratio of polyunsaturated fatty acids (PUFA) to saturated fatty acids (SFA), the ratio of monounsaturated fatty acids (MUFA) to SFA, and the ratio of (MUFA+PUFA) to SFA on genome-wide DNA methylation patterns in normal-weight and obese children. more...
#> 853                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Obesity is associated with a chronic, low-grade, systemic inflammation that may contribute to the development of insulin resistance and type 2 diabetes. Resveratrol, a natural compound with anti-inflammatory properties, is shown to improve glucose tolerance and insulin sensitivity in obese mice and humans. Here we tested the effect of a 2-year resveratrol administration on the pro-inflammatory profile and insulin resistance caused by a high-fat, high-sugar (HFS) diet in white adipose tissue (WAT) from rhesus monkeys. more...
#> 854                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              To identify genes with expression levels that are associated with T1D progression from AbP (islet autoantibody positive),   global gene expression changes were analyzed in AbP subjects with different T1D progression rate.
#> 855                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Monozygotic (MZ) twin pair discordance for childhood-onset Type 1 Diabetes (T1D) is ~50%, implicating roles for genetic and non-genetic factors in the aetiology of this complex autoimmune disease. Although significant progress has been made in elucidating the genetics of T1D in recent years, the non-genetic component has remained poorly defined. We hypothesized that epigenetic variation could underlie some of the non-genetic component of T1D aetiology and, thus, performed an epigenome-wide association study (EWAS) for this disease. more...
#> 856                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Access to an unlimited number of human pancreatic beta cells represents a major challenge in the field of diabetes to better dissect human beta cell functions and to make significant progress in drug discovery and cell replacement therapies. We previously reported the generation of the EndoC-bH1 human beta cell line that was generated by targeted oncogenesis in human fetal pancreases followed by in vivo cell differentiation in mice. more...
#> 857                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Results Platelets in non-diabetic patients demonstrated miRNA expression profiles comparable to previously published data. The miRNA expression profiles of platelets in diabetics were similar. Statistical analysis unveiled only three miRNAs (miR-377-5p, miR-628-3p, miR-3137) with high reselection probabilities in resampling techniques, corresponding to signatures with only modest discriminatory performance. more...
#> 858                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        This dataset was used to establish whole blood transcriptional modules (n=260) that represent groups of coordinately expressed transcripts that exhibit altered abundance within individual datasets or across multiple datasets.  This modular framework was generated to reduce the dimensionality of whole blood microarray data processed on the Illumina Beadchip platform yielding data-driven transcriptional modules with biologic meaning.
#> 859                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Pancreatic islets are central in type 2-diabetes development, which coincides with increased activity of innate immunity. Intriguingly, human pancreatic islets express many complement genes. The most highly expressed gene was the complement inhibitor CD59 that is GPI anchored to the cell membrane, which unexpectedly was found in high amounts intracellularly in beta cells. Silencing of CD59 strongly suppressed insulin secretion. more...
#> 860                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Intensive lifestyle modification is believed to mediate cardiovascular disease (CVD) risk through traditional pathways that affect endothelial function and progression of atherosclerosis; however, the extent, persistence, and clinical significance of molecular change during lifestyle modification are not well known. Our study reveals that gene expression signatures are significantly modulated by rigorous lifestyle behaviors and track with CVD risk profiles over time.
#> 861                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To unravel genes and molecular pathways involved in the pathogenesis of type 1 diabetes (T1D), we performed genome-wide gene expression profiling of prospective venous blood samples from children developing T1D-associated autoantibodies or progressing towards clinical diagnosis.
#> 862                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              This SuperSeries is composed of the SubSeries listed below.  Due to privacy concerns, the SNP data is not available with unrestricted access.
#> 863                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To unravel genes and molecular pathways involved in the pathogenesis of type 1 diabetes (T1D), we performed genome-wide gene expression profiling of prospective venous blood samples from children developing T1D-associated autoantibodies or progressing towards clinical diagnosis.
#> 864                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To unravel genes and molecular pathways involved in the pathogenesis of type 1 diabetes (T1D), we performed genome-wide gene expression profiling of prospective venous blood samples from children developing T1D-associated autoantibodies or progressing towards clinical diagnosis.
#> 865                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    To unravel genes and molecular pathways involved in the pathogenesis of type 1 diabetes (T1D), we performed genome-wide gene expression profiling of prospective venous blood samples from children developing T1D-associated autoantibodies or progressing towards clinical diagnosis.
#> 866                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The aim of this study was to compare miRNA expression in urinary exosomes from type 1 diabetic patients with and without incipient diabetic nephropathy. Overnight urine collections were obtained from normo- and microalbuminuric type 1 diabetic patients. Urines were pre-cleared by both centrifugation and filtration, urinary exosomes were isolated by two consecutive ultracentrifugation steps and total RNA extracted. more...
#> 867                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Identification of the inflammatory signature in visceral adipose tissue CD14+ cells (adipose tissue macrophage) Total RNA obtained from CD14+ cells (Immunoselcted cells from stromal adipose tissue cells)
#> 868                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico was recently established to better understand the impacts of prenatal exposure to inorganic arsenic (iAs). In this study, we examined a subset (n = 40) of newborn cord blood samples for microRNA (miRNA) expression changes associated with in utero arsenic exposure. Levels of iAs in maternal drinking water (DW-iAs) and maternal urine were assessed. more...
#> 869                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The Biomarkers of Exposure to ARsenic (BEAR) pregnancy cohort in Gómez Palacio, Mexico was recently established to better understand the impacts of prenatal exposure to inorganic arsenic (iAs). In this study, we examined a subset (n = 40) of newborn cord blood samples for microRNA (miRNA) expression changes associated with in utero arsenic exposure. Levels of iAs in maternal drinking water (DW-iAs) and maternal urine were assessed. more...
#> 870                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Pancreatic beta-cell dysfunction and death are central in the pathogenesis of type 2 diabetes. Saturated fatty acids cause beta-cell failure and contribute to diabetes development in genetically predisposed individuals. Here we used RNA-sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. more...
#> 871                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We determined the genes that were differentially expressed between fulminant type 1 diabetes and classical type 1A diabetes or healthy control using gene expression microarray in peripheral blood cells.
#> 872                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We determined the genes that were differentially expressed between fulminant type 1 diabetes and classical type 1A diabetes using gene expression microarray in peripheral blood cells.
#> 873                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 874                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                With broad high-throughput evaluation of microRNA expression across the spectrum of colon cancer stages, we identidied a microRNA signature that is associated with more aggressive disease
#> 875                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Compariosn of mRNA and miRNA profile in colon cancer
#> 876                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 We profiled gene expression in peripheral blood cells from 28 obese patients by microarray analysis and visceral fat accumulation caused the gene expression proliles especially in circadian rhythm, inflammation, oxidative stress, and immune response.
#> 877                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 878                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death.
#> 879                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Fetal growth restriction (FGR) develops when fetal nutrient availability is compromised and increases the risk for perinatal complications and predisposes for offspring obesity, diabetes and cardiovascular disease later in life. Emerging evidence implicates changes in placental function in altered fetal growth and the subsequent development of adult disease.  The susceptibility for disease in response to an adverse intrauterine environment differs distinctly between boys and girls, with girls typically having better outcomes. more...
#> 880                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We compared human female hiPSC lines (all derived from IMR-90 fibroblasts) that were XIST RNA-positive and XIST RNA-negative.  We also examined the gene expression patterns for 2 female hIPSCs (derived from different disease model fibroblasts) that were also negative for XIST RNA. hiPS 12D-1 is derived from Huntington's Disease patient and 6C-1 is derived from a Type I Diabetes Mellitus patient (Park et al Nature 2008).
#> 881                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Type 2 diabetes mellitus (T2DM) is a multi-factorial disease characterized by the inability of beta-cells in the endocrine pancreas to produce sufficient amounts of insulin to overcome insulin resistance in peripheral tissue. To investigate the function of miRNAs in T2DM, we sequenced the small RNAs of human islets cells from diabetic and non-diabetic organ donors and identified a cluster of miRNAs in an imprinted locus on human chromosome 14 to be dramatically down-regulated in T2DM islets. more...
#> 882                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Using the Illumina 450K array and a stringent statistical analysis with age and gender correction, we report genome-wide differences in DNA methylation between pathology-free regions derived from human multiple sclerosis–affected and control brains. Differences were subtle, but widespread and reproducible in an independent validation cohort. The transcriptional consequences of differential DNA methylation were further defined by genome-wide RNA-sequencing analysis and validated in two independent cohorts. more...
#> 883                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              To explore the molecular mechanisms of obesity and insulin resistance in the patients with polycystic ovary syndrome (PCOS) at the level of human embryonic stem cells (hESCs).Three PCOS-derived and one non-PCOS-derived hESC lines were induced into adipocytes, and then total mRNA was extracted from these adipocytes. The differential genes between PCOS-derived and non-PCOS-derived adipocytes were identified with GeneChip, and then were validated with real-time PCR.There were 153 differential genes. more...
#> 884                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Type 2 diabetes mellitus (T2DM) is a complex disease characterized by the inability of the insulin-producing β-cells in the endocrine pancreas to overcome insulin resistance in peripheral tissues. To determine if microRNAs are involved in the pathogenesis of human T2DM, we sequenced the small RNAs of human islets from diabetic and non-diabetic organ donors. We identified a cluster of miRNAs in an imprinted locus on human chromosome 14q32 that is highly and specifically expressed in human β-cells and dramatically down-regulated in islets from T2DM organ donors. more...
#> 885                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          MicroRNAs are powerful gene expression regulators, but their corneal repertoire and potential changes in corneal diseases remain unknown. Our purpose was to identify miRNAs altered in the human diabetic cornea by microarray analysis, and to examine their effects on wound healing in cultured telomerase-immortalized human corneal epithelial cells (HCEC) in vitro. Using microarrays, 29 miRNAs were identified as differentially expressed in diabetic samples. more...
#> 886                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Chromatin-based functional genomic analyses and genomewide association studies (GWASs) together implicate enhancers as critical elements influencing gene expression and risk for common diseases. Here, we performed systematic chromatin and transcriptome pro- filing in human pancreatic islets. Integrated analysis of islet data with those generated by the ENCODE project in nine cell types identified specific and significant enrichment of type 2 diabetes and related quantitative trait GWAS variants in islet enhancers. more...
#> 887                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Chromatin-based functional genomic analyses and genomewide association studies (GWASs) together implicate enhancers as critical elements influencing gene expression and risk for common diseases. Here, we performed systematic chromatin and transcriptome profiling in human pancreatic islets. Integrated analysis of islet data with those generated by the ENCODE project in nine cell types identified specific and significant enrichment of type 2 diabetes and related quantitative trait GWAS variants in islet enhancers. more...
#> 888                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Lifestyle intervention can improve insulin sensitivity in obese youth yet few studies have examined the biological mechanisms underlying improvements. Therefore, the purpose of this study was to explore biological pathways associated with intervention-induced improvements in insulin sensitivity. Fifteen (7M/8F) overweight/obese (BMI percentile=96.3±1.1) Latino adolescents (15.0±0.9 years) completed a 12-week lifestyle intervention that included weekly nutrition education and 180 minutes of moderate-vigorous exercise per week. more...
#> 889                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        This dataset encompassing the profiles of 150 lung cancer tumors was developed to serve as test dataset in the SBV IMPROVER Diagnostic Signature Challenge (sbvimprover.com). The aim of this subchallenge was to verify that it is possible to extract a robust diagnostic signature from gene expression data that can identify stages of different types of lung cancer. Participants were asked to develop and submit a classifier that can stratify lung cancer patients in one of four groups – Stage 1 of Adenocarcinoma (AC Stage 1), Stage 2 of Adenocarcinoma (AC Stage 2), Stage 1 of Squamous cell carcinoma (SCC Stage 1) or Stage 2 of Squamous cell carcinoma (SCC Stage 2). more...
#> 890                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The aim of this study was to investigate the association of gene expression profiles in subcutaneous adipose tissue with percent of total body weight change in 26 kidney transplant recipients. Using multivariate linear regression analysis controlled for race and gender, expression levels of 1553 genes were significantly (p<0.05) associated with weight change.
#> 891                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Polyphenolic compounds, such as resveratrol, have recently received widespread interest due to their ability to mimic effects of calorie restriction. The objective of the present study was to gain more insight into the effects of 30 days resveratrol supplementation on adipose tissue morphology and underlying processes. Nine healthy obese men were supplemented with placebo and 150mg/day resveratrol for 30 days, separated by a 4-week washout period. more...
#> 892                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Glomerular abnormalities have been demonstrated in kidney biopsies of patient after orthotopic liver transplantation (OLT). We hypothesize that these changes exist prior to OLT and may play a role in the development of renal failure after OLT. We use gene expression microarrays to investigate the mechanism of kidney disease in patients listed for OLT. Gene expression profiles of biopsies of cirrhotic patients were compared with pre-implantation living donor biopsies. more...
#> 893                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Regulatory T cells (Treg) prevent the emergence of autoimmune disease. Prototypic natural Treg (nTreg) are programmed by Forkhead-box P3 (FOXP3) and can be reliably identified by demethylation at the FOXP3 locus. To explore the nTreg methylation landscape we performed genome-wide methylation studies on human naïve resting nTreg (rTreg) and conventional naïve CD4+ T cells (Naïve). We detected 2,315 differentially methylated CpGs between these two cell types, many of which clustered into 127 regions of differential methylation (RDMs). more...
#> 894                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Tissues from another series of 74 patients with colorectal cancer were collected by laser micro-dissection with the Leica Laser Microdissection System (Leica Microsystems).
#> 895                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Insulin-secreting β cells and glucagon-secreting α cells maintain physiological blood glucose levels, and their malfunction drives diabetes development. Using ChIP sequencing and RNA sequencing analysis, we determined the epigenetic and transcriptional landscape of human pancreatic α, β, and exocrine cells. We found that, compared with exocrine and β cells, differentiated α cells exhibited many more genes bivalently marked by the activating H3K4me3 and repressing H3K27me3 histone modifications. more...
#> 896                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Diabetes and obesity are widespread diseases with signifciant socioeconomic implications.  We used three different types of human adipose tissue (epigastric, visceral, and subcutaneous) in order to determine differences in global gene expression between these adipose depots in severely obese patients. In this dataset, we include the expression data obtained from three types of adipose tissue; epigastric, subcutaneous, and visceral all obtained through open gastric bypass surgery.
#> 897                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  To search for new markers of active lesions that might help better understand the molecular basis of MPA and aid in its diagnosis, DNA microarray analysis was performed with peripheral blood mononuclear cells (PBMCs).
#> 898                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Primary endothelial cells from umbilical cord vein (HUVEC) obtained at delivery from gestational diabetic (GD) women, represent an expedient model for the study of the effects of chronic HG in vivo. In fetal tissues genome-wide epigenetic changes are likely to occur with specific long term and even trans-generational effects. We have utilized this model to study the effects of chronic hyperglycemia on the transcriptome and to verify the presence of specific epigenetic changes associated to chronic HG in vascular cells.
#> 899                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Inherited genetic variants of insulin receptor induced cellular signaling have long been suspected to contribute to the development of type-2- diabetes mellitus. In this report we discuss a heterozygous mutation in the first coding exon of the proto-oncogene Ha-Ras (Ha-RasA11P) that we have identified in a patient with familial premature aging syndrome. The patient has atopic sklerodermic skin alterations, insulin resistance as well as disturbances in lipid metabolism. more...
#> 900                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Lipodystrophies resemble syndromes of disturbed adipocyte biology or development and severe congenital forms (CGL) lack adipose tissue. The ubiquitous immediate-early gene c-fos is one essential transcription factor to initiate adipocyte differentiation. In a CGL patient we identified a single homozygous point mutation in the promoter of c-fos gene. The mutation facilitates the formation of a novel specific protein/ DNA complex and ubiquitously reduces basal and inducible c-fos transcription activity. more...
#> 901                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 902                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        To identify genes with cell-lineage-specific expression not accessible by experimental micro-dissection, we developed a genome-scale iterative method, in-silico nano-dissection, which leverages high-throughput functional-genomics data from tissue homogenates using a machine-learning framework. This study applied nano-dissection to chronic kidney disease and identified transcripts specific to podocytes, key cells in the glomerular filter responsible for hereditary proteinuric syndromes and acquired CKD. more...
#> 903                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        To identify genes with cell-lineage-specific expression not accessible by experimental micro-dissection, we developed a genome-scale iterative method, in-silico nano-dissection, which leverages high-throughput functional-genomics data from tissue homogenates using a machine-learning framework. This study applied nano-dissection to chronic kidney disease and identified transcripts specific to podocytes, key cells in the glomerular filter responsible for hereditary proteinuric syndromes and acquired CKD. more...
#> 904                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C).
#> 905                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 906                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C).
#> 907                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The overall objective of the heritage project is to study the role of the genotype in cardiovascular,metabolic and hormonal responses to aerobic exercise training and the contribution of regular exercise to changes in several cardiovascular disease and diabetes risk factors.  PLEASE NOTE THE POST-TRAINING GENE CHIP FILES HAVE NEVER BEEN RELEASED ON GEO. PLEASE ALSO NOTE THAT DUE TO THE OUTDATED INSULIN ASSAY UTILISED IN THE HERITAGE STUDY, THE INSULIN DATA WAS NOT COMPARABLE WITH ANY MORE RECENT MODERN STUDIES.
#> 908                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Recent advances in the understanding of the genetics of type 2 diabetes (T2D) susceptibility have focused attention on the regulation of transcriptional activity within the pancreatic beta-cell. MicroRNAs (miRNAs) represent an important component of regulatory control, and have proven roles in the development of human disease and control of glucose homeostasis. We set out to establish the miRNA profile of human pancreatic islets and of enriched beta-cell populations, and to explore their potential involvement in T2D susceptibility. more...
#> 909                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 910                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      A need exists for biomarkers in T1D that can 1) sensitively and specifically detect disease-related immune activity prior to, and independent of, measurement of auto-antibodies towards islet cell antigens; 2) define immunopathological mechanisms; and 3) monitor changes in the inflammatory state associated with disease progression or response to therapeutic intervention.  In an effort to fill this gap, we have applied a novel bioassay to both human and BB rat T1D whereby the complex milieu of inflammatory mediators present in plasma can be indirectly detected through their ability to drive transcription in peripheral blood mononuclear cells drawn from healthy, unrelated donors. more...
#> 911                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Overall, the widely disparate transcriptomes identified prior to RT among the three clusters support the notion that at least some of the inter-individual heterogeneity in propensity for RT-induced myofiber hypertrophy is likely pre-determined.
#> 912                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Transcriptional Profiling of Insulin Sensitive and Insulin Resistant Samples
#> 913                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Metabolic Syndrome (MetS) is a strong predictor for diabetes and cardiovascular disease and is defined by a constellation of phenotypes including increased and adverse body fat distribution, insulin resistance, abnormalities in lipids and lipoproteins, malfunctional cardiovascular performance, and abnormal levels of adipokines and cytokines. We assayed in a subset of our family cohort phentoyped for MetS phentoypes, the genome-wde transcript levels using the Illumina Human WG-6 v3 expression arrays.
#> 914                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Metabolic Syndrome (MetS) is a strong predictor for diabetes and cardiovascular disease and is defined by a constellation of phenotypes including increased and adverse body fat distribution, insulin resistance, abnormalities in lipids and lipoproteins, malfunctional cardiovascular performance, and abnormal levels of adipokines and cytokines. We assayed in a subset of our family cohort phentoyped for MetS phentoypes, the genome-wde transcript levels using the Illumina Human WG-6 v2 expression arrays.
#> 915                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Diabetes is a disorder characterized by loss of beta cell mass and/or beta cell function, leading to deficiency of insulin relative to metabolic need. To determine whether stem cell derived-beta cells faithfully reflect the phenotypes of a diabetic subject, we generated induced pluripotent stem cells from diabetic subjects (MODY2) with heterozygous loss-of-function of the gene encoding glucokinase (GCK). more...
#> 916                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Expression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes
#> 917                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 918                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Transcription has the capacity to modify mechanically DNA topology, DNA structure, and nucleosome arrangement. Resulting from ongoing transcription, these modifications in turn, may provide instant feedback to the transcription machinery. To substantiate the connection between transcription and DNA dynamics, we charted an ENCODE map of transcription-dependent dynamic supercoiling in human Burkitt lymphoma cells using psoralen photobinding to probe DNA topology in vivo. more...
#> 919                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Nuclear RNA from Raji human B cells was hybridized to NimbleGen arrays to quantify gene expression levels.
#> 920                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               In this study, we examined the impact of modulating the TGF-β/PAI-1 axis in CD34+ cells function from diabetic patients and controls.  Using gene array studies, we found that diabetics, protected from microvascular complications despite suboptimal glycemic control, had reduced level of TGF- β1 and PAI-1 transcripts in their CD34+ cells compared to age, sex, duration and degree of glycemic control -matched diabetics with microvascular complications. more...
#> 921                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Objective was to examine acute gene expression responses to physiologic oral glucose ingestion in human circulating leukocytes. Microarray study of human circulating leukocytes sampled before, 1 hour after and 2 hours after glucose ingestion was performed. The present study demonstrated 36 genes which showed acute gene expression change in human leukocytes within 1 hour after glucose ingestion and suggest that leukocytes participate in the inflammatory process induced by acute hyperglycemia.
#> 922                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      This study employed Affymetrix GeneChips to profile transcriptome of human pulmonary microvascular endothelial cells (HMVEC-L) treated with PBEFsiRNA to gain insight into transcriptional regulations of PBEF on the endothelial function. We isolated and labeled mRNAs from PBEF siRNA transfected HMVEC-L and hybridized them to Affymetrix GeneChip HG-U133 plus 2. Differentially expressed genes and canonical pathways were analyzed. more...
#> 923                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Monozygotic twins discordant for type 2 diabetes constitute an ideal model to study environmental contributions to type 2 diabetic traits. We aimed to examine whether global DNA methylation differences exist in major glucose metabolic tissues from twelve 53–80 year-old monozygotic discordant twin pairs.
#> 924                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Through gene expression profiling in cultured lymphocytes and PBMCs from a large set of T1D patients and controls, we demonstrate that IL-1ra may protect against the development of islet autoimmunity and T1D through down-regulating a large number of inflammatory genes and pathways.  Keywords: autoimmunity; IL-1Ra;Type 1 diabetes (T1D)
#> 925                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     A genome-wide eQTL analysis was performed in whole blood samples collected from 76 Japanese subjects. RNA microarray analysis was performed for 3 independent samples that were genotyped in a genome-wide scan. The correlations between the genotypes of 534,404 autosomal single nucleotide polymorphisms (SNPs) and the expression levels of 30,465 probes were examined for each sample. The SNP-probe pairs with combined correlation coefficients of all 3 samples corresponding to P < 3.10 × 10-12 (i.e., Bonferroni-corrected P < 0.05) were considered significant. more...
#> 926                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     A genome-wide eQTL analysis was performed in whole blood samples collected from 76 Japanese subjects. RNA microarray analysis was performed for 3 independent samples that were genotyped in a genome-wide scan. The correlations between the genotypes of 534,404 autosomal single nucleotide polymorphisms (SNPs) and the expression levels of 30,465 probes were examined for each sample. The SNP-probe pairs with combined correlation coefficients of all 3 samples corresponding to P < 3.10 × 10-12 (i.e., Bonferroni-corrected P < 0.05) were considered significant. more...
#> 927                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     A genome-wide eQTL analysis was performed in whole blood samples collected from 76 Japanese subjects. RNA microarray analysis was performed for 3 independent samples that were genotyped in a genome-wide scan. The correlations between the genotypes of 534,404 autosomal single nucleotide polymorphisms (SNPs) and the expression levels of 30,465 probes were examined for each sample. The SNP-probe pairs with combined correlation coefficients of all 3 samples corresponding to P < 3.10 × 10-12 (i.e., Bonferroni-corrected P < 0.05) were considered significant. more...
#> 928                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     A genome-wide eQTL analysis was performed in whole blood samples collected from 76 Japanese subjects. RNA microarray analysis was performed for 3 independent samples that were genotyped in a genome-wide scan. The correlations between the genotypes of 534,404 autosomal single nucleotide polymorphisms (SNPs) and the expression levels of 30,465 probes were examined for each sample. The SNP-probe pairs with combined correlation coefficients of all 3 samples corresponding to P < 3.10 × 10-12 (i.e., Bonferroni-corrected P < 0.05) were considered significant. more...
#> 929                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Gene expression profiles of biopsy samples of visceral adipose of three female patients of type 2 diabetes and three non-diabetic female patients were generated using Illumina HumanHT-12 v3 Expression BeadChip arrays. The primary indications of surgery were non-infective and non-malignant conditions, namely, cholelethiasis, hernia and trauma.
#> 930                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Gene expression profiles of biopsy samples of subcutaneous adipose of three female patients of type 2 diabetes and three non-diabetic female patients were generated using Illumina HumanHT-12 v3 Expression BeadChip arrays.  The primary indications of surgery were non-infective and non-malignant conditions, namely, cholelethiasis, hernia and trauma.
#> 931                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Gene expression profiles of biopsy samples of skeletal muscle of three male patients of type 2 diabetes and three non-diabetic male patients were generated using Illumina HumanHT-12 v3 Expression BeadChip arrays. The primary indications of surgery were non-infective and non-malignant conditions, namely, cholelethiasis, hernia and trauma.
#> 932                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Global gene expression profile of whole blood in patients with coronary artery disease (CAD) showed significant upregulation of 343 genes and down regulation of 151 genes as compared to controls (p<0.05). There was predominant differential regulation of inflammatory and immune response genes as well as early growth response genes in our dataset. Of the ten candidate genes selected for validation by real time PCR in an independent cohort, CXCL1, EGR3, IL8, PTGS2 and CD69 genes were up regulated and IFNG and FASLG down regulated in cases relative to controls.
#> 933                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The remarkable differentiation capacity of pluripotent stem cells into any adult cell types have enabled researchers to model human embryonic development and disease process in dishes, as well as deriving specialized cells for replacing damaged tissues. Type 1 diabetes is a degenerative disease characterized by autoimmune destruction of the insulin-producing beta islet cells in the pancreas. Recent advances have led to the establishment of different methods to direct differentiation of human or mouse pluripotent stem cells toward beta cell lineages. more...
#> 934                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        The remarkable differentiation capacity of pluripotent stem cells into any adult cell types have enabled researchers to model human embryonic development and disease process in dishes, as well as deriving specialized cells for replacing damaged tissues. Type 1 diabetes is a degenerative disease characterized by autoimmune destruction of the insulin-producing beta islet cells in the pancreas. Recent advances have led to the establishment of different methods to direct differentiation of human or mouse pluripotent stem cells toward beta cell lineages. more...
#> 935                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Polycystic ovary Syndrome (PCOS) is a heterogeneous endocrine disorder that shows evidence of genetic predidposition among affected individuals. We have utilized the Microarray data from  granulosa cells of normal and PCOS women for network construction.
#> 936                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 937                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 938                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 939                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 940                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions.  Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). more...
#> 941                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Myotonic Dystrophy Type-2 (DM2) is an autosomal dominant disease caused by the expansion of a CCTG tetraplet repeat. It is a multisystemic disorder, affecting skeletal muscles, the heart, the eye, the central nervous system and the endocrine system The expression of 365 miRNAs was measured in the muscle of DM2 patients and compared it to controls and were identified distinct miRNAs modulated in DM2 patients compared to controls.
#> 942                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Purpose:  Despite advances in radical surgery and chemotherapy delivery, ovarian cancer is the most lethal gynecologic malignancy.  Most of these patients are treated with platinum-based chemotherapies, but there is no biomarker model to guide their responses to these therapeutic agents.   We have developed and independently tested our novel multivariate molecular predictors for forecasting patients' responses to individual drugs on a cohort of 58 ovarian cancer patients. more...
#> 943                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          A study which examines differences in microRNA expression profiles across different sarcoma histological subtypes
#> 944                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Aims/hypothesis: Duct cells isolated from adult human pancreas can be reprogrammed to express islet beta cell genes by adenoviral transduction of the developmental transcription factor neurogenin3 (Ngn3). In this study we aimed to fully characterize the extent of this reprogramming and intended to improve it. Methods: The extent of the Ngn3-mediated duct-to-endocrine cell reprogramming was measured employing genome wide mRNA profiling. more...
#> 945                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Close to 50 genetic loci have been associated with type 2 diabetes (T2D), but they explain only 15% of the heritability. In an attempt to identify additional T2D genes, we analyzed global gene expression in human islets from 63 donors.
#> 946                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 947                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Expression data was used in Paradigm analysis for exploration of networks affected by copy number and gene expression changes based on mutation spectra of recurrently mutated genes in breast cancer.
#> 948                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   The TCF7L2 transcription factor is linked to a variety of human diseases, including type 2 diabetes and cancer. One mechanism by which TCF7L2 could influence expression of genes involved in diverse diseases is by binding  to distinct regulatory regions in different tissues. To test this hypothesis, we performed ChIP-seq for TCF7L2 in 6 human cell lines. We identified 116,000 non-redundant TCF7L2 binding sites, with only 1,864  sites common to the 6 cell lines. more...
#> 949                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. more...
#> 950                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 951                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in  histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. more...
#> 952                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in  histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. more...
#> 953                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in  histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. more...
#> 954                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        OBJECTIVE: Novel biomarkers of disease progression after type 1 diabetes onset are needed. RESEARCH DESIGN AND METHODS: We profiled peripheral blood (PB) monocyte gene expression in 6 healthy subjects and 16 children with type 1 diabetes diagnosed ~3 months previously, and analyzed clinical features from diagnosis to 1 year. RESULTS: Monocyte expression profiles clustered into two distinct subgroups, representing mild and severe deviation from healthy controls, along the same continuum. more...
#> 955                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Skin and intact fascia were collected from 15 normal control (NC) patients with no hernia history and 18 patients presenting for recurrent incisional hernia (RH) repair. Microarray analysis was performed using whole genome microarray chips on NC (n = 8) and RH (n = 9). These samples were further investigated using a pathway-specific PCR array containing fibrosis-related genes.
#> 956                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Low-grade chronic inflammation plays an important role in the development of obesity and obesity-associated disorders such as insulin resistance, type 2 diabetes, the metabolic syndrome and atherosclerosis. One possible link between obesity and inflammation is the enhanced activation of circulating monocytes making them more prone to infiltration into the adipose and vascular tissues of obese persons. more...
#> 957                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Low-grade chronic inflammation plays an important role in the development of obesity and obesity-associated disorders such as insulin resistance, type 2 diabetes, the metabolic syndrome and atherosclerosis. One possible link between obesity and inflammation is the enhanced activation of circulating monocytes making them more prone to infiltration into the adipose and vascular tissues of obese persons. more...
#> 958                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Objectives –To determine whether inflammation biomarkers can be used as indicators of therapeutic response, an exploratory study was performed to ascertain whether short term improvements in risk parameters will have measureable effects on a pre-defined panel of plaque inflammation biomarkers. Methods and Results – Patients (n=121) with peripheral arterial disease were enrolled into one of three sub-studies based upon the presence of hypercholesterolemia, hypertension, or diabetes. more...
#> 959                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Data on the temporal dynamics of human placental gene expression is scarce. We have completed the first whole-genome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®) from early to mid- gestation (10 samples; gestational weeks 5 to 18) and report 154 genes with considerable change in transcript levels (FDR P<0.1). Functional enrichment analysis revealed >200 GO categories that are statistically over-represented among 105 genes with dynamically increasing transcript levels. more...
#> 960                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Faced by an alarming incidence of metabolic diseases including obesity and type 2 diabetes worldwide, there is an urgent need for effective strategies for preventing and treating these common diseases. The nuclear receptor PPARγ (peroxisome proliferator-activated receptor gamma) plays a crucial role in metabolism. We isolated the amorfrutins from edible parts of the plants Glychyrrhiza foetida and Amorpha fruticosa, and identified these natural products as a new chemical class to treat insulin resistance and diabetes by selectively activating PPARγ. more...
#> 961                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              The prognosis of pancreatic cancer is still very poor, how to detect pancreatic cancer from high-risk group in an early stage is essential for improving its long-time survival. Therefore, the purpose of this study was to explore specific biomarkers that can differentiate pancreatic cancer-associated diabetes from type-2 diabetes for the early detection of pancreatic cancer. In the current study, we used global gene transcription analysis with affymetrix gene chip to identify genes specifically expressed in pancreatic cancer-associated diabetes mellitus from peripheral blood samples in stead of from tissue samples.
#> 962                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   SPARC is  a matricellular glycoprotein that plays critical roles in the pathologies associated with obesity and diabetes, as well as tumorigenesis. The objective of this study was to investigate the role of SPARC in the process of trophoblast invasion which shares many similarities with tumor cells invasion. Our results reveals that hormones, cell adhesion molecules, ECM molecules, growth factors and cytokines all are mediated by SPARC in EVT invasion.
#> 963                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Little is known about the contribution of the epigenome to the pathophysiology of type 2 diabetes (T2D). Here we have used genome-wide DNA methylation profiling to obtain the first comprehensive DNA methylation data set for human T2D pancreatic islets. Therefore, we analyzed the methylation profile of 27,578 CpG sites affiliated to more than 14,000 genes in 16 samples of pancreatic islets, 11 normal and 5 type 2-diabetic. more...
#> 964                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Glucose intolerance and diabetes mellitus are classical parts of endogenous Cushing’s syndrome (CS), and insulin resistance is a feature of cortisol excess. CS patients display characteristics including hyperglycemia, abdominal obesity, reduced high-density lipoprotein cholesterol levels and elevated triglycerides, and arterial hypertension. Hypercortisolism is a well known cause of bone loss, and patients with CS frequently display low bone mass and fragility fractures. more...
#> 965                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Objective:  Insulin regulates amino acid metabolism. We investigated whether glycemia and 43 genetic risk variants for hyperglycemia/type 2 diabetes affect amino acid levels in a large population-based cohort. Subjects and Methods: A total of 9,371 non-diabetic or newly-diagnosed type 2 diabetic Finnish men from the population-based METSIM Study were studied. Proton NMR spectroscopy was used to measure plasma levels of 8 amino acids. more...
#> 966                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    TGF-beta1 is the major cytokine driver of fibrotic scarring observed in diabetic nephropathy and other fibrosis-related diseases. RNA-sequencing offers the potential for more sensitive assessment of the TGF-ß1-driven transcriptome.
#> 967                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Mitochondria have been implicated in insulin resistance and beta cell dysfunction, both of which comprise the core pathophysiology of type 2 diabetes mellitus (T2DM). It has also recently been found that mtDNA haplogroups are distinctively associated with susceptibility to T2DM at least in Koreans and Japanese. To investigate the functional consequences of different mtDNA, we compared gene expression profiles between cybrid clones harboring three different mtDNA haplogroups (D5, F, and N9a). more...
#> 968                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Increased morbidity and mortality associated with post-ischemic heart failure (HF) in diabetic patients underscore the need for a better understanding of the underlying molecular events. Indeed, effective HF therapy in diabetic patients requires a complex strategy encompassing the development of improved diagnostic and prognostic markers and innovative pharmacological approaches. Whole mRNAs expression was measured in the heart of patients with heart failure (HF) with or without concomitant Type 2 diabetes mellitus (T2DM)  and compared it to control non-failing hearts. more...
#> 969                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We have determined the whole genome sequence of an individual at high accuracy and performed an integrated analysis of omics profiles over a 1.5 year period that included healthy and two virally infected states. Omics profiling of transcriptomes, proteomes, cytokines, metabolomes and autoantibodyomes from blood components have revealed extensive, dynamic and broad changes in diverse molecular components and biological pathways that occurred during healthy and disease states. more...
#> 970                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We have determined the whole genome sequence of an individual at high accuracy and performed an integrated analysis of omics profiles over a 1.5 year period that included healthy and two virally infected states. Omics profiling of transcriptomes, proteomes, cytokines, metabolomes and autoantibodyomes from blood components have revealed extensive, dynamic and broad changes in diverse molecular components and biological pathways that occurred during healthy and disease states. more...
#> 971                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We have used RNA-seq to identify transcripts, including splice variants, expressed in human islets of Langerhans under control condition or following exposure to the pro-inflammatory cytokines interleukin-1β (IL-1β) and interferon-γ (IFN-γ). A total of 29,776 transcripts were identified as expressed in human islets. Expression of around 20% of these transcripts was modified by pro-inflammatory cytokines, including apoptosis- and inflammation-related genes. more...
#> 972                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Dietary fat quality may influence skeletal muscle lipid handling and fat accumulation, thereby modulating insulin sensitivity. Objective: To examine acute effects of meals with various fatty acid (FA) compositions on skeletal muscle FA handling and postprandial insulin sensitivity in obese insulin resistant men. Design: In a single-blinded randomized crossover study, 10 insulin resistant men consumed three high-fat mixed-meals (2.6MJ). more...
#> 973                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Autologous nonmyeloablative hematopoietic stem cell transplantation (AHST) was the first therapeutic approaches that can improveβcell function in type 1 diabetic (T1D) patients. This study was designed to investigate the potential mechanisms involved.We applied AHST to nine T1D patients diagnosed within six months and analyzed the acute response in peripheral blood  genomic expression profiling at the six-month follow-up.
#> 974                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Background. Differential gene expression in adipose tissue during diet-induced weight loss followed by a weight stability period is not well characterized. Markers of these processes may provide a deeper understanding of the underlying mechanisms.  Objective. To identify differentially expressed genes in human adipose tissue during weight loss and weight maintenance after weight loss.  Design. RNA from subcutaneous abdominal adipose tissue from nine obese subjects was obtained and analyzed at baseline, after weight reduction on a low calorie diet (LCD), and after a period of group therapy in order to maintain weight stability. more...
#> 975                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 976                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      MicroRNAs expression profiling of human nucleus pulposus cells derived from patients with disc degeneration in comparison with those derived from patients with scoliosis as control.
#> 977                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Stroke is a “brain attack” cutting off vital blood, and consequently the nutrients and oxygen vital to the brain cells that control everything we do. Stroke is a complex disease with unclear pathogenesis resulting from environmental and genetic factors. To better understand IS´s etiology, we performed genomic expression profiling of patients and controls.
#> 978                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Gene expression profiling in arterial tissue from type 2 diabetic patients
#> 979                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Resveratrol is a naturally occurring compound that profoundly affects energy metabolism and mitochondrial function and serves as a calorie restriction mimetic, at least in animal models of obesity. Here we treated 10 healthy, obese men with placebo and 150 mg/day resveratrol in a randomized double-blind cross-over study for 30 days. Resveratrol supplementation significantly reduced sleeping- and resting metabolic rate. more...
#> 980                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Sub-optimal fetal development is associated with an increased risk of developing cardiovascular disease, type 2 diabetes (T2D) and adiposity later in life. However, definitions of intrauterine growth restriction (IUGR) and small for gestational age (SGA) are based on simple statistical approaches that may misclassify infants with a normal developmental profile and vice versa. We used an unbiased global profiling approach to identify gene expression patterns in umbilical cord tissue from 38 infants and identified a set of 466 genes which separated the subjects into 2 distinct groups – one biased towards lower birth weight and one biased towards normal birth weight. more...
#> 981                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Inter-individual DNA methylation variations were frequently hypothesized to alter individual susceptibility to Type 2 Diabetes Mellitus (T2DM). Sequence-influenced methylations were described in T2DM-associated genomic regions, but evidence for direct, sequence-independent association with disease risk is missing. Here we explore disease-contributing DNA methylation through a stepwise study design: first, a pool-based, genome-scale screen among 1,169 case and control individuals revealed an excess of differentially methylated sites in genomic regions that were previously associated with T2DM through genetic studies. more...
#> 982                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 983                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The exchange of the oocyte's genome with the genome of a somatic cell, followed by the derivation of pluripotent stem cells, could enable the generation of specific cell types affected in degenerative human diseases.  Such cells, carrying the patient's genome, might be useful for cell replacement. Here we report that the development of human oocytes activated after genome exchange invariably arrests at the late cleavage stages in association with transcriptional abnormalities. more...
#> 984                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The exchange of the oocyte’s genome with the genome of a somatic cell, followed by the derivation of pluripotent stem cells, could enable the generation of specific cell types affected in degenerative human diseases.  Such cells, carrying the patient’s genome, might be useful for cell replacement. Here we report that the development of human oocytes activated after genome exchange invariably arrests at the late cleavage stages in association with transcriptional abnormalities. more...
#> 985                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Podocytes are cells of the visceral epithelium in the kidneys and form a crucial component of the glomerular filtration barrier, contributing to size selectivity and maintaining a massive filtration surface.
#> 986                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          INTRODUCTION. Fixation with formalin, a widely adopted procedure to preserve tissue samples, leads to extensive degradation of nucleic acids and thereby compromises procedures like microarray-based gene expression profiling. We hypothesized that RNA fragmentation is caused by activation of RNAses during the interval between formalin penetration and tissue fixation. To prevent RNAse activation, a series of tissue samples were kept under-vacuum at 4°C until fixation and then fixed at 4°C, for 24 hours, in formalin followed by 4 hours in ethanol 95%. more...
#> 987                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Background: Changes in DNA methylation patterns with age frequently have been observed and implicated in the normal aging process and its associated increasing risk of disease, particularly cancer. Additionally, the offspring of older parents are at significantly increased risk of cancer, diabetes, and neurodevelopmental disorders. Only a proportion of these increased risks among the children of older parents can be attributed to nondisjunction and chromosomal rearrangements. more...
#> 988                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Tissues from another series of 132 patients with colorectal cancer were collected by laser micro-dissection with the Leica Laser Microdissection System (Leica Microsystems).
#> 989                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Samples were prospectively collected from patients with histologically normal surgical resection margins. 96 tissue samples (histologically normal margins, oral carcinoma and adjacent normal tissues) from 24 patients comprised the training set. Our study design was guided by the hypothesis that the expression of genes present in oral squamous cell carcinoma (OSCC) but not in healthy oral tissues would be indicative of recurrence in advance of histological alteration. more...
#> 990                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
#> 991                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
#> 992                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
#> 993                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 994                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Obesity is a major risk factor for several chronic diseases including diabetes, fatty liver disease and cancer. Despite similar propensities for obesity, Hispanics and African Americans exhibit unique and distinct differences in obesity related outcomes such as greater risk of, obesity-related cancers in AA and non alcoholic fatty liver disease (NAFLD) in Hispanics. This study was aimed to determine whether differences in subcutaneous adipose tissue (SAT) gene expression in obese, Hispanic and AA young adults might explain ethnic differences in obesity-related phenotypes.
#> 995                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Aims: establishment of reference samples to investigate gene expression selective for endocrine or ductal-exocrine cells within the adult human pancreas. To this end, human islet endocrine cells, FACS-enriched in insulin+ cells, (n=3) and human exocrine ductal cells (n=2) are compared on Affymetrix HG133A platform with duplicate hybridizations of a panel of other primary human tissues.
#> 996                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Expansion of beta cells from the limited number of adult human islet donors is an attractive prospect for increasing cell availability for cell therapy of diabetes. However, while evidence supports the replicative capacity of adult beta cells in vivo, attempts at expanding human islet cells in tissue culture resulted in loss of beta-cell phenotype. Using a genetic lineage-tracing approach we have provided evidence for massive proliferation of beta-cell-derived (BCD) cells within these cultures. more...
#> 997                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Exploratory microarray analysis identified significant changes in gene expression in adipose tissue.  These included changes in genes regulating lipid and steroid metabolic processes and electron carrier activity in HIV-infected patients receiving antiretroviral therapy (ART).  Additional genes involved in metabolic processes and mitochondrial function were found to be up-regulated in the adipose tissue of HIV-positive patients compared with HIV-negative controls.
#> 998                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Dysregulation of ceramide synthesis has been associated with metabolic disorders such as atherosclerosis and diabetes mellitus. Using a human hepatoma cell line (Huh7), we investigated the changes in lipid homeostasis and gene expression when the synthesis of ceramide is perturbed by knocking down serine transferases subunits 1, 2 and 3 (SPTLC123) or dihydroceramide desaturase (DEGS1). While the inhibition of serine palmitoyl transferase (SPTLC) affects ceramide production differently at the subspecies level depending upon which SPTLC subunit is silenced; depleting DEGS1 is sufficient to produce a similar outcome as knocking down all SPTLC subunits. more...
#> 999                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                This SuperSeries is composed of the SubSeries listed below.
#> 1000                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             The aim of this study was to characterize expression profiles of visceral and subcutaneous adipose tissue in children. Adipose tissue samples were collected from children having elective surgery (n=71, [54 boys], 6.0 +- 4.3 years). Affymetrix microarrays (n=20) were performed to characterize the functional profile and identify genes of interest in adipose tissue. Visceral adipose tissue had an overrepresentation of Gene Ontology themes related to immune and inflammatory responses and subcutaneous adipose tissue had an overrepresentation of themes related to adipocyte growth and development. more...
#> 1001                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Adipose tissue abundance relies partly on the factors that regulate adipogenesis, i.e. proliferation and differentiation of adipocytes. While the transcriptional program that initiates adipogenesis is well-known, the importance of microRNAs in adipogenesis is less well studied. We thus set out to investigate whether miRNAs would be actively modulated during adipogenesis and obesity. Several models exist to study adipogenesis in vitro, of which the cell line 3T3-L1 is probably the most well known, albeit not the most physiologically appropriate. more...
#> 1002                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            We use ChIP-seq to discover the genome-wide sites of acetylation of lysine 56 of the histone H3 (H3K56), which is a target of three histone modifying enzymes with known roles in diabetes and insulin resistance, in human adipocytes derived from mesenchymal stem cells. Surprisingly, we find that a very large fraction of genes show some level of acetylation on H3K56, but the highest levels of acetylation are associated with genes previously reported to be involved  in type 2 diabetes. more...
#> 1003                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               TGFbeta is the major cytokine driver of fibrosis in the kidney and other tissue. Epithelial-mesenchymal transition has been postulated to contibrute to renal fibrosis in diseases such as diabetic nephropathy. We wished to identify novel genes that were upregulated in human kidney epithelial cells in response to TGFb1.The transcriptional responses for human proximal tubule epithelial cells to 10 ng/ml TGFbeta1 was examined over 24 and 48 hr
#> 1004                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                To study the role of miRNAs in the transition from latent to active TB and to discover candidate biomarkers that may help predict TB progression, we have employed miRNA microarray expression profiling as a discovery platform to probe the transcriptome of peripheral blood mononuclear cells (PBMCs) with active TB, latent TB infection (LTBI), and healthy donors.Patients were recruited at the Shanghai Public Health Clinical Centre (Shanghai, China) from December, 2008 to May, 2009. more...
#> 1005                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Type 1 Diabetes (T1D) is considered to be a Th1 autoimmune disease characterised by an absolute lack of insulin caused by an autoimmune destruction of the insulin producing pancreatic beta cells. Th1 lymphocytes are responsible for the infiltration of the islets of Langerhans and for the cytokine release that supports cytotoxic (Tc) lymphocytes to mediate destruction of the beta cells. The preclinical disease stage is characterized by the generation of the self-reactive lymphocytes that infiltrate the pancreas and selectively destroy the insulin-producing beta cells present in the islets. more...
#> 1006                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        HNF4a is an important liver transcription factor that regulates at least a thousand genes in the liver. Here we used expression profiling in HepG2 cells, a hepatocellular carcinoma cell line, in which HNF4a was knocked down by RNAi to identify some of those target genes. This dataset accompanies the article in Hepatology 2010 Feb;51(2):642-53. Integrated approach for the identification of human hepatocyte nuclear factor 4alpha target genes using protein binding microarrays by Bolotin E, Liao H, Ta TC, Yang C, Hwang-Verslues W, Evans JR, Jiang T, Sladek FM.
#> 1007                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Insulin resistance in skeletal muscle is a key phenotype associated with type 2 diabetes (T2D) and is even present in offspring of diabetic parents. However, molecular mediators of insulin resistance remain unclear. We find that the top-ranking gene set in expression analysis of muscle from humans with T2D and normoglycemic insulin resistant subjects with parental family history (FH+) of T2D is increased expression of actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator MKL1. more...
#> 1008                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Insulin (INS) synthesis and secretion from pancreatic β cells are tightly regulated;  their deregulation causes diabetes. Here we map INS-associated loci in human  pancreatic islets by 4C and 3C techniques and show that the INS gene physically  interacts with the SYT8 gene, located over 300 kb away. This interaction is  elevated by glucose and accompanied by increases in SYT8 expression.  Inactivation of the INS promoter by promoter-targeting siRNA reduces SYT8  gene expression. more...
#> 1009                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has a large number of biological effects, including skin, cardiovascular, neurologic disease, diabetes, infertility and cancer. We analysed the in vitro TCDD effects on human CD34+ cells and tested the gene expression modulation by means of microarray analyses before and after TCDD exposure. We identified 253 differentially modulated probe sets, identifying 217 well-characterized genes. more...
#> 1010                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       The goal of this study was to investigate the effects of the cardioprotective nucleoside adenosine on gene expression in early and late endothelial progenitor cells. Adenosine mod
#> 1011                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               To investigate the effects of bariatric surgery on gene expression profile changes in whole blood in obese subjects with type 2 diabetes in a pilot study setting.  Whole blood from eleven obese subjects with type 2 diabetes was collected in PAXgene tubes prior to and 6-12 months after bariatric surgery. Total RNA was isolated, amplified, labeled and hybridized to Illumina gene expression microarrays. more...
#> 1012                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Mutations in growth signaling pathways extend life span, as well as protect against age-dependent DNA damage in yeast and decrease insulin resistance and cancer in mice. To test their effect in humans, we monitored for 22 years Ecuadorian individuals who carry mutations in the growth hormone receptor (GHR) gene that lead to severe GHR and IGF-1 (insulin-like growth factor-1) deficiencies. We combined this information with surveys to identify the cause and age of death for individuals in this community who died before this period. more...
#> 1013                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Genomic expression profiles of blood and placenta reveal significant immune-related pathways and categories in Chinese women with Gestational Diabetes Gestational diabetes mellitus (GDM) is a complex metabolic disease which occurs in pregnancy with high prevalence, and its pathogenesis remains elusive. Thus far, there has been no comprehensive gene expression profiling in Chinese women with GDM. In this study, we attempt to define the genes and/or pathways that are involved in GDM with Chinese ethnicity, by the Illumina microarray technique. more...
#> 1014                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               This SuperSeries is composed of the SubSeries listed below.
#> 1015                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Dysregulation in expression of microRNAs (miRNAs) in various tissues has been linked to a wide spectrum of diseases, including Type 2 Diabetes mellitus (T2D). In this study, we compared the expression profiles of miRNAs in blood samples from Impaired Fasting Glucose (IFG) and T2D male patients with tissues from T2D rat models. Healthy adult males with no past history of T2D (n=158) and with desirable cholesterol and blood pressure profiles were enrolled in this study. more...
#> 1016                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               DNA methylation patterns were analyzed in blood samples from humans unexposed or exposed to arsenic Using a state-of-the-art technique to map the methylomes of our study subjects, we identified a large interactome of hypermethylated genes that are enriched for their involvement in arsenic-associated diseases, such as cancer, heart disease, and diabetes. Notably, we have uncovered an arsenic-induced “suppressorome” - a complex of 17 known and putative tumor suppressors silenced in human cancers. more...
#> 1017                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              There is growing evidence that genomic DNA sequence changes occur in individual somatic cells during the lifetime of an individual and accumulation of these changes may influence aging and disease. In light of this, and contradicting reports regarding discordant copy number profiles between MZ twins(BARANZINI et al. 2010; BRUDER et al. 2008), we set out to identify de novo somatic copy number mutations in DNA from blood for MZ twin pairs of Mexican American descent who were participants of the San Antonio Family Heart Study (SAFHS) or San Antonio Family Diabetes/Gallbladder study (SAFDGS). more...
#> 1018                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     We performed microarray analysis to evaluate differences in the transcriptome of type 2 diabetic human islets compared to non-diabetic islet samples.
#> 1019                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Custom array designed to tile Linkage Disequilibrium Blocks of T2D GWAS SNPs, monogenic candidates for T2D and Obesity, and all plausible imprinted loci from human and mouse data.
#> 1020                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  There are an estimated 21million diabetics in the United States and 150 million diabetics worldwide.  The World Health Organization anticipates that these numbers will double in the next 20 years. Metabolic syndrome is a well recognized set of symptoms that increases a patient’s risk of developing diabetes.  Insulin resistance is a factor in both metabolic syndrome and Type 2 diabetes. It is characterized by decreased insulin stimulated glucose uptake in peripheral tissues, decreased adiponectin levels, increased adipocyte  FFA and cytokine production, and increased insulin and hepatic glucose output. more...
#> 1021                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Skeletal muscle mitochondrial dysfunction is secondary to T2DM and can be improved by long-term regular exercise training  Mitochondrial dysfunction has long been implicated to play a causative role in development of type 2 diabetes (T2DM). However, a growing number of recent studies provide data that mitochondrial dysfunction is a consequence of T2DM development. The aim of our study is to clarify in further detail the causal role of mitochondrial dysfunction in T2DM by a comprehensive ex vivo analysis of mitochondrial function combined with global gene expression analysis in muscle of pre-diabetic newly diagnosed untreated T2DM subjects and long-standing insulin treated T2DM subjects compared with age- and BMI-matched controls. more...
#> 1022                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          The orphan nuclear receptor TR4 (human testicular receptor 4 or NR2C2) plays a pivotal role in a variety of biological and metabolic processes. With no known ligand and few known target genes, the mode of TR4 function was unclear. We report the first genome-wide identification and characterization of TR4 in vivo binding. Using chromatin immunoprecipitation followed by high throughput sequencing (ChIP-seq), we identified TR4 binding sites in 4 different human cell types and found that the majority of target genes were shared among different cells. more...
#> 1023                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Genome scale characterization of chromatin modification, RNA expression, and cytosine methylation in a diverse panel of primary human cells and tissues, stem cells, and iPS cells derived from deidentified human subjects  **************** For data usage terms and conditions, please refer to: http://www.drugabuse.gov/funding/funding-opportunities/nih-common-fund/epigenomics-data-access-policies ****************
#> 1024                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Identifying cis-regulatory elements is important to understand how human pancreatic islets modulate gene expression in physiologic or pathophysiologic (e.g., diabetic) conditions. We conducted genome-wide analysis of DNase I hypersensitive sites, histone H3 lysine methylation marks (K4me1, K4me3, K79me2), and CCCTC factor (CTCF) binding in human islets. This identified ~18,000 putative promoters (several hundred novel and islet-active). more...
#> 1025                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Congenital hypothyroidism from thyroid dysgenesis (CHTD) is a sporadic disease characterized by defects in the differentiation, migration or growth of thyroid tissue. Of these defects, incomplete migration resulting in ectopic thyroid tissue is the most common (up to 80%). We obtained flashfrozen samples of ectopic thyroid tissue removed from 3 girls aged 8, 10 and 15 yr, because it caused local symptoms. more...
#> 1026                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         Type 1 diabetes is an autoimmune destruction of pancreatic islet beta cell disease, and it is important to find new alternative source of the islet beta cells to replace the damaged cells. Human embryonic stem (hES) cells possess unlimited self-renewal and pluripotency and thus have the potential to provide an unlimited supply of different cell types for tissue replacement. The hES-T3 cells with normal female karyotype were first differentiated into embryoid bodies and then induced to generate the pancreatic islet-like cell clusters, which expressed pancreatic islet cell-specific markers of insulin, glucagon and somatostatin. more...
#> 1027                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Diabetic neuropathy (DN) is a common complication of diabetes.  While multiple pathways are implicated in the pathophysiology of DN, there are no specific treatments for DN and currently it is not possible to predict DN onset or progression. To examine gene expression signatures related to DN, microarray experiments were performed on a subset of human sural nerves collected during a 52-week clinical trial of acetyl-L-carnitine. more...
#> 1028                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Rationale: Physical inactivity is a risk factor for insulin resistance. We examined the effect of nine days of bed rest on basal and insulin stimulated expression of genes potentially involved in insulin action by applying hypothesis-generating microarray in parallel with candidate gene real-time PCR approaches in 20 healthy, young men. Furthermore, we investigated whether bed rest affected DNA methylation in the promoter region of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) gene. more...
#> 1029                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Inflammation is common to many disorders and responsible for tissue and organ damage. However, the associated peripheral cytokine milieu is frequently dilute and difficult to measure, necessitating development of more sensitive and informative biomarkers for mechanistic studies, earlier diagnosis, and monitoring therapeutic interventions. Previously, we have shown that sera from type 1 diabetes (T1D) patients induces a unique disease-specific pro-inflammatory transcriptional profile in fresh peripheral blood mononuclear cells (PBMCs) compared to sera of healthy controls. more...
#> 1030                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Genome-wide DNA methylation was studied to identify regions with extreme inter-individual variability, half of which show stability within-person, and some of which show covariation with body mass index consistently and are located in or near genes previously implicated in regulating body weight or diabetes.
#> 1031                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Gene expression in peripheral blood is shown sufficient to differentiate patients with metabolic disorders from control. The signatures of metabolic syndrome, coronary artery disease and type 2 diabetes also have significant overlap.
#> 1032                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            (original Title) Phenothiazine Neuroleptics Signal To The Human Insulin Promoter As Revealed By A Novel Human b-Cell Line Based High-Throughput Screen.  To address the current deficiency in human beta-cell models, we have developed a cell line from human islets in which the expression of insulin and other beta-cell restricted genes are modulated by an inducible form of the bHLH transcription factor E47. more...
#> 1033                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Lung squamous cell carcinoma gene expression (LSCC) is highly variable.  This study discovered and validated LSCC gene expression subtypes.
#> 1034                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               Gene expression changes in Peripheral Blood Mononuclear cells (PBMC) induced by physical activity was investigated in  sedentary middle-aged men (mean age 52.6 years and BMI 29.1) who undertook a 24-week physical activity programme with blood sampling in the pre-exercise period ,  at the end of 24-weeks prescribed physical activity , and following a two-week detraining period.
#> 1035                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                A number of chronic, age-related diseases are associated with elevated markers of inflammation such as interleukin-6 (IL-6). In this study, we investigated the hypothesis that sedentary individuals with disparate basal serum IL-6 respond differentially to a structured physical activity programme. Gene expression changes in Peripheral Blood Mononuclear cells (PBMC) induced by physical activity was investigated in  sedentary, middle-aged men (mean age 52.6 years and BMI 29.1), with relatively high or low basal serum IL-6 levels (mean of 2.13 and 0.59pg/ml respectively), who undertook a 24-week physical activity programme with blood sampling in the pre-exercise period and at the end of 24-weeks prescribed physical activity.
#> 1036                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secreted proteins, termed hepatokines. To identify hepatic secretory proteins involved in insulin resistance, we performed liver biopsies in humans with or without type 2 diabetes and conducted a comprehensive analysis of gene expression profiles.
#> 1037                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Glomerular diseases account for the majority of cases with chronic renal failure. Several genes have been identified with key relevance for glomerular function. Quite a few of these genes show a specific or preferential mRNA expression in the renal glomerulus. To identify additional candidate genes involved in glomerular function in humans we generated a human renal glomerulus-specific transcript dataset (GTD) by comparing gene expression profiles from human glomeruli and tubulointerstitium obtained from six transplant living donors using Affymetrix HG-U133A arrays. more...
#> 1038                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Insulin is a potent pleiotropic hormone that affects processes such as cellular growth, differentiation, apoptosis, ion flux, energy expenditure, and carbohydrate, lipid, and protein metabolism. We used microarrays to detail the global programme of gene expression underlying the influence of insulin in human skeletal muscle collected from different human individuals including 20 insulin sensitive, 20 insulin resistant and 15 diabetic patients. more...
#> 1039                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Background: In diabetes chronic hyperinsulinemia is responsible for the instability of the atherosclerotic plaque and stimulates cellular proliferation through the activation of the MAP kinases, which in turn regulate cellular proliferation. However, it is not known whether insulin itself could increase the transcription of specific genes for cellular proliferation in the endothelium. Hence, the characterization of transcriptional modifications in endothelium is an important step for a better understanding of the mechanism of insulin action and the relationship between endothelial cell dysfunction and insulin resistance. more...
#> 1040                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Objective: Potential regulators of adipogenesis include microRNAs (miRNAs), small non-coding RNAs that have been recently shown related to adiposity and differentially expressed in fat depots. However, to date no study is available regarding the relationship of miRNAs expression profile, biological pathway and cellular phenotype during human adipogenesis. Thereby, the aim of this study was to investigate whether miRNA expression profile in human adipocytes is related to adipogenesis and to test whether miRNA profile in human subcutaneous adipose tissue is associated to human obesity and co-morbidities. more...
#> 1041                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                In this study, we compared the expression profiles of miRNAs in blood samples from Impaired Fasting Glucose (IFG) and T2D male patients. Healthy adult males with no past history of T2D (n=158) and with desirable cholesterol and blood pressure profiles were enrolled in this study. They were then classified according to fasting glucose levels to have T2D, IFG or as healthy controls (CTL), for comparison of miRNA expression profiles. more...
#> 1042                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Epidemiological studies have revealed concurrence of specific cancers with other disease states such as metabolic syndrome, inflammatory disease and autoimmune disease. Patients with these chronic conditions have a higher incidence of various cancers, more aggressive tumors, and a higher mortality rate. It has been proposed that obesity, inflammation and chronic disease should be correlated with cancer at the molecular level, but common gene signatures or networks have yet to be described. more...
#> 1043                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Type 2 diabetes mellitus (DM) is characterized by insulin resistance and pancreatic beta-cell dysfunction. In high-risk subjects, the earliest detectable abnormality is insulin resistance in skeletal muscle. Impaired insulin-mediated signaling, gene expression, and glycogen synthesis, and accumulation of intramyocellular triglycerides have all been linked with insulin resistance, but no specific defect responsible for insulin resistance and DM has been identified in humans. more...
#> 1044                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) results in the condition called “ER stress” which induces the unfolded protein response (UPR) which is a complex cellular process that includes changes in expression of many genes. Failure to restore homeostasis in the ER is associated with human diseases. To identify the underlying changes in gene expression in response to ER stress, we induced ER stress in human B-cells and then measured gene expression at 10 time-points. more...
#> 1045                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Changes in gene expression in pancreatic beta-cells from type 2 diabetes could provide insights into their abnormal insulin secretion and beta-cell turnover. The laser capture microdissection technique was used to acquire beta-cells from pancreatic tissue sections obtained from type 2 diabetic (T2D) and non-diabetic controls. We found that 4% of analyzed transcripts were differentially expressed between the two groups at the lower confidence bound cutoff of 1.2, and, among the differentially expressed transcripts, 62% were up-regulated and 38% down-regulated in samples of T2D subjects compared to non-diabetic controls. more...
#> 1046                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in whole blood samples from a case-control study of 192 Irish patients with type 1 diabetes mellitus (T1D). Cases had T1D and nephropathy whereas controls had T1D but no evidence of renal disease. emails: christopher.bell@cancer.ucl.ac.uk, a.teschendorff@ucl.ac.uk  Keywords: DNA methylation
#> 1047                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Perturbations of the intrauterine environment can affect fetal development during critical periods of plasticity, and can increase susceptibility to a number of age-related diseases (e.g. type 2 diabetes mellitus; T2DM), manifesting sometimes decades later.  We hypothesized that this biological memory is mediated by permanent alterations of the epigenome in stem cell populations.  Our studies focused specifically on DNA methylation in CD34+ hematopoietic stem and progenitor cells from cord blood, and utilized a two-stage design involving genome-wide discovery followed by quantitative, single-locus validation. more...
#> 1048                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Microarray analysis reveals up-regulation of retinoic acid and hepatocyte growth factor related signaling pathways by pro-insulin C-peptide in kidney proximal tubular cells: Antagonism of the pro-fibrotic effects of TGF-b1 Novel signaling roles for C-peptide have recently been discovered with evidence that it can ameliorate complications of type 1 diabetes.  Here we sought to identify new pathways regulated by C-peptide of relevance to the pathophysiology of diabetic nephropathy. more...
#> 1049                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            We used microarray technology to profile mRNA expression in the skeletal muscle of normal (NGT), glucose intolerant (IGT) and type 2 diabetic (DM) subjects. Groups were classified using WHO criteria and, importantly, the DM group were free of anti hypoglycaemic medication for one week prior to biopsy.
#> 1050                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       We have employed whole microRNA microarray with the potential to distinguish H.pylori infection.Among the 470 human miRNAs represented on the array chip, 228 were undetectable or expressed below the background and so were eliminated, leaving 242 miRNAs for the supervised analysis. When comparing 10 H. pylori-negative and nine H. pylori-positive subjects, 55 miRNAs were deemed significantly different on the basis of microRNA arrays.
#> 1051                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     The NIH Roadmap Epigenomics Mapping Consortium aims to produce a public resource of epigenomic maps for stem cells and primary ex vivo tissues selected to represent the normal counterparts of tissues and organ systems frequently involved in human disease.  Study of chromatin accessibility and expression using exon arrays.   **************** For data usage terms and conditions, please refer to: http://www.drugabuse.gov/funding/funding-opportunities/nih-common-fund/epigenomics-data-access-policies ****************
#> 1052                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Insulin resistance and Type 2 Diabetes Mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. To identify the underlying molecular processes in preadipocytes of T2DM patients that are a characteristic of the development of T2DM, preadipocyte cell cultures were prepared from subcutaneous fat biopsies of T2DM patients and compared with age- and BMI matched control subjects. more...
#> 1053                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Background: Endothelial progenitor cells play an important role in vascular wall repair. Patients with type 1 diabetes have reduced levels of endothelial progenitor cells of which their functional capacity is impaired. Reduced nitric oxide bioavailability and increased oxidative stress play a role in endothelial progenitor cell dysfunction in these patients. Folic acid, a B-vitamin with anti-oxidant properties, may be able to improve endothelial progenitor cell function. more...
#> 1054                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Despite years of effort, exact pathogenesis of non-alcoholic fatty liver disease (NAFLD) remains obscure. To gain an insight into the regulatory roles of microRNAs (miRNAs) in aberrant energy metabolic status and pathogenesis of NAFLD, we analyzed the expression of miRNAs in livers of ob/ob mice, streptozotocin (STZ)-induced type 1 diabetic mice and normal C57BL/6 mice by miRNA microarray. Compared to normal C57BL/6 mice, ob/ob mice showed up-regulation of 8 miRNAs and down-regulation of 4 miRNAs in fatty livers. more...
#> 1055                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Several reports have focused on the identification of biological elements involved in the development of abnormal systemic biochemical alterations in chronic kidney disease, but this abundant literature results most of the time fragmented. To better define the cellular machinery associated to this condition, we employed an innovative high-throughput approach based on a whole transcriptomic analysis and classical biomolecular methodologies. more...
#> 1056                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Individuals of African descent in the United States suffer disproportionately from diseases with a metabolic etiology (obesity, metabolic syndrome, and diabetes), and from the pathological consequences of these disorders (hypertension and cardiovascular disease).  Using a combination of genetic/genomic and bioinformatics approaches, we identified a large number of genes that were both differentially expressed between American subjects self-identified to be of either African or European ancestry and that also contained single nucleotide polymorphisms that distinguish distantly related ancestral populations. more...
#> 1057                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Alcohol affects gene expression in several brain regions. The amygdala is a key structure in the brain’s emotional system and in recent years the crucial importance of the amygdala in drug-seeking and relapse has been increasingly recognized. In this study gene expression screening was used to identify genes involved in alcoholism in the human basolateral amygdala. The results show that alcoholism affects a broad range of genes and many systems including genes involved in synaptic transmission, neurotransmitter transport, structural plasticity, metabolism, energy production, transcription and RNA processing and the circadian cycle. more...
#> 1058                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               The goal of this study was to compare the gene expression profiles of chronically inflamed human peri-implant and chronically inflamed human periodontal tissues in order to elucidate potential changes at the molecular level. Cells out of the pocket depth of the inflamed peri-implant and periodontal ligament as well as from the middle third of healthy periodontal ligament were applied. Genome-wide gene expression was compared with the help of microarray analysis, and the data were validated by real-time RT-PCR. more...
#> 1059                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Diabetes is associated with a more aggressive form of atherosclerosis. Thrombospondin-1 (TSP-1), an extracellular matrix protein, is an acute phase reactant that induces vascular smooth muscle (VSMC) migration and proliferation in areas of vascular injury, and is also upregulated in VSMCs exposed to hyperglycemia. We hypothesized that hyperglycemia amplifies the expression of genes induced by TSP-1 in VSMCs. more...
#> 1060                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           The human embryonic stem cells (hESCs) are a unique model system for investigating the mechanisms of human development due to their ability to replicate indefinitely while retaining the capacity to differentiate into a host of functionally distinct cell types. In addition, these cells could be potentially used as therapeutic agents in regenerative medicine. Differentiation of hESCs involves selective activation or silencing of genes, a process controlled in part by the epigenetic state of the cell. more...
#> 1061                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          Pancreatic islet transplantation as a cure for type 1 diabetes (T1D) cannot be scaled up due to a scarcity of human pancreas donors. In vitro expansion of beta cells from mature human pancreatic islets provides an alternative source of insulin-producing cells. The exact nature of the expanded cells produced by diverse expansion protocols, and their potential for differentiation into functional beta cells, remain elusive. more...
#> 1062                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               This SuperSeries is composed of the SubSeries listed below.
#> 1063                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    MicroRNAs (miRNAs) are non-coding RNA molecules involved in post-transcriptional control of gene expression of a wide number of genes, including those involved in glucose homeostasis. Type 2 diabetes (T2D) is characterized by hyperglycaemia and defects in insulin secretion and action at target tissues. Using a miRNA microarray platform, we sought to establish differences in miRNA expression in two insulin-target tissues (liver and adipose tissue) from seven-month-old spontaneously diabetic (Goto-Kakizaki [GK]) and non-diabetic (Brown-Norway [BN]) rats. more...
#> 1064                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Non-small-cell lung cancer (NSCLC), which is comprised mainly of adenocarcinoma and squamous cell carcinoma (SCC), is the cause of 80% of all lung cancer deaths in the US. NSCLC is also associated with a high rate of relapse following clinical treatment and therefore requires robust prognostic markers to better manage therapy options. The aim of this study was to identify miRNA expression profiles in squamous cell carcinoma (SSC) of the lung that would better predict prognosis.
#> 1065                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Melioidosis is a severe infectious disease caused by Burkholderia pseudomallei, a gram-negative bacillus classified by the NIAID as a category B priority agent. Septicemia is the most common presentation of the disease with 40% mortality rate even with appropriate treatments. Faster diagnostic procedures are required to improve therapeutic response and survival rates. We have used microarray technology to generate genome-wide transcriptional profiles (>48,000 transcripts) of whole blood obtained from patients with septicemic melioidosis (n=32), patients with sepsis caused by other pathogens (n=31), and uninfected controls (n=29). more...
#> 1066                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Obesity is becoming increasingly widespread in developed countries, and is often associated with heart diseases and diabetes.  Elevated levels of plasma free fatty acids are a biochemical hallmark of obesity.  Unlike plants and bacteria, mammals cannot utilize fatty acids to generate glucose because of the lack of glyoxylate shunt enzymes. Instead, fatty acids are used for energy storage, and their utilization is regulated at multiple levels ranging from hormonal to metabolic ensuring that glucose is preferentially oxidized before fatty acids. more...
#> 1067                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Genes showing differential expression in visceral adipose tissue obtained from Asia Indian obese women suffering from type-2 diabetes mellitus as compared to age and BMI matched normal glucose tolerant women were identified by genome wide transcriptomic profiling in 5 diabetic and 5 control subjects respectively.
#> 1068                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      Hepatic lipid accumulation is an important complication of obesity linked to risk for type 2 diabetes. To identify novel transcriptional changes in human liver which could contribute to hepatic lipid accumulation and associated insulin resistance and type 2 diabetes (DM2), we evaluated gene expression and gene set enrichment in surgical liver biopsies from 13 obese (9 with DM2) and 5 control subjects, obtained in the fasting state at the time of elective abdominal surgery for obesity or cholecystectomy. more...
#> 1069                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Gene expression in human umbilical vein endothelial cells (HUVEC) was investigated by microarray analysis after 4 h infection with S. aureus isolated from healthy nasal carriers (n=5) and from blood (n=5) of septic patients. All bacterial isolates were spa-typed and characterized with a DNA microarray to determine the presence of virulence genes.  Keywords: infection studies, pathogen, S. aureus
#> 1070                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                The frequent use of rodent hepatic in vitro systems in pharmacological and toxicological investigations challenges extrapolation of in vitro results to the situation in vivo and interspecies extrapolation from rodents to humans. The toxicogenomics approach may aid in evaluating relevance of these model systems for human risk assessment by direct comparison of toxicant-induced gene expression profiles and infers mechanisms between several systems. more...
#> 1071                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         MicroRNAs (miRNAs), which are a newly identified class of small single-stranded non-coding RNAs, regulate their target genes via post-transcriptional pathway. It has been proved that miRNAs play important roles in many biological processes. To better understand miRNA function with type 2 diabetes, we have used an oligonucleotide microarray to monitor miRNA expression profiles of GK and Wistar rats’ muscle. more...
#> 1072                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                We examined gene expression signatures in healthy and diseased gingival tissues in 90 patients. Analysis of the gingival tissue transcriptome in states of periodontal health and disease may reveal novel insights of the pathobiology of periodontitis. Keywords: gingival tissue disease state analysis
#> 1073                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             In the present study, we performed transcriptome expression analyses in three independent peripheral blood-derived monocyte subpopulations from patients with chronic coronary occlusions (CTO) and tested for arteriogenesis. Whole-genome mRNA expression analyses were performed on these three monocyte subpopulations, namely: (1) unstimulated-, (2) 3 hours LPS-stimulated-, (3) monocyte-derived macrophages. more...
#> 1074                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             Insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes. Studies have shown that thiazolidinediones (TZD) improve metabolic disturbances in PCOS patients. We hypothesized that the effect of TZD in PCOS is in part mediated by changes in the transcriptional profile of muscle favoring insulin sensitivity.  Using Affymetrix microarrays, we examined the effect of pioglitazone (30 mg/day for 16 weeks) on gene expression in skeletal muscle of 10 obese women with PCOS metabolically characterized by a euglycemic-hyperinsulinemic clamp. more...
#> 1075                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Microarray-based studies of skeletal muscle from patients with type 2 diabetes and high-risk individuals have demonstrated that insulin resistance and reduced mitochondrial biogenesis co-exist early in the pathogenesis of type 2 diabetes independent of hyperglycaemia and obesity. It is unknown whether reduced mitochondrial biogenesis or other transcriptional alterations co-exist with impaired insulin-responsiveness in primary human muscle cells from patients with type 2 diabetes. more...
#> 1076                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                We designed a strategy for microarray analysis that is based on the identification of transcriptional modules formed by genes coordinately expressed in multiple disease data sets. Mapping changes in gene expression at the module level generated disease-specific transcriptional fingerprints that provide a stable framework for the visualization and functional interpretation of microarray data.
#> 1077                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 The analysis of patient blood transcriptional profiles offers a means to investigate the immunological mechanisms relevant to human diseases on a genome-wide scale. In addition, such studies provide a basis for the discovery of clinically relevant biomarker signatures. We designed a strategy for microarray analysis that is based on the identification of transcriptional modules formed by genes coordinately expressed in multiple disease data sets. more...
#> 1078                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   Abstract  The metabolic syndrome is a cluster of conditions that predispose for diabetes and cardiovascular disease. Nine metabolic syndrome patients were recruited to 48 workouts of interval training. At the end of the study, all patients significantly reduced their risk of cardiovascular disease (in terms of VO2max, blood pressure and plasma lipid). Exercise-induced transcriptional changes may provide new mechanistically insights in the area of improved health by exercise. more...
#> 1079                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             To uncover the genetic determinants affecting expression in a metabolically active tissue relevant to the study of obesity, diabetes, atherosclerosis, and other common human diseases, we profiled 427 human liver samples on a comprehensive gene expression microarray targeting greater than 40,000 transcripts and genotyped DNA from each of these samples at greater than 1,000,000 SNPs.  The relatively large sample size  of this study and the large number of SNPs genotyped provided the means to assess the relationship between genetic variants and gene expression and it provided this look for the first time in a non-blood derived, metabolically active tissue. more...
#> 1080                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    We used a whole genome approach to identify major functional gene categories (including xenobiotic transporters and metabolizing enzymes) whose expression depends on gestational age. STUDY DESIGN: We compared gene expression profiles of 1st (45-59 days) and 2nd trimester (109-115 days), and C-section term placentae. RESULTS: In 1st trimester placentae, genes related to cell cycle, DNA, aminoacids and carbohydrate metabolism were significantly overrepresented, while genes related to signal transduction were downregulated. more...
#> 1081                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          To determine whether optic nerve head astrocytes, a key cellular component of glaucomatous neuropathy, exhibit differential gene expression in primary culture of astrocytes from normal African American donors, compared to astrocytes from normal Caucasian American donors. All donors have no histories of eye disease, diabetes, or chronic CNS disease. Keywords: Gene expression profile
#> 1082                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           Periodontal infections have been associated with systemic inflammation and risk for atherosclerosis and vascular disease. We investigated the effects of comprehensive periodontal therapy on gene expression of peripheral blood monocytes. Approximately 1/3 of the patients showed substantial changes in expression in genes relevant to innate immunity, apoptosis, and cell signaling. We concluded that periodontal therapy may alter monocytic gene expression in a manner consistent with a systemic anti-inflammatory effect. more...
#> 1083                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Although increased vascular stiffness is more prominent in aging males than females, and males are more prone to vascular disease with aging, no study has investigated the genes potentially responsible for gender differences in vascular aging.  We tested the hypothesis that the transcriptional adaptation to aging differs in males and females using a monkey model, which is not only physiologically and phylogenetically closer to humans than the more commonly studied rodent models, but also is not afflicted with the most common forms of vascular disease that accompany the aging process in humans, e.g., atherosclerosis, hypertension, and diabetes. more...
#> 1084                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Recently, abnormalities in mitochondrial oxidative phosphorylation (OXPHOS) have been implicated in the pathogenesis of skeletal muscle insulin resistance in type 2 diabetes. In the present study, we hypothesized that decreased expression of OXPHOS genes could be of similar importance for insulin resistance in the polycystic ovary syndrome (PCOS). Using the HG-U133 Plus 2.0 expression array from Affymetrix, we analyzed gene expression in skeletal muscle from obese women with PCOS (n=16) and age- and body mass index-matched control women (n=13) metabolically characterized by euglycemic-hyperinsulinemic clamp and indirect calorimetry. more...
#> 1085                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         This SuperSeries is related to a manuscript published in Genome Biology. The abstract of this manuscript follows here: Background Investigations performed in mice and humans have acknowledged obesity as a low-grade inflammatory disease. Several molecular mechanisms have been convincingly involved in activating inflammatory processes and altering cell composition in white adipose tissue (WAT); however, the overall importance of these alterations, and their long-term impact on the metabolic functions of the WAT and on its morphology, remain unclear. more...
#> 1086                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                Extracellular matrix (ECM) remodelling occurs during tissue repair and inflammation-related pathologies with deposition of specific proteins.  White adipose tissue (WAT) was recently shown to be the site of substantial interstitial fibrosis. ECM components, such as fibronectin, and their receptors integrins control cell migration, proliferation and differentiation. Adipocyte differentiation which is under the control of a specific transcriptional network is associated with decrease of fibronectin-rich matrix. more...
#> 1087                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            This study was undertaken to test the hypothesis that short term exposure (4 hours) to physiologic hyperinsulinemia in normal, healthy subjects without a family history of diabetes would induce a low grade inflammatory response, independently of glycemic status. We performed euglycemic hyperinsulinemic (80 mU/m2/min) clamps in 12 healthy, insulin sensitive subjects with no family history of diabetes followed by biopsies of the vastus lateralis muscle taken basally and after 30 and 240 minutes of insulin infusion. more...
#> 1088                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Objective: We hypothesized that type 1 diabetes (T1D) is accompanied by changes in gene expression in peripheral blood mononuclear cells (PBMCs) due to dysregulation of adaptive and innate immunity, counterregulatory responses to immune dysregulation, insulin deficiency and hyperglycemia. Research Design and Methods: Microarray analysis was performed on PBMCs from 43 patients with newly diagnosed T1D, 12 patients with newly diagnosed type 2 diabetes (T2D) and 24 healthy controls. more...
#> 1089                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Objectives: While cardiac scar tissue is damaged irreversibly, hibernating myocardium is characterized by reversible contractile dysfunction. Limited data are available in humans regarding the molecular biology of hibernating myocardium. The aim of this study was to identify new molecular mechanisms distinctive for human hibernating myocardium  by gene expression analysis. Results: Of 4,171 transcripts examined, we identified 86 to be differentially expressed. more...
#> 1090                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  Reversible acetylation of histone and nonhistone proteins plays pivotal role in cellular homeostasis. Dysfunction of histone acetyltransferases (HATs) leads to several diseases including cancer, neurodegenaration, asthma, diabetes, AIDS and cardiac hypertrophy. We describe the synthesis and characterization of a set of p300-HAT specific small molecule inhibitors from a natural nonspecific HAT inhibitor, garcinol, which is highly toxic to cells. more...
#> 1091                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  To identify insulin responsive genes in humans, in the first protocol, skeletal muscle biopsies from six non-diabetic subjects were obtained before and after a two-hour of hyperinsulinaemic (infusion rate 40 mU/m2/min) euglycemic clamp. A variable infusion of glucose (180 g/l) enriched with tritiated glucose (100 μCi/500 ml) maintained euglycemia during insulin infusion, with monitoring of plasma glucose concentration every 5 to 10 min during the basal and clamp periods using an automated glucose oxidation method (Glucose Analyzer 2, Beckman Instruments, Fullerton, CA). more...
#> 1092                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Failure of ligamentous support of the genital tract to resist intra-abdominal pressure is a plausible underlying mechanism for the development of pelvic organ prolapse, but the nature of molecular response of pelvic tissue support remains unknown. We hypothesized that the expression of genes coding for proteins involved in maintaining the cellular and extracellular integrity would be altered in cases of pelvic organ prolapse. more...
#> 1093                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. more...
#> 1094                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     Sample tissue: peripheral blood  Samples for gene expression analysis were obtained before and after the event. Keywords: time course, event response
#> 1095                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Müller cells are the principal glial cells in the retina. Alterations in Müller cell behaviour are observed in retinal tissue from patients with proliferative diabetic retinopathy. The purpose of this study was to compare gene and protein expression profile of normal human Müller cells (NHMC) with two spontaneously human Müller cell lines generated from type 1 (HMCL-I) and type 2 (HMCL-II) diabetic donors using Serial Analysis Gene Expression (SAGE). more...
#> 1096                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Sample tissue: peripheral blood Disease: normal subject, patients with type 2 diabetes (diabetic nephropathy +, -) Samples for gene expression analysis were obtained before and after the event. Keywords: equivalent probe, disease response
#> 1097                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   This experiment was designed to study if there are differences in gene expression in the adipose tissue of women affected by polycystic ovary syndrome (PCOS) compared to non-hyperandrogenic women. PCOS is the most common endocrinopathy in women of reproductive age, and is characterized by hyperandrogenism and chronic anovulation. This disease is frequently associated with obesity, insulin resistance, and defects in insulin secretion, predisposing these women to type 2 diabetes, atherosclerosis, and cardiovascular disease. more...
#> 1098                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Insulin action in target tissues involved precise regulation of gene expression. To define the set of insulin-regulated genes in human skeletal muscle, we analyzed the global changes in mRNA levels during a 3-h hyperinsulinemic euglycemic clamp in vastus lateralis muscle of six healthy subjects. Using 29,308 cDNA element microarrays, we found that the mRNA expression of 762 genes, including 353 expressed sequence tags, was significantly modified during insulin infusion. more...
#> 1099                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       Hepatocyte nuclear factor 1beta (HNF1beta, TCF2) is a tissue-specific transcription factor whose mutation in humans leads to renal cysts, genital malformations, pancreas atrophy and maturity onset diabetes of the young (MODY5). Furthermore, HNF1beta overexpression has been observed in clear cell cancer of the ovary. To identify potential HNF1beta target genes whose activity may be deregulated in human patients we established a human embryonic kidney cell line (HEK293) expressing HNF1beta conditionally. more...
#> 1100                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Even though autoimmune diseases are heterogeneous, believed to result from the interaction between genetic and environmental components, patients with these disorders exhibit reproducible patterns of gene expression in their peripheral blood mononuclear cells. A portion of this gene expression profile reflects family resemblance rather than the actual presence of an autoimmune disease.  Here we wanted to identify that portion of this gene expression pattern that is independent of family resemblance and determine if it is a product of disease duration, disease onset, or other factors. more...
#> 1101                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              Summary:   Genetic disorders of muscle cause muscular dystrophy, and are some of the most common inborn errors of metabolism. Muscle also rapidly remodels in response to training and innervation. Muscle weakness and wasting is important in such conditions as aging, critical care medicine, space flight, and diabetes. Finally, muscle can also be used to investigate systemic defects, and the compensatory mechansisms invoked by cells to overcome biochemical and genetic abnormalities. more...
#> 1102                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Expression profile was obtained for GeneChip probe sets among colon cancer specimens with or without the methylation of MLH1 promoter. Keywords: other
#> 1103                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    A physiological state of insulin resistance is required to preferentially direct maternal nutrients toward the feto-placental unit, allowing adequate growth of the fetus. When women develop gestational diabetes mellitus (GDM), insulin resistance is more severe and disrupts the intrauterine milieu, resulting in accelerated fetal development with increased risk of macrosomia. As a natural interface between mother and fetus, the placenta is the obligatory target of such environmental changes. more...
#> 1104                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                 Sample tissue: peripheral blood Disease: diabetes Samples for gene expression analysis were obtained before the meal and 1.5 hours after the event. Event: listening to a Japanese comic story or a monotonous academic lecture without humor. Keywords: equivalent probe
#> 1105                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other
#> 1106                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        Skeletal muscle biopsies from atypical diabetics at presentation and remission. Protein expression determined with antibody arrays Keywords: other
#> 1107                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    Global transcript profiling to identify differentially expressed skeletal muscle genes in insulin resistance, a major risk factor for Type II (non-insulin-dependent) diabetes mellitus.  Compared gene expression profiles of skeletal muscle tissues from 18 insulin-sensitive versus 17 insulin-resistant equally obese, non-diabetic Pima Indians. Keywords: other
#>                                                                                                                                                                                                                                                                                                                                                                                              Organism
#> 1                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 2                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 3                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 4                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 5                                                                                                                                                                                                                                                                                                                                                                          Homo sapiens; Mus musculus
#> 6                                                                                                                                                                                                                                                                                                                                                                          Mus musculus; Homo sapiens
#> 7                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 8                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 9                                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens
#> 10                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 11                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 12                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 13                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 14                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 15                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 16                                                                                                                                                                                                                                                                                                                                                                         Homo sapiens; Mus musculus
#> 17                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 18                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 19                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 20                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 21                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 22                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 23                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 24                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 25                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 26                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 27                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 28                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 29                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 30                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 31                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 32                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 33                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 34                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 35                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 36                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 37                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 38                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 39                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 40                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 41                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 42                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 43                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 44                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 45                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 46                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 47                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 48                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 49                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 50                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 51                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 52                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 53                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 54                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 55                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 56                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 57                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 58                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 59                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 60                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 61                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 62                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 63                                                                                                                                                                                                                                                                                                                                                                       Macaca mulatta; Homo sapiens
#> 64                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 65                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 66                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 67                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 68                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 69                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 70                                                                                                                                                                                                                                                                                                                                                                         Mus musculus; Homo sapiens
#> 71                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 72                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 73                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 74                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 75                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 76                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 77                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 78                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 79                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 80                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 81                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 82                                                                                                                                                                                                                                                                                                                                                                         Homo sapiens; Mus musculus
#> 83                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 84                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 85                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 86                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 87                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 88                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 89                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 90                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 91                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 92                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 93                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 94                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 95                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 96                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 97                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 98                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 99                                                                                                                                                                                                                                                                                                                                                                                       Homo sapiens
#> 100                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 101                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 102                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 103                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 104                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 105                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 106                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 107                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 108                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 109                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 110                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 111                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 112                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 113                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 114                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 115                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 116                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 117                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 118                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 119                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 120                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 121                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 122                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 123                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 124                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 125                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 126                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 127                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 128                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 129                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 130                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 131                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 132                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 133                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 134                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 135                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 136                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 137                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 138                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 139                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 140                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 141                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 142                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 143                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 144                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 145                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 146                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 147                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 148                                                                                                                                                                                                                                                                                                                                                     Mus musculus; Rattus norvegicus; Homo sapiens
#> 149                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 150                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 151                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 152                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 153                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 154                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 155                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 156                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 157                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 158                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 159                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 160                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 161                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 162                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 163                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 164                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 165                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 166                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 167                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 168                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 169                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 170                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 171                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 172                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 173                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 174                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 175                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 176                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 177                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 178                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 179                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 180                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 181                                                                                                                                                                                                                                                                                                                                                                   Homo sapiens; Rattus norvegicus
#> 182                                                                                                                                                                                                                                                                                                                                                                   Rattus norvegicus; Homo sapiens
#> 183                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 184                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 185                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 186                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 187                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 188                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 189                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 190                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 191                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 192                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 193                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 194                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 195                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 196                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 197                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 198                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 199                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 200                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 201                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 202                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 203                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 204                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 205                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 206                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 207                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 208                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 209                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 210                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 211                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 212                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 213                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 214                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 215                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 216                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 217                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 218                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 219                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 220                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 221                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 222                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 223                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 224                                                                                                                                                                                                                                                                                                                                                                 Homo sapiens; synthetic construct
#> 225                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 226                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 227                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 228                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 229                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 230                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 231                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 232                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 233                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 234                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 235                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 236                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 237                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 238                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 239                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 240                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 241                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 242                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 243                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 244                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 245                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 246                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 247                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 248                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 249                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 250                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 251                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 252                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 253                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 254                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 255                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 256                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 257                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 258                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 259                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 260                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 261                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 262                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 263                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 264                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 265                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 266                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 267                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 268                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 269                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 270                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 271                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 272                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 273                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 274                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 275                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 276                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 277                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 278                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 279                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 280                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 281                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 282                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 283                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 284                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 285                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 286                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 287                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 288                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 289                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 290                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 291                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 292                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 293                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 294                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 295                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 296                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 297                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 298                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 299                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 300                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 301                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 302                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 303                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 304                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 305                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 306                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 307                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 308                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 309                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 310                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 311                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 312                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 313                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 314                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 315                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 316                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 317                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 318                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 319                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 320                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 321                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 322                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 323                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 324                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 325                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 326                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 327                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 328                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 329                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 330                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 331                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 332                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 333                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 334                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 335                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 336                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 337                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 338                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 339                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 340                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 341                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 342                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 343                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 344                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 345                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 346                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 347                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 348                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 349                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 350                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 351                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 352                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 353                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 354                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 355                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 356                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 357                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 358                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 359                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 360                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 361                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 362                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 363                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 364                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 365                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 366                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 367                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 368                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 369                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 370                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 371                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 372                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 373                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 374                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 375                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 376                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 377                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 378                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 379                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 380                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 381                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 382                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 383                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 384                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 385                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 386                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 387                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 388                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 389                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 390                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 391                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 392                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 393                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 394                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 395                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 396                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 397                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 398                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 399                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 400                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 401                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 402                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 403                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 404                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 405                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 406                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 407                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 408                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 409                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 410                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 411                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 412                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 413                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 414                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 415                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 416                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 417                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 418                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 419                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 420                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 421                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 422                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 423                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 424                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 425                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 426                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 427                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 428                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 429                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 430                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 431                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 432                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 433                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 434                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 435                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 436                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 437                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 438                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 439                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 440                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 441                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 442                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 443                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 444                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 445                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 446                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 447                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 448                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 449                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 450                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 451                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 452                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 453                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 454                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 455                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 456                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 457                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 458                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 459                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 460                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 461                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 462                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 463                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 464                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 465                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 466                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 467                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 468                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 469                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 470                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 471                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 472                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 473                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 474                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 475                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 476                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 477                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 478                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 479                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 480                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 481                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 482                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 483                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 484                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 485                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 486                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 487                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 488                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 489                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 490                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 491                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 492                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 493                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 494                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 495                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 496                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 497                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 498                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 499                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 500                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 501                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 502                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 503                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 504                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 505                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 506                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 507                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 508                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 509                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 510                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 511                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 512                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 513                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 514                                                                                                                                                                                                                                                                                                                                                                     Papio hamadryas; Homo sapiens
#> 515                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 516                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 517                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 518                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 519                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 520                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 521                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 522                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 523                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 524                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 525                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 526                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 527                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 528                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 529                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 530                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 531                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 532                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 533                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 534                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 535                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 536                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 537                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 538                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 539                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 540                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 541                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 542                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 543                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 544                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 545                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 546                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 547                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 548                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 549                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 550                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 551                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 552                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 553                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 554                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 555                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 556                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 557                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 558                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 559                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 560                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 561                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 562                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 563                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 564                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 565                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 566                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 567                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 568                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 569                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 570                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 571                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 572                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 573                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 574                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 575                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 576                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 577                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 578                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 579                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 580                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 581                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 582                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 583                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 584                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 585                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 586                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 587                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 588                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 589                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 590                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 591                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 592                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 593                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 594                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 595                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 596                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 597                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 598                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 599                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 600                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 601                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 602                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 603                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 604                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 605                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 606                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 607                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 608                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 609                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 610                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 611                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 612                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 613                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 614                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 615                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 616                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 617                                Homo sapiens; Macacine alphaherpesvirus 1; Merkel cell polyomavirus; Human gammaherpesvirus 4; JC polyomavirus; Human immunodeficiency virus 1; Human gammaherpesvirus 8; Human alphaherpesvirus 2; Saimiriine gammaherpesvirus 2; Betapolyomavirus hominis; Human alphaherpesvirus 1; Human betaherpesvirus 5; Human betaherpesvirus 6B; Betapolyomavirus macacae
#> 618                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 619                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 620                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 621                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 622                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 623                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 624                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 625                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 626                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 627                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 628                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 629                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 630                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 631                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 632                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 633                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 634                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 635                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 636                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 637                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 638                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 639                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 640                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 641                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 642                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 643                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 644                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 645                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 646                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 647                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 648                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 649                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 650                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 651                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 652                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 653                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 654                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 655                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 656                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 657                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 658                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 659                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 660                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 661                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 662                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 663                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 664                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 665                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 666                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 667                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 668                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 669                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 670                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 671                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 672                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 673                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 674                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 675                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 676                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 677                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 678                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 679                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 680                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 681                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 682                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 683                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 684                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 685                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 686                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 687                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 688                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 689                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 690                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 691                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 692                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 693                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 694                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 695                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 696                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 697                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 698                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 699                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 700                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 701                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 702                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 703                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 704                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 705                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 706                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 707                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 708                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 709                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 710                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 711                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 712                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 713                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 714                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 715                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 716                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 717                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 718                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 719                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 720                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 721                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 722                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 723                                                                                                                                                                                                                                                                                                                                                                         Homo sapiens; Danio rerio
#> 724                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 725                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 726                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 727                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 728                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 729                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 730                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 731                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 732                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 733                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 734                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 735                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 736                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 737                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 738                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 739                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 740                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 741                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 742                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 743                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 744                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 745                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 746                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 747                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 748                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 749                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 750                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 751                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 752                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 753                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 754                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 755                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 756                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 757                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 758                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 759                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 760                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 761                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 762                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 763                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 764                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 765                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 766                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 767                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 768                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 769                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 770                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 771                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 772                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 773                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 774                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 775                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 776                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 777                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 778                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 779                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 780                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 781                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 782                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 783                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 784                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 785                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 786                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 787                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 788                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 789                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 790                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 791                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 792                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 793                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 794                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 795                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 796                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 797                                                                                                                                                                                                                                                                                                                                                                   Rattus norvegicus; Homo sapiens
#> 798                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 799                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 800                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 801                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 802                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 803                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 804                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 805                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 806                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 807                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 808                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 809                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 810                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 811                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 812                                                                                                                                                                                                                                                                                                                                                                 Homo sapiens; synthetic construct
#> 813                                                                                                                                                                                                                                                                                                                                                                 Homo sapiens; synthetic construct
#> 814                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 815                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 816                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 817  Human gammaherpesvirus 8; Mus musculus cytomegalovirus 2; Betapolyomavirus macacae; Homo sapiens; Human betaherpesvirus 5; Murid gammaherpesvirus 4; Betapolyomavirus hominis; Human alphaherpesvirus 1; Human alphaherpesvirus 2; Human gammaherpesvirus 4; Mus musculus; Rattus norvegicus; Murid betaherpesvirus 1; JC polyomavirus; Human immunodeficiency virus 1; Merkel cell polyomavirus
#> 818                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 819                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 820                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 821                                                                                                                                         JC polyomavirus; Human gammaherpesvirus 8; Betapolyomavirus macacae; Rattus norvegicus; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Human gammaherpesvirus 4; Human immunodeficiency virus 1; Homo sapiens; Betapolyomavirus hominis
#> 822                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 823                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 824                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 825                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 826                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 827                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 828                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 829                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 830                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 831                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 832                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 833                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 834                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 835                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 836                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 837                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 838                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 839                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 840                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 841                                                                                                                                                                                                                                                                                                                                                                 Homo sapiens; synthetic construct
#> 842                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 843                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 844                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 845                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 846                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 847                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 848                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 849                                                                                                                                                                                                                                                                                                                                                                        Homo sapiens; Mus musculus
#> 850                                                                                        Mus musculus; Human alphaherpesvirus 1; Human gammaherpesvirus 4; Rattus norvegicus; Murid betaherpesvirus 1; JC polyomavirus; Human gammaherpesvirus 8; Betapolyomavirus macacae; Homo sapiens; Human betaherpesvirus 5; Human immunodeficiency virus; Murid gammaherpesvirus 4; Betapolyomavirus hominis
#> 851                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 852                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 853                                                                                                                                                                                                                                                                                                                                                                      Macaca mulatta; Homo sapiens
#> 854                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 855                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 856                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 857                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 858                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 859                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 860                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 861                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 862                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 863                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 864                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 865                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 866                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 867                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 868                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 869                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 870                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 871                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 872                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 873                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 874                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 875                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 876                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 877                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 878                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 879                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens; Papio hamadryas
#> 880                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 881                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 882                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 883                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 884                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 885                                                                                                                                                                                                                                                                                                                                                                 synthetic construct; Homo sapiens
#> 886                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 887                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 888                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 889                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 890                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 891                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 892                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 893                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 894                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 895                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 896                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 897                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 898                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 899                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 900                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 901                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 902                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 903                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 904                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 905                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 906                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 907                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 908                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 909                                                                                                                                                                                                                                                                                                                                                                   Rattus norvegicus; Homo sapiens
#> 910                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 911                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 912                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 913                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 914                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 915                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 916                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 917                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 918                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 919                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 920                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 921                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 922                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 923                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 924                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 925                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 926                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 927                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 928                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 929                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 930                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 931                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 932                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 933                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 934                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 935                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 936                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 937                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 938                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 939                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 940                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 941                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 942                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 943                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 944                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 945                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 946                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 947                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 948                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 949                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 950                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 951                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 952                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 953                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 954                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 955                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 956                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 957                           Human gammaherpesvirus 8; Mus musculus cytomegalovirus 2; Betapolyomavirus macacae; Rattus norvegicus; Human alphaherpesvirus 2; JC polyomavirus; Merkel cell polyomavirus; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Human gammaherpesvirus 4; Human immunodeficiency virus 1; Homo sapiens; Murid gammaherpesvirus 4; Betapolyomavirus hominis
#> 958                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 959                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 960                                                                                                                                                                                                                                                                                                                                                                        Mus musculus; Homo sapiens
#> 961                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 962                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 963                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 964                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 965                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 966                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 967                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 968                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 969                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 970                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 971                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 972                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 973                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 974                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 975                                                                                                                                                                                                                                                                                                    Gallus gallus; Oryctolagus cuniculus; Mus musculus; Escherichia coli; Bos taurus; Homo sapiens
#> 976                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 977                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 978                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 979                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 980                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 981                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 982                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 983                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 984                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 985                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 986                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 987                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 988                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 989                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 990                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 991                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 992                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 993                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 994                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 995                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 996                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 997                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 998                                                                                                                                                                                                                                                                                                                                                                                      Homo sapiens
#> 999                                                                                      Rattus norvegicus; Murid gammaherpesvirus 4; Betapolyomavirus hominis; Human alphaherpesvirus 1; Human betaherpesvirus 5; Betapolyomavirus macacae; Homo sapiens; Mus musculus; Murid betaherpesvirus 1; Human gammaherpesvirus 4; JC polyomavirus; Human immunodeficiency virus 1; Human gammaherpesvirus 8
#> 1000                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1001                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1002                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1003                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1004                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1005                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1006                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1007                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1008                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1009                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1010                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1011                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1012                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1013                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1014                                                                                     Human gammaherpesvirus 8; Betapolyomavirus macacae; Homo sapiens; Human betaherpesvirus 5; Murid gammaherpesvirus 4; Betapolyomavirus hominis; Mus musculus; Human alphaherpesvirus 1; Human gammaherpesvirus 4; Rattus norvegicus; Murid betaherpesvirus 1; JC polyomavirus; Human immunodeficiency virus 1
#> 1015                                                                                     JC polyomavirus; Human gammaherpesvirus 8; Betapolyomavirus macacae; Rattus norvegicus; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Murid betaherpesvirus 1; Human gammaherpesvirus 4; Human immunodeficiency virus 1; Homo sapiens; Murid gammaherpesvirus 4; Betapolyomavirus hominis
#> 1016                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1017                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1018                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1019                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1020                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1021                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1022                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1023                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1024                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1025                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1026                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1027                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1028                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1029                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1030                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1031                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1032                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1033                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1034                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1035                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1036                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1037                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1038                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1039                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1040                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1041                                                                                     Human gammaherpesvirus 8; Betapolyomavirus macacae; Rattus norvegicus; Murid betaherpesvirus 1; JC polyomavirus; Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Human gammaherpesvirus 4; Human immunodeficiency virus 1; Homo sapiens; Murid gammaherpesvirus 4; Betapolyomavirus hominis
#> 1042                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1043                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1044                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1045                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1046                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1047                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1048                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1049                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1050                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1051                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1052                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1053                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1054                                                                                                                                                                                                                                                                                                                                                    Homo sapiens; Mus musculus; Rattus norvegicus
#> 1055                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1056                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1057                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1058                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1059                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1060                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1061                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1062                                                                                                                                                                                                                                                                                                                                                    Homo sapiens; Mus musculus; Rattus norvegicus
#> 1063                                                                                                                                                                                                                                                                                                                                                    Homo sapiens; Mus musculus; Rattus norvegicus
#> 1064                                                                                                                                                                                                                                                                                                                                                    Mus musculus; Rattus norvegicus; Homo sapiens
#> 1065                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1066                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1067                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1068                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1069                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1070                                                                                                                                                                                                                                                                                                                                                                  Rattus norvegicus; Homo sapiens
#> 1071                                                                                                                                                                                                                                                                                                                                                    Homo sapiens; Rattus norvegicus; Mus musculus
#> 1072                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1073                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1074                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1075                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1076                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1077                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1078                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1079                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1080                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1081                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1082                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1083                                                                                                                                                                                                                                                                                                                                                                Macaca fascicularis; Homo sapiens
#> 1084                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1085                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1086                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1087                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1088                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1089                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1090                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1091                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1092                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1093                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1094                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1095                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1096                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1097                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1098                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1099                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1100                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1101                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1102                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1103                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1104                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1105                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1106                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#> 1107                                                                                                                                                                                                                                                                                                                                                                                     Homo sapiens
#>                                                                                                                                                                                                                                   Type
#> 1                                                                                                                                                                                         Methylation profiling by genome tiling array
#> 2                                                                                                                                                                     Expression profiling by array; Non-coding RNA profiling by array
#> 3                                                                                                                                                                               Non-coding RNA profiling by high throughput sequencing
#> 4                                                                                                                                                                                   Expression profiling by high throughput sequencing
#> 5                                                                                                                                                                                   Expression profiling by high throughput sequencing
#> 6                                                                                                                                                                     Genome binding/occupancy profiling by high throughput sequencing
#> 7                                                                                                                                                                                   Expression profiling by high throughput sequencing
#> 8                                                                                                                                                                                   Expression profiling by high throughput sequencing
#> 9                                                                                                                                                                                   Expression profiling by high throughput sequencing
#> 10                                                                                                                                                                                                      Methylation profiling by array
#> 11                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 12                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 13                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 14                                                                                                                                                                                        Methylation profiling by genome tiling array
#> 15                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 16                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 17                                                                                                                                                                              Non-coding RNA profiling by high throughput sequencing
#> 18                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 19                                                                                                                Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 20                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 21                                                                                                                                                                                                       Expression profiling by array
#> 22                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 23                                                                                                                                                                                 Methylation profiling by high throughput sequencing
#> 24                                                                                                                             Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
#> 25                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 26                                                                                                                                                                              Non-coding RNA profiling by high throughput sequencing
#> 27                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 28                                                                                                                                                                                 Methylation profiling by high throughput sequencing
#> 29                                                                                                                                                                                 Methylation profiling by high throughput sequencing
#> 30                                                                                                                                                                                 Methylation profiling by high throughput sequencing
#> 31                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 32                                                                                                                                                                                                   Non-coding RNA profiling by array
#> 33                                                                                                                                                                    Genome binding/occupancy profiling by high throughput sequencing
#> 34                                                                                                                                                                    Genome binding/occupancy profiling by high throughput sequencing
#> 35                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 36                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 37                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 38                                                                                                                                                                              Non-coding RNA profiling by high throughput sequencing
#> 39                                                                                                                                                                                                   Non-coding RNA profiling by array
#> 40                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 41                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 42                                                                                                                                                                                 Methylation profiling by high throughput sequencing
#> 43                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 44                                                                                                                                                                                        Methylation profiling by genome tiling array
#> 45                                                                                                                                                                    Expression profiling by array; Non-coding RNA profiling by array
#> 46                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 47                                                                                                                Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 48                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 49                                                                                                                                                                    Genome binding/occupancy profiling by high throughput sequencing
#> 50                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 51                                                                                                                                                                                                       Expression profiling by array
#> 52                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 53                                                                                                                                                                                                       Expression profiling by array
#> 54                                                                                                                                                                                                  Protein profiling by protein array
#> 55                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 56                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 57                                                                                                                                                                              Non-coding RNA profiling by high throughput sequencing
#> 58                                                                                                                                                                           Expression profiling by high throughput sequencing; Other
#> 59                                                                                                                          Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 60                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 61                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 62                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 63                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 64                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 65                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 66                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 67                                                                                                                                                                                        Methylation profiling by genome tiling array
#> 68                                                                                                                                                                                        Methylation profiling by genome tiling array
#> 69                                                                                                                                                                                                      Methylation profiling by array
#> 70                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 71                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 72                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 73                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 74                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 75                                                                                                                                                                    Expression profiling by array; Non-coding RNA profiling by array
#> 76                                                                                                                                                                                                   Non-coding RNA profiling by array
#> 77                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 78                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 79                                                                                                                                                                                                       Expression profiling by array
#> 80                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 81                                                                                                                                                                    Non-coding RNA profiling by array; Expression profiling by array
#> 82                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 83                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 84                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 85                                                                                                                                                                                                       Expression profiling by array
#> 86                                                                                                                                                                                                       Expression profiling by array
#> 87                                                                                                                                                                           Expression profiling by high throughput sequencing; Other
#> 88                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 89                                                                                                                                                                                                                               Other
#> 90                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 91                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 92                                                                                                                                                                    Genome binding/occupancy profiling by high throughput sequencing
#> 93                                                                                                                                                                                                      Methylation profiling by array
#> 94                                                                                                                          Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 95                                                                                                                                                                              Non-coding RNA profiling by high throughput sequencing
#> 96                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 97                                                                                                                                                                                  Expression profiling by high throughput sequencing
#> 98                                                                                                                                                                           Expression profiling by high throughput sequencing; Other
#> 99                                                                                                                                                                                                       Expression profiling by array
#> 100                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 101                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 102                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 103                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 104                                                                                                                                                                                                      Expression profiling by array
#> 105                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 106                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 107                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 108                                                                                                                                                                                                      Expression profiling by array
#> 109                                                                                                                                                                                                      Expression profiling by array
#> 110                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 111                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 112                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 113                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 114                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 115                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 116                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 117                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 118                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 119                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 120                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 121                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 122                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 123                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 124                                                                                                                                                                                                      Expression profiling by array
#> 125                                                                                                                                                                          Expression profiling by high throughput sequencing; Other
#> 126                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 127                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 128                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 129                                                                                                                                                                                                      Expression profiling by array
#> 130                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 131                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 132                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 133                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 134                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 135                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 136                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 137                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 138                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 139                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 140                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 141                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 142                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 143                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 144                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 145                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 146                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 147                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 148                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 149                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 150                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 151                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 152                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 153                                                                                                                                                                                                 Protein profiling by protein array
#> 154                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 155                                                                                                                                                  Expression profiling by high throughput sequencing; Expression profiling by array
#> 156                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 157                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 158                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 159                                                                                                                                                                                                                              Other
#> 160                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 161                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 162                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 163                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 164                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 165                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 166                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 167                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 168                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 169                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 170                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 171                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 172                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 173                                                                                                                                                                                                      Expression profiling by array
#> 174                                                                                                                                                                                            Genome variation profiling by SNP array
#> 175                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 176                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 177                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 178                                                                                                                                                               Genome variation profiling by SNP array; SNP genotyping by SNP array
#> 179                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 180                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 181                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 182                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 183                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 184                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 185                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 186                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 187                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 188                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 189                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 190                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 191                                                                                                                                                                                                      Expression profiling by array
#> 192                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 193                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 194                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 195                                                                                                                                                                                                      Expression profiling by array
#> 196                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 197                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 198                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 199                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 200                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 201                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 202                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 203                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 204                                                          Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 205                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 206                                                                                                                                                                                                      Expression profiling by array
#> 207                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 208                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 209                                                                                                                                                                                                      Expression profiling by array
#> 210                                                                                                                                                                                                      Expression profiling by array
#> 211                                                                                                                                                                                                      Expression profiling by array
#> 212                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 213                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 214                                                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 215                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 216                                                                                                                                                                                                 Protein profiling by protein array
#> 217                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 218                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 219                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 220                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 221                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 222                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 223                                                                                                                                                                                                      Expression profiling by array
#> 224                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 225                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 226                                                                                                                                                                                                                              Other
#> 227                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 228                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 229                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 230                                                                                                                                                                                                     Methylation profiling by array
#> 231                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 232                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 233                                                                                                                                                                                                      Expression profiling by array
#> 234                                                                                                                                                                                                      Expression profiling by array
#> 235                                                                                                                                                        Expression profiling by array; Methylation profiling by genome tiling array
#> 236                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 237                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 238                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 239                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 240                                                                                                                                                                                                      Expression profiling by array
#> 241                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 242                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 243                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 244                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 245                                                                                                                                                                                                      Expression profiling by array
#> 246                                                                                                                                                                                                                              Other
#> 247                                                                                                        Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
#> 248                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 249                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 250                                                                                                                                                                                                      Expression profiling by array
#> 251                                                                                                                                                                                                      Expression profiling by array
#> 252                                                                                                                                                                                                      Expression profiling by array
#> 253                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 254                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 255                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 256                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 257                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 258                                                                                                                                                                                                                              Other
#> 259                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 260                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 261                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 262                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 263                                                                                                                                                                                                Genome variation profiling by array
#> 264                                                                                                                                                                                                      Expression profiling by array
#> 265                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 266                                                                                                                                                                                                      Expression profiling by array
#> 267                                                                                                                                                                                                      Expression profiling by array
#> 268                                                                                                                                                   Methylation profiling by genome tiling array; Methylation profiling by SNP array
#> 269                                                                                                                         Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 270                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 271                                                                                                                                                                                                      Expression profiling by array
#> 272                                                                                                                                                                                                      Expression profiling by array
#> 273                                                                                                                                                                                                      Expression profiling by array
#> 274                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 275                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 276                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 277                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by array
#> 278                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 279                                                                                                                                                                                                     Methylation profiling by array
#> 280                                                                                                                                                                                                 Protein profiling by protein array
#> 281                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 282                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 283                                                                                                                            Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 284                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 285                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 286                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 287                                                                                                                                                                                                                              Other
#> 288                                                                                                                                                                                                      Expression profiling by array
#> 289                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 290                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 291                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 292                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 293                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 294                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 295                                                                                                                                                                                                      Expression profiling by array
#> 296                                                                                                                                                                                                      Expression profiling by array
#> 297                                                                                                                                                                                                      Expression profiling by array
#> 298                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 299                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 300                                                                                                                            Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
#> 301                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 302                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 303                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 304                                                                                                                                                                                                      Expression profiling by array
#> 305                                                                                                                                                                                                      Expression profiling by array
#> 306                                                                                                                                                                                                      Expression profiling by array
#> 307                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 308                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 309                                                                                                                                                                                                                              Other
#> 310                                                                                                        Expression profiling by high throughput sequencing; Other; Genome binding/occupancy profiling by high throughput sequencing
#> 311                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 312                                                                                                                                                                                                                              Other
#> 313                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 314                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 315                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 316                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 317                                                                                                                                                                                                      Expression profiling by array
#> 318                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 319                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 320                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 321                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 322                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 323                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 324                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 325                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 326                                                                                                                                                                                                      Expression profiling by array
#> 327                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 328                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 329                                                                                                                                                                                                      Expression profiling by array
#> 330                                                                                                                                                                                                      Expression profiling by array
#> 331                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 332                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 333                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 334                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 335                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 336                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 337                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 338                                                                                                                                                                                                                              Other
#> 339                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 340                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 341                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 342                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 343                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 344                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 345                                                                                                                                                                                                      Expression profiling by array
#> 346                                                                                                                                                                                                      Expression profiling by array
#> 347                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 348                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 349                                                                                                                                                                                                      Expression profiling by array
#> 350                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 351                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 352                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 353                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 354                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 355                                                                                                                                                                                  Genome variation profiling by genome tiling array
#> 356                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 357                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 358                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 359                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 360                                                                                                                                                                   Genome variation profiling by array; SNP genotyping by SNP array
#> 361                                                                                                              Methylation profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 362                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 363                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 364                                                                                                                                                                                                      Expression profiling by array
#> 365                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 366                                                                                                                                                                                                        SNP genotyping by SNP array
#> 367                                                                                                                                                                                                      Expression profiling by array
#> 368                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 369                                                                                                                                                                                                                              Other
#> 370                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 371                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 372                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 373                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 374                                                                                                                                                                                                      Expression profiling by array
#> 375                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 376                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 377                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 378                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 379                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 380                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 381                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 382                                                                                                                                                  Expression profiling by array; Expression profiling by high throughput sequencing
#> 383                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 384                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 385                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 386                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 387                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 388                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 389                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 390                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 391                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 392                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 393                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 394                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 395                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 396                                                                                                                                                                                                      Expression profiling by array
#> 397                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 398                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 399                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 400                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 401                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 402                                                                                                                                                                                                      Expression profiling by array
#> 403                                                                                                                                                                                                                              Other
#> 404                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 405                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 406                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 407                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 408                                                                                                                                                                                                      Expression profiling by array
#> 409                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 410                                                                                                                                                                                                      Expression profiling by array
#> 411                                                                                                                                                                                                      Expression profiling by array
#> 412                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 413                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 414                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 415                                                                                                                                                                      Other; Non-coding RNA profiling by high throughput sequencing
#> 416                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 417                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 418                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 419                                                                                                                                                                                                                              Other
#> 420                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 421                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 422                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 423                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 424                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 425                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 426                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 427                                                                                                                                                                                                 Protein profiling by protein array
#> 428                                                                                                                                                                                                 Protein profiling by protein array
#> 429                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 430                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 431                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 432                                                                                                                                                                                                      Expression profiling by array
#> 433                                                                                                                                                                                                      Expression profiling by array
#> 434                                                                                                                                                                                                      Expression profiling by array
#> 435                                                                                                                                                                                                      Expression profiling by array
#> 436                                                                                                                                                                                                      Expression profiling by array
#> 437                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 438                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 439                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 440                                                                                                                                                                                                                              Other
#> 441                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 442                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 443                                                                                                                                                                                                      Expression profiling by array
#> 444                                                                                                                                                                                                 Protein profiling by protein array
#> 445                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 446                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 447                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 448                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 449                                                                                                                                                                                                      Expression profiling by array
#> 450                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 451                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 452                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 453                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 454                                                                                                                                                                          Expression profiling by high throughput sequencing; Other
#> 455                                                                                                                                                                                                 Protein profiling by protein array
#> 456                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 457                                                                                                                                                                                                      Expression profiling by array
#> 458                                                                                                                                                                                                      Expression profiling by array
#> 459                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 460                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 461                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 462                                                                                                                                                                                                      Expression profiling by array
#> 463                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 464                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 465                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 466                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 467                                                                                                                                                                                            Genome variation profiling by SNP array
#> 468                                                                                                                                                                                                      Expression profiling by array
#> 469                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 470                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 471                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 472                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 473                                                                                                                                                                                                      Expression profiling by array
#> 474                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 475                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 476                                                                                                                                                                                                      Expression profiling by array
#> 477                                                                                                                                                                                                      Expression profiling by array
#> 478                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 479                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 480                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 481                                                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 482                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 483                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 484                                                                                                                                                                                                      Expression profiling by array
#> 485                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 486                                                                                                                                   Methylation profiling by genome tiling array; Expression profiling by high throughput sequencing
#> 487                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 488                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 489                                                                                                                                                                                                 Protein profiling by protein array
#> 490                                                                                                                                                            Genome binding/occupancy profiling by high throughput sequencing; Other
#> 491                                                                                                                                                            Genome binding/occupancy profiling by high throughput sequencing; Other
#> 492                                                                                                                                                            Genome binding/occupancy profiling by high throughput sequencing; Other
#> 493                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 494                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 495                                                                                                                                                                                                      Expression profiling by array
#> 496                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 497                                                                                                                                                                                                                              Other
#> 498                                                                                                                                                                                                      Expression profiling by array
#> 499                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 500                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 501                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 502                                                                                                                                                                                                      Expression profiling by array
#> 503                                                                                                                                                                                                      Expression profiling by array
#> 504                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 505                                                                                                                                                                                                      Expression profiling by array
#> 506                                                Other; Genome binding/occupancy profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 507                                                                                                                                                                                                      Expression profiling by array
#> 508                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 509                                                                                                                                                                                                      Expression profiling by array
#> 510                                                                                                                                                                                                Genome variation profiling by array
#> 511                                                                                                                                                                                                      Expression profiling by array
#> 512                                                                                                                                                                                                      Expression profiling by array
#> 513                                                                                                                                                                                                      Expression profiling by array
#> 514                                                                                                                                                                                                      Expression profiling by array
#> 515                                                                                                                                                                                                                              Other
#> 516                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 517                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 518                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 519                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 520                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 521                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 522                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 523                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 524                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 525                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 526                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 527                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 528                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 529                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 530                                                                                                                                                                                                      Expression profiling by array
#> 531                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 532                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 533                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 534                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 535                                                                                                                                                                                                      Expression profiling by array
#> 536                                                                                                                                                                                                      Expression profiling by array
#> 537                                                                                                                                                                                                      Expression profiling by array
#> 538                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 539                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 540                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 541                                                                                                                                                                                                      Expression profiling by array
#> 542                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 543                                                                                                                                                                                                      Expression profiling by array
#> 544                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 545                                                                                                                                                                                                      Expression profiling by array
#> 546                                                                                                                                                 Expression profiling by array; Methylation profiling by high throughput sequencing
#> 547                                                                                                                                                                                                      Expression profiling by array
#> 548                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 549                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 550                                                                                                                                                                                                      Expression profiling by array
#> 551                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 552                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 553                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 554                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 555                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 556                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 557                                                                                                                                                                   Non-coding RNA profiling by array; Expression profiling by array
#> 558                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 559                                                                                                                                                                                                      Expression profiling by array
#> 560                                                                                                                                                                                                      Expression profiling by array
#> 561                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 562                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 563                                                                                                                                                                                                      Expression profiling by array
#> 564                                                                                                                                                                                                      Expression profiling by array
#> 565                                                                                                                                                                                                      Expression profiling by array
#> 566                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 567                                                                                                                                                                                                      Expression profiling by array
#> 568                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 569                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 570                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 571                                                                                                                                                        Expression profiling by array; Methylation profiling by genome tiling array
#> 572                                                                                                                                                                                                      Expression profiling by array
#> 573                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 574                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 575                                                                                                                                                                                                                              Other
#> 576                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 577                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 578                                                                                                                                                                                                      Expression profiling by array
#> 579                                                                                                                                                                                                      Expression profiling by array
#> 580                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 581                                                                                                                                                                                                      Expression profiling by array
#> 582                                                                                                                                                                                                      Expression profiling by array
#> 583                                                                                                                                                                                                      Expression profiling by array
#> 584                                                                                                                                                                                                      Expression profiling by array
#> 585                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 586                                                                                                                                                                                                      Expression profiling by array
#> 587                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 588                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 589                                                                                                                         Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 590                                                                                                                                                                                                      Expression profiling by array
#> 591                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 592                                                                                                                                                                                                      Expression profiling by array
#> 593                                                                                                                                                                                                      Expression profiling by array
#> 594                                                                                                                                                                                                      Expression profiling by array
#> 595                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 596                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 597                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 598                                                                                                                                                                                                      Expression profiling by array
#> 599                                                                                                                                                             Expression profiling by array; Genome variation profiling by SNP array
#> 600                                                                                                                                                                                                      Expression profiling by array
#> 601                                                                                                                                                                                            Genome variation profiling by SNP array
#> 602                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 603                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 604                                                                                                                                                                                                  Expression profiling by SNP array
#> 605                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 606                                                                                                                                                                                                      Expression profiling by array
#> 607                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 608                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 609                                                                                                                                                                                                      Expression profiling by array
#> 610                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 611                                                                                                                                                                                                      Expression profiling by array
#> 612                                                                                                                                                                                                      Expression profiling by array
#> 613                                                                                                                                                                                                      Expression profiling by array
#> 614                                                                                                                                                                                                      Expression profiling by array
#> 615                                                                                                                                                                                                      Expression profiling by array
#> 616                                                                                                                                                                                                      Expression profiling by array
#> 617                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 618                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 619                                                                                                                                                                                                     Methylation profiling by array
#> 620                                                                                                                                                                                                 Protein profiling by protein array
#> 621                                                                                                                                                                                                      Expression profiling by array
#> 622                                                                                                                                                                                                      Expression profiling by array
#> 623                                                                                                                                                                                                      Expression profiling by array
#> 624                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 625                                                                                                                                                                                                      Expression profiling by array
#> 626                                                                                                                                                                                                      Expression profiling by array
#> 627                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 628                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 629                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 630                                                                                                                                                               SNP genotyping by SNP array; Genome variation profiling by SNP array
#> 631                                                                                                                                                                                                      Expression profiling by array
#> 632                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 633                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 634                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 635                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 636                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 637                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 638                                                                                                                                                                                                      Expression profiling by array
#> 639                                                                                                                                                                                                      Expression profiling by array
#> 640                                                                                                                                                                                                     Methylation profiling by array
#> 641                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 642                                                                                                                                                                                                     Methylation profiling by array
#> 643                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 644                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 645                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 646                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 647                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 648                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 649                                                                                                                                                                                                      Expression profiling by array
#> 650                                                                                                                                                                                                      Expression profiling by array
#> 651                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 652                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 653                                                                                                                                                                                                      Expression profiling by array
#> 654                                                                                                                                                                                                      Expression profiling by array
#> 655                                                                                                                                                                                                      Expression profiling by array
#> 656                                                                                                                                                                                                      Expression profiling by array
#> 657                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 658                                                                                                                                                                                                      Expression profiling by array
#> 659                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 660                                                                                                                                                                                                      Expression profiling by array
#> 661                                                                                                                                                                                                      Expression profiling by array
#> 662                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 663                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 664                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 665                                                                                                                                                                                                                              Other
#> 666                                                                                                                                                                                                      Expression profiling by array
#> 667                                                                                                                                                                                                      Expression profiling by array
#> 668                                                                                                                                                                                                      Expression profiling by array
#> 669                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 670                                                                                                                                                                                                      Expression profiling by array
#> 671                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 672                                                                                                                                                  Expression profiling by high throughput sequencing; Expression profiling by array
#> 673                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 674                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 675                                                                                                                                                                                                      Expression profiling by array
#> 676                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 677                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 678                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 679                                                                                                                                                                                                      Expression profiling by array
#> 680                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 681                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 682                                                                                                                                                                                                      Expression profiling by array
#> 683                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 684                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 685                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 686                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 687                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 688                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 689                                                                                                                                                                                                      Expression profiling by array
#> 690                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 691                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 692                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 693                                                                                                                                                                                                      Expression profiling by array
#> 694                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 695                                                                                                                                                                                                      Expression profiling by array
#> 696                                                                                                                                                                                                      Expression profiling by array
#> 697                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 698                                                                                                                                                                                                      Expression profiling by array
#> 699                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 700                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 701                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 702                                                                                                                                                                                                      Expression profiling by array
#> 703                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 704                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 705                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 706                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 707                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 708                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 709                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 710                                                                                                                                                                                                      Expression profiling by array
#> 711                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 712                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 713                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 714                                                                                                                                                                                                     Methylation profiling by array
#> 715                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 716                                                                                                                                                                                                      Expression profiling by array
#> 717                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 718                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 719                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 720                                                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 721                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 722                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 723                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 724                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 725                                                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 726                                                                                                                                                                                                     Methylation profiling by array
#> 727                                                                                                                                                                                                      Expression profiling by array
#> 728                                                                                                                                                                                                     Methylation profiling by array
#> 729                                                                                                                                                                                                      Expression profiling by array
#> 730                                                                                                                                                                                                      Expression profiling by array
#> 731                                                                                                                                                          Methylation profiling by genome tiling array; SNP genotyping by SNP array
#> 732                                                                                                                                                                                                        SNP genotyping by SNP array
#> 733                                                                                                                                                                                                        SNP genotyping by SNP array
#> 734                                                                                                                                                                                                      Expression profiling by array
#> 735                                                                                                                                                                                                      Expression profiling by array
#> 736                                                                                                                                                                                                      Expression profiling by array
#> 737                                                                                                                                                                                                      Expression profiling by array
#> 738                                                                                                                                                                                                      Expression profiling by array
#> 739                                                                                                                                                                                                      Expression profiling by array
#> 740                                                                                                                                                                                                      Expression profiling by array
#> 741                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 742                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 743                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 744                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 745                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 746                                                                                                                                                                                                      Expression profiling by array
#> 747                                                                                                                                                                                                        SNP genotyping by SNP array
#> 748                                                                                                                                                                                                      Expression profiling by array
#> 749                                                                                                                                                                                                      Expression profiling by array
#> 750                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 751                                                                                                                                                                                                      Expression profiling by array
#> 752                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 753                                                                                                                                                                                                                              Other
#> 754                                                                                                                                                                                                      Expression profiling by array
#> 755                                                                                                                                                                                                      Expression profiling by array
#> 756                                                                                                                                                                                                      Expression profiling by array
#> 757                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 758                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 759                                                                                                                                                                                                      Expression profiling by array
#> 760                                                                                                                                                                                                      Expression profiling by array
#> 761                                                                                                                                                                                              Expression profiling by RT-PCR; Other
#> 762                                                                                                                                                                                                      Expression profiling by array
#> 763                                                                                                                                                                                                      Expression profiling by array
#> 764                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 765                                                                                                                                                                                                      Expression profiling by array
#> 766                                                                                                                                                                                                      Expression profiling by array
#> 767                                                                                                                                                                                                      Expression profiling by array
#> 768                                                                                                                                                                                                      Expression profiling by array
#> 769                                                                                                                                                                                                      Expression profiling by array
#> 770                                                                                                                                                                      Expression profiling by array; Methylation profiling by array
#> 771                                                                                                                                                                                                      Expression profiling by array
#> 772                                                                                                                                                                                                     Methylation profiling by array
#> 773                                                                                                                                                                                                      Expression profiling by array
#> 774                                                                                                                                                                                                      Expression profiling by array
#> 775                                                                                                                                                                                                      Expression profiling by array
#> 776                                                                                                                                                                                                      Expression profiling by array
#> 777                                                                                                                                                                                                      Expression profiling by array
#> 778                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 779                                                                                                                                                                                                      Expression profiling by array
#> 780                                                                                                                                                                                                      Expression profiling by array
#> 781                                                                                                                                                                                                      Expression profiling by array
#> 782                                                                                                                                                                                                      Expression profiling by array
#> 783                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 784                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 785                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 786                                                                                                                                                                                                      Expression profiling by array
#> 787                                                                                                                                                                                                      Expression profiling by array
#> 788                                                                                                                                                                                                      Expression profiling by array
#> 789                                                                                                                                                                                                      Expression profiling by array
#> 790                                                                                                                                                                                                      Expression profiling by array
#> 791                                                                                                                                                                                                      Expression profiling by array
#> 792                                                                                                                                                                                                      Expression profiling by array
#> 793                                                                                                                                                            Expression profiling by array; Other; Non-coding RNA profiling by array
#> 794                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 795                                                                                                                                                                                                                              Other
#> 796                                                                                                                                                                                                      Expression profiling by array
#> 797                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 798                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 799                                                                                                                                                                                                      Expression profiling by array
#> 800                                                                                                                                                                                                      Expression profiling by array
#> 801                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 802                                                                                                                                                                                                      Expression profiling by array
#> 803                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 804                                                                                                                                                                                                      Expression profiling by array
#> 805                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 806                                                                                                                                                                                                      Expression profiling by array
#> 807                                                                                                                                                                                                      Expression profiling by array
#> 808                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 809                                                                                                                                                                                  Genome variation profiling by genome tiling array
#> 810                                                                                                                                                                                                      Expression profiling by array
#> 811                                                                                                                                                                                                      Expression profiling by array
#> 812                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 813                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 814                                                                                                                                                                                                      Expression profiling by array
#> 815                                                                                                                                                                                       Methylation profiling by genome tiling array
#> 816                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 817                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 818                                                                                                                                                                                                      Expression profiling by array
#> 819                                                                                                                                                                                                      Expression profiling by array
#> 820                                                                                                                                                                                                      Expression profiling by array
#> 821                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 822                                                                                                                                                                   Non-coding RNA profiling by array; Expression profiling by array
#> 823                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 824                                                                                                                                                                                                      Expression profiling by array
#> 825                                                                                                                                                                                                      Expression profiling by array
#> 826                                                                                                                                                                                                      Expression profiling by array
#> 827                                                                                                                                                                                                      Expression profiling by array
#> 828                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 829                                                                                                                                                                                            Genome variation profiling by SNP array
#> 830                                                                                                                                                                                                      Expression profiling by array
#> 831                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 832                                                                                                                                                                                                        SNP genotyping by SNP array
#> 833                                                                                                           Genome variation profiling by SNP array; SNP genotyping by SNP array; Expression profiling by high throughput sequencing
#> 834                                                                                                                                                               SNP genotyping by SNP array; Genome variation profiling by SNP array
#> 835                                                                                                                                                                                                      Expression profiling by array
#> 836                                                                                                                                                                                                      Expression profiling by array
#> 837                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 838                                                                                                                                                                                Methylation profiling by high throughput sequencing
#> 839                                                                                                                                                                                                      Expression profiling by array
#> 840                                                                                                                                                                                                      Expression profiling by array
#> 841                                                                                                                                                                   Expression profiling by array; Non-coding RNA profiling by array
#> 842                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 843                                                                                                                                                                                                      Expression profiling by array
#> 844                                                                                                                                                                                                 Protein profiling by protein array
#> 845                                                                                                                                                                                                      Expression profiling by array
#> 846                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 847                                                                                                                                                         Expression profiling by high throughput sequencing; Third-party reanalysis
#> 848                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 849                                                                                                                                                        Expression profiling by array; Methylation profiling by genome tiling array
#> 850                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 851                                                                                                                                                                                                      Expression profiling by array
#> 852                                                                                                                                                                                                     Methylation profiling by array
#> 853                                                                                                                                                                                                      Expression profiling by array
#> 854                                                                                                                                                                                                      Expression profiling by array
#> 855                                                                                                                                                                                                     Methylation profiling by array
#> 856                                                                                                                                                                              Expression profiling by array; Third-party reanalysis
#> 857                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 858                                                                                                                                                                                                      Expression profiling by array
#> 859                                                                                                                                                                                                      Expression profiling by array
#> 860                                                                                                                                                                                                      Expression profiling by array
#> 861                                                                                                                                                                                                      Expression profiling by array
#> 862                                                                                                                                                                                                      Expression profiling by array
#> 863                                                                                                                                                                                                      Expression profiling by array
#> 864                                                                                                                                                                                                      Expression profiling by array
#> 865                                                                                                                                                                                                      Expression profiling by array
#> 866                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 867                                                                                                                                                                                                      Expression profiling by array
#> 868                                                                                                                                                                                                      Expression profiling by array
#> 869                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 870                                                                                                                                                         Expression profiling by high throughput sequencing; Third-party reanalysis
#> 871                                                                                                                                                                                                      Expression profiling by array
#> 872                                                                                                                                                                                                      Expression profiling by array
#> 873                                                                                                                                                                                               Expression profiling by array; Other
#> 874                                                                                                                                                                                                                              Other
#> 875                                                                                                                                                                                                      Expression profiling by array
#> 876                                                                                                                                                                                                      Expression profiling by array
#> 877                                                                                                                                                                          Genome binding/occupancy profiling by genome tiling array
#> 878                                                                                                                                                                                                      Expression profiling by array
#> 879                                                                                                                                                                                                      Expression profiling by array
#> 880                                                                                                                                                                                                      Expression profiling by array
#> 881                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 882                                                                                                                                                                                                     Methylation profiling by array
#> 883                                                                                                                                                                                                      Expression profiling by array
#> 884                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 885                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 886                                                                                                                                                                   Genome binding/occupancy profiling by high throughput sequencing
#> 887                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 888                                                                                                                                                                                                      Expression profiling by array
#> 889                                                                                                                                                                                                      Expression profiling by array
#> 890                                                                                                                                                                                                      Expression profiling by array
#> 891                                                                                                                                                                                                      Expression profiling by array
#> 892                                                                                                                                                                                                      Expression profiling by array
#> 893                                                                                                                                                                                                     Methylation profiling by array
#> 894                                                                                                                                                                                                      Expression profiling by array
#> 895                                                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
#> 896                                                                                                                                                                                                      Expression profiling by array
#> 897                                                                                                                                                                                                      Expression profiling by array
#> 898                                                                                                                                                                                                      Expression profiling by array
#> 899                                                                                                                                                                                                      Expression profiling by array
#> 900                                                                                                                                                                                                      Expression profiling by array
#> 901                                                                                                                                                                                                      Expression profiling by array
#> 902                                                                                                                                                                                                      Expression profiling by array
#> 903                                                                                                                                                                                                      Expression profiling by array
#> 904                                                                                                                                                                                                      Expression profiling by array
#> 905                                                                                                                                                                                                      Expression profiling by array
#> 906                                                                                                                                                                                                      Expression profiling by array
#> 907                                                                                                                                                                                                      Expression profiling by array
#> 908                                                                                                                                                                             Non-coding RNA profiling by high throughput sequencing
#> 909                                                                                                                                                                                                      Expression profiling by array
#> 910                                                                                                                                                                                                      Expression profiling by array
#> 911                                                                                                                                                                                                      Expression profiling by array
#> 912                                                                                                                                                                                                      Expression profiling by array
#> 913                                                                                                                                                                                                      Expression profiling by array
#> 914                                                                                                                                                                                                      Expression profiling by array
#> 915                                                                                                                                                                                                      Expression profiling by array
#> 916                                                                                                                                                                                                      Expression profiling by array
#> 917                                                                                                                                                                           Other; Genome variation profiling by genome tiling array
#> 918                                                                                                                                                                                  Genome variation profiling by genome tiling array
#> 919                                                                                                                                                                                                                              Other
#> 920                                                                                                                                                                                                      Expression profiling by array
#> 921                                                                                                                                                                                                      Expression profiling by array
#> 922                                                                                                                                                                                                      Expression profiling by array
#> 923                                                                                                                                                                                                     Methylation profiling by array
#> 924                                                                                                                                                                                                      Expression profiling by array
#> 925                                                                                                                                                               Genome variation profiling by SNP array; SNP genotyping by SNP array
#> 926                                                                                                                                                                                                      Expression profiling by array
#> 927                                                                                                                                                                                                      Expression profiling by array
#> 928                                                                                                                                                                                                      Expression profiling by array
#> 929                                                                                                                                                                                                      Expression profiling by array
#> 930                                                                                                                                                                                                      Expression profiling by array
#> 931                                                                                                                                                                                                      Expression profiling by array
#> 932                                                                                                                                                                                                      Expression profiling by array
#> 933                                                                                                                                                                                                      Expression profiling by array
#> 934                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 935                                                                                                                                                                                                      Expression profiling by array
#> 936                                                                                                                                                                                                      Expression profiling by array
#> 937                                                                                                                                                                                                      Expression profiling by array
#> 938                                                                                                                                                                                                      Expression profiling by array
#> 939                                                                                                                                                                                                      Expression profiling by array
#> 940                                                                                                                                                                                                      Expression profiling by array
#> 941                                                                                                                                                                                                     Expression profiling by RT-PCR
#> 942                                                                                                                                                                                                      Expression profiling by array
#> 943                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 944                                                                                                                                                                                                      Expression profiling by array
#> 945                                                                                                                                                                                                      Expression profiling by array
#> 946                                                                                                                                                   Expression profiling by array; Genome variation profiling by genome tiling array
#> 947                                                                                                                                                                                                      Expression profiling by array
#> 948                                                                                                               Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
#> 949                                                                                                                                                                                                      Expression profiling by array
#> 950                                                                                                                                           Expression profiling by array; Genome binding/occupancy profiling by genome tiling array
#> 951                                                                                                                                                                          Genome binding/occupancy profiling by genome tiling array
#> 952                                                                                                                                                                          Genome binding/occupancy profiling by genome tiling array
#> 953                                                                                                                                                                                                      Expression profiling by array
#> 954                                                                                                                                                                                                      Expression profiling by array
#> 955                                                                                                                                                                                                      Expression profiling by array
#> 956                                                                                                                                                                                                      Expression profiling by array
#> 957                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 958                                                                                                                                                                                                      Expression profiling by array
#> 959                                                                                                                                                                                                      Expression profiling by array
#> 960                                                                                                                                                                                                      Expression profiling by array
#> 961                                                                                                                                                                                                      Expression profiling by array
#> 962                                                                                                                                                                                                      Expression profiling by array
#> 963                                                                                                                                                                                                     Methylation profiling by array
#> 964                                                                                                                                                                                                      Expression profiling by array
#> 965                                                                                                                                                                                                      Expression profiling by array
#> 966                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 967                                                                                                                                                                                                      Expression profiling by array
#> 968                                                                                                                                                                                                      Expression profiling by array
#> 969                                                                                                                         Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 970                                                                                                                                                                                                 Protein profiling by protein array
#> 971                                                                                                                                                                                 Expression profiling by high throughput sequencing
#> 972                                                                                                                                                                                                      Expression profiling by array
#> 973                                                                                                                                                                                                      Expression profiling by array
#> 974                                                                                                                                                                                                      Expression profiling by array
#> 975                                                                                                                                                                                                 Protein profiling by protein array
#> 976                                                                                                                                                                                                  Non-coding RNA profiling by array
#> 977                                                                                                                                                                                                      Expression profiling by array
#> 978                                                                                                                                                                                                      Expression profiling by array
#> 979                                                                                                                                                                                                      Expression profiling by array
#> 980                                                                                                                                                                                                      Expression profiling by array
#> 981                                                                                                                                                                                                 Methylation profiling by SNP array
#> 982                                                                                                                                                                                                      Expression profiling by array
#> 983                                                                                                                                                                                                      Expression profiling by array
#> 984                                                                                                                                                                                                      Expression profiling by array
#> 985                                                                                                                                                                                                      Expression profiling by array
#> 986                                                                                                                                                                                                      Expression profiling by array
#> 987                                                                                                                                                                                                     Methylation profiling by array
#> 988                                                                                                                                                                                                      Expression profiling by array
#> 989                                                                                                                                                                                                      Expression profiling by array
#> 990                                                                                                                                                                                                      Expression profiling by array
#> 991                                                                                                                                                                                                      Expression profiling by array
#> 992                                                                                                                                                                                                      Expression profiling by array
#> 993                                                                                                                                                                                                      Expression profiling by array
#> 994                                                                                                                                                                                                      Expression profiling by array
#> 995                                                                                                                                                                                                      Expression profiling by array
#> 996                                                                                                                                                                                                      Expression profiling by array
#> 997                                                                                                                                                                                                      Expression profiling by array
#> 998                                                                                                                                                                                                      Expression profiling by array
#> 999                                                                                                                                                                   Non-coding RNA profiling by array; Expression profiling by array
#> 1000                                                                                                                                                                                                     Expression profiling by array
#> 1001                                                                                                                                                                                                     Expression profiling by array
#> 1002                                                                                                                                                                  Genome binding/occupancy profiling by high throughput sequencing
#> 1003                                                                                                                                                                                                     Expression profiling by array
#> 1004                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1005                                                                                                                                                                                                     Expression profiling by array
#> 1006                                                                                                                                                                                                     Expression profiling by array
#> 1007                                                                                                                                                                                                     Expression profiling by array
#> 1008                                                                                                                                                                                                                             Other
#> 1009                                                                                                                                                                                                     Expression profiling by array
#> 1010                                                                                                                                                                                                     Expression profiling by array
#> 1011                                                                                                                                                                                                     Expression profiling by array
#> 1012                                                                                                                                                                                                     Expression profiling by array
#> 1013                                                                                                                                                                                                     Expression profiling by array
#> 1014                                                                                                                                                                  Expression profiling by array; Non-coding RNA profiling by array
#> 1015                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1016                                                                                                                                                                                      Methylation profiling by genome tiling array
#> 1017                                                                                                                                                                                           Genome variation profiling by SNP array
#> 1018                                                                                                                                                                                                     Expression profiling by array
#> 1019                                                                                                                                                                                      Methylation profiling by genome tiling array
#> 1020                                                                                                                                                                                                     Expression profiling by array
#> 1021                                                                                                                                                                                                     Expression profiling by array
#> 1022                                                                                                                                                                  Genome binding/occupancy profiling by high throughput sequencing
#> 1023                                                                                                                                                                  Genome binding/occupancy profiling by high throughput sequencing
#> 1024                                                                                                                                                                  Genome binding/occupancy profiling by high throughput sequencing
#> 1025                                                                                                                                                                                                     Expression profiling by array
#> 1026                                                                                                                                                                                                     Expression profiling by array
#> 1027                                                                                                                                                                                                     Expression profiling by array
#> 1028                                                                                                                                                                                                     Expression profiling by array
#> 1029                                                                                                                                                                                                     Expression profiling by array
#> 1030                                                                                                                                                                                      Methylation profiling by genome tiling array
#> 1031                                                                                                                                                                                                     Expression profiling by array
#> 1032                                                                                                                                                                                                     Expression profiling by array
#> 1033                                                                                                                                                                                                     Expression profiling by array
#> 1034                                                                                                                                                                                                     Expression profiling by array
#> 1035                                                                                                                                                                                                     Expression profiling by array
#> 1036                                                                                                                                                                                                     Expression profiling by array
#> 1037                                                                                                                                                                                                     Expression profiling by array
#> 1038                                                                                                                                                                                                     Expression profiling by array
#> 1039                                                                                                                                                                                                     Expression profiling by array
#> 1040                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1041                                                                                                                                                                  Expression profiling by array; Non-coding RNA profiling by array
#> 1042                                                                                                                                                                                                     Expression profiling by array
#> 1043                                                                                                                                                                                                     Expression profiling by array
#> 1044                                                                                                                                                                                                     Expression profiling by array
#> 1045                                                                                                                                                                                                     Expression profiling by array
#> 1046                                                                                                                                                                                                    Methylation profiling by array
#> 1047                                                                                                                                                                                      Methylation profiling by genome tiling array
#> 1048                                                                                                                                                                                                     Expression profiling by array
#> 1049                                                                                                                                                                                                     Expression profiling by array
#> 1050                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1051                                                                               Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array; Expression profiling by high throughput sequencing
#> 1052                                                                                                                                                                                                     Expression profiling by array
#> 1053                                                                                                                                                                                                     Expression profiling by array
#> 1054                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1055                                                                                                                                                                                                     Expression profiling by array
#> 1056                                                                                                                                                                                                     Expression profiling by array
#> 1057                                                                                                                                                                                                     Expression profiling by array
#> 1058                                                                                                                                                                                                     Expression profiling by array
#> 1059                                                                                                                                                                                                     Expression profiling by array
#> 1060 Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
#> 1061                                                                                                                                                                                                     Expression profiling by array
#> 1062                                                                                                                                                                  Expression profiling by array; Non-coding RNA profiling by array
#> 1063                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1064                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1065                                                                                                                                                                                                     Expression profiling by array
#> 1066                                                                                                                                                                                                     Expression profiling by array
#> 1067                                                                                                                                                                                                     Expression profiling by array
#> 1068                                                                                                                                                                                                     Expression profiling by array
#> 1069                                                                                                                                                                                                     Expression profiling by array
#> 1070                                                                                                                                                                                                     Expression profiling by array
#> 1071                                                                                                                                                                                                 Non-coding RNA profiling by array
#> 1072                                                                                                                                                                                                     Expression profiling by array
#> 1073                                                                                                                                                                                                     Expression profiling by array
#> 1074                                                                                                                                                                                                     Expression profiling by array
#> 1075                                                                                                                                                                                                     Expression profiling by array
#> 1076                                                                                                                                                                                                     Expression profiling by array
#> 1077                                                                                                                                                                                                     Expression profiling by array
#> 1078                                                                                                                                                                                                     Expression profiling by array
#> 1079                                                                                                                                                                                                     Expression profiling by array
#> 1080                                                                                                                                                                                                     Expression profiling by array
#> 1081                                                                                                                                                                                                     Expression profiling by array
#> 1082                                                                                                                                                                                                     Expression profiling by array
#> 1083                                                                                                                                                                                                     Expression profiling by array
#> 1084                                                                                                                                                                                                     Expression profiling by array
#> 1085                                                                                                                                                                                                     Expression profiling by array
#> 1086                                                                                                                                                                                                     Expression profiling by array
#> 1087                                                                                                                                                                                                     Expression profiling by array
#> 1088                                                                                                                                                                                                     Expression profiling by array
#> 1089                                                                                                                                                                                                     Expression profiling by array
#> 1090                                                                                                                                                                                                     Expression profiling by array
#> 1091                                                                                                                                                                                                     Expression profiling by array
#> 1092                                                                                                                                                                                                     Expression profiling by array
#> 1093                                                                                                                                                                                                     Expression profiling by array
#> 1094                                                                                                                                                                                                     Expression profiling by array
#> 1095                                                                                                                                                                                                      Expression profiling by SAGE
#> 1096                                                                                                                                                                                                     Expression profiling by array
#> 1097                                                                                                                                                                                                     Expression profiling by array
#> 1098                                                                                                                                                                                                     Expression profiling by array
#> 1099                                                                                                                                                                                                     Expression profiling by array
#> 1100                                                                                                                                                                                                     Expression profiling by array
#> 1101                                                                                                                                                                                                     Expression profiling by array
#> 1102                                                                                                                                                                     Expression profiling by array; Methylation profiling by array
#> 1103                                                                                                                                                                                                     Expression profiling by array
#> 1104                                                                                                                                                                                                     Expression profiling by array
#> 1105                                                                                                                                                                                                     Expression profiling by array
#> 1106                                                                                                                                                                                                Protein profiling by protein array
#> 1107                                                                                                                                                                                                     Expression profiling by array
#>                        Platforms                        Contains
#> 1                       GPL13534                      18 Samples
#> 2                       GPL23126                       9 Samples
#> 3                       GPL15520                      54 Samples
#> 4                       GPL16791                      61 Samples
#> 5     GPL19057 GPL18573 GPL24247                      38 Samples
#> 6              GPL18573 GPL19057                      14 Samples
#> 7                       GPL16791                     111 Samples
#> 8                       GPL20795                       6 Samples
#> 9                       GPL11154                      16 Samples
#> 10                      GPL16353                       9 Samples
#> 11                      GPL17303                      30 Samples
#> 12                      GPL16791                      35 Samples
#> 13                      GPL24676                       8 Samples
#> 14                      GPL23976                      60 Samples
#> 15                      GPL24676                      21 Samples
#> 16             GPL24676 GPL24247                      59 Samples
#> 17                      GPL18573                       8 Samples
#> 18                      GPL21290                      92 Samples
#> 19                      GPL24676                       8 Samples
#> 20                      GPL18573                      14 Samples
#> 21                      GPL16686                      18 Samples
#> 22                      GPL24676                      84 Samples
#> 23                      GPL24676                      82 Samples
#> 24                      GPL24676                     166 Samples
#> 25                      GPL15433                      17 Samples
#> 26             GPL22790 GPL21697                      10 Samples
#> 27                      GPL20795                      12 Samples
#> 28             GPL11154 GPL24676                     211 Samples
#> 29                      GPL24676                     101 Samples
#> 30                      GPL11154                     110 Samples
#> 31                      GPL16791                      90 Samples
#> 32                      GPL20712                      10 Samples
#> 33                      GPL16791                      43 Samples
#> 34                      GPL16791                      12 Samples
#> 35                      GPL16791                      12 Samples
#> 36                      GPL20301                       6 Samples
#> 37                      GPL24676                      24 Samples
#> 38                      GPL16791                      78 Samples
#> 39                      GPL25243                      60 Samples
#> 40                      GPL24676                      21 Samples
#> 41                      GPL18573                      28 Samples
#> 42                      GPL18573                      55 Samples
#> 43                      GPL20795                       5 Samples
#> 44                      GPL21145                     100 Samples
#> 45                      GPL20115                       2 Samples
#> 46                      GPL20795                      12 Samples
#> 47                      GPL18573                      89 Samples
#> 48                      GPL18573                      80 Samples
#> 49                      GPL18573                       9 Samples
#> 50                      GPL18573                      48 Samples
#> 51                        GPL570                      50 Samples
#> 52                      GPL20795                       4 Samples
#> 53                      GPL17692                     288 Samples
#> 54                      GPL29450                       4 Samples
#> 55                      GPL20301                      60 Samples
#> 56                      GPL24676                       8 Samples
#> 57                      GPL20301                      18 Samples
#> 58                      GPL18573                       4 Samples
#> 59                      GPL24676                      12 Samples
#> 60                      GPL24676                      47 Samples
#> 61                      GPL18573                      11 Samples
#> 62                      GPL18573                       6 Samples
#> 63             GPL24522 GPL20795                      19 Samples
#> 64                      GPL20795                       3 Samples
#> 65                      GPL20795                      12 Samples
#> 66                      GPL20301                       9 Samples
#> 67                      GPL21145                      28 Samples
#> 68                      GPL13534                      48 Samples
#> 69                      GPL13534                      42 Samples
#> 70             GPL20301 GPL24247                       8 Samples
#> 71                      GPL20795                       6 Samples
#> 72                      GPL24676                      34 Samples
#> 73                      GPL11154                       6 Samples
#> 74                      GPL24676                       6 Samples
#> 75                      GPL22120                       6 Samples
#> 76                      GPL28148                      12 Samples
#> 77                      GPL18573                       2 Samples
#> 78                      GPL24676                      18 Samples
#> 79                        GPL570                      12 Samples
#> 80                      GPL21697                       8 Samples
#> 81                      GPL16956                      18 Samples
#> 82             GPL19057 GPL18573                      50 Samples
#> 83                      GPL18573                      36 Samples
#> 84                      GPL18573                      43 Samples
#> 85                      GPL20844                      40 Samples
#> 86                      GPL20844                      40 Samples
#> 87                      GPL20301                      24 Samples
#> 88                      GPL20301                       8 Samples
#> 89                      GPL20301                      16 Samples
#> 90                      GPL17303                       6 Samples
#> 91                      GPL20795                     560 Samples
#> 92                      GPL20301                      74 Samples
#> 93                      GPL23976                      40 Samples
#> 94                      GPL11154                      82 Samples
#> 95                      GPL11154                      41 Samples
#> 96                      GPL11154                      41 Samples
#> 97                      GPL21290                       9 Samples
#> 98                      GPL18573                    3343 Samples
#> 99                      GPL16699                       8 Samples
#> 100                     GPL21145                      60 Samples
#> 101                     GPL18573                      13 Samples
#> 102                     GPL16791                      15 Samples
#> 103                     GPL16791                      15 Samples
#> 104                     GPL21827                       6 Samples
#> 105                     GPL24676                      29 Samples
#> 106                     GPL16791                       6 Samples
#> 107                     GPL20301                      21 Samples
#> 108                     GPL25864                     204 Samples
#> 109                     GPL25864                     166 Samples
#> 110                     GPL16791                       4 Samples
#> 111                     GPL18573                      70 Samples
#> 112                     GPL11154                       8 Samples
#> 113                     GPL11154                       4 Samples
#> 114                     GPL11154                       4 Samples
#> 115                     GPL28038                      20 Samples
#> 116                      GPL5082                      40 Samples
#> 117                     GPL24676                       6 Samples
#> 118                     GPL20301                       4 Samples
#> 119                     GPL20301                       7 Samples
#> 120                     GPL16791                    9600 Samples
#> 121                     GPL16791                       9 Samples
#> 122                     GPL24676                      54 Samples
#> 123                     GPL15433                      24 Samples
#> 124                     GPL23159                      16 Samples
#> 125                     GPL21697                      23 Samples
#> 126            GPL24335 GPL30889                      31 Samples
#> 127                     GPL20301                       6 Samples
#> 128                     GPL18573                       6 Samples
#> 129                     GPL29503                     318 Samples
#> 130            GPL21273 GPL20795                      14 Samples
#> 131            GPL24676 GPL18573                      16 Samples
#> 132                     GPL15520                      12 Samples
#> 133                     GPL20795                       2 Samples
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#> 777                      GPL6104                      16 Samples
#> 778                     GPL15520                      10 Samples
#> 779                       GPL570                      19 Samples
#> 780                     GPL13667                     802 Samples
#> 781                     GPL11532                      14 Samples
#> 782                      GPL6244                      42 Samples
#> 783                     GPL10850                      96 Samples
#> 784                      GPL8786                       4 Samples
#> 785                     GPL11154                      24 Samples
#> 786                     GPL10558                     138 Samples
#> 787                      GPL6244                      53 Samples
#> 788                       GPL570                       4 Samples
#> 789                      GPL6244                      40 Samples
#> 790                       GPL570                     114 Samples
#> 791                        GPL80                      96 Samples
#> 792                     GPL17586                       8 Samples
#> 793   GPL17537 GPL19631 GPL16686                      20 Samples
#> 794                     GPL17537                       8 Samples
#> 795                     GPL19631                       6 Samples
#> 796                     GPL16686                       6 Samples
#> 797            GPL16770 GPL14860                      28 Samples
#> 798                     GPL16770                      16 Samples
#> 799                      GPL4133                     102 Samples
#> 800                       GPL570                      38 Samples
#> 801            GPL16791 GPL11154                       6 Samples
#> 802                      GPL5175                      20 Samples
#> 803                         <NA>  4 related Platforms 36 Samples
#> 804                     GPL18056                      16 Samples
#> 805                     GPL13534                      60 Samples
#> 806                     GPL14550                      23 Samples
#> 807                       GPL570                      99 Samples
#> 808                     GPL13534                      70 Samples
#> 809                      GPL9777                      49 Samples
#> 810                     GPL16956                       6 Samples
#> 811                       GPL571                     480 Samples
#> 812            GPL19296 GPL19295                     220 Samples
#> 813                     GPL19295                     101 Samples
#> 814                      GPL6244                      36 Samples
#> 815            GPL19520 GPL19521                      86 Samples
#> 816                     GPL15456                     134 Samples
#> 817                     GPL11434                       6 Samples
#> 818                     GPL13607                      64 Samples
#> 819                      GPL6102                      97 Samples
#> 820                       GPL570                      23 Samples
#> 821                      GPL7724                      22 Samples
#> 822                     GPL15314                      10 Samples
#> 823                     GPL11154                      30 Samples
#> 824                     GPL10558                      12 Samples
#> 825                     GPL14951                      12 Samples
#> 826                     GPL19316                     104 Samples
#> 827                      GPL6244                       9 Samples
#> 828                     GPL11154                       6 Samples
#> 829                      GPL6801                       4 Samples
#> 830                     GPL10558                       2 Samples
#> 831                     GPL16956                      12 Samples
#> 832                     GPL18545                     969 Samples
#> 833            GPL16288 GPL18544                      40 Samples
#> 834                     GPL18544                      30 Samples
#> 835                     GPL11532                      12 Samples
#> 836                     GPL17930                      23 Samples
#> 837                     GPL10999                       2 Samples
#> 838                     GPL11154                       4 Samples
#> 839                      GPL5175                      16 Samples
#> 840                      GPL6884                       9 Samples
#> 841               GPL8786 GPL570                      44 Samples
#> 842                      GPL8786                      22 Samples
#> 843                       GPL570                      22 Samples
#> 844                     GPL13669                      59 Samples
#> 845                      GPL6244                      89 Samples
#> 846                     GPL13886                       8 Samples
#> 847                         <NA>                            <NA>
#> 848                     GPL14767                      20 Samples
#> 849    GPL15207 GPL1261 GPL13534                      24 Samples
#> 850                     GPL18716                      12 Samples
#> 851                       GPL570                     286 Samples
#> 852                      GPL8490                      22 Samples
#> 853                     GPL10558                      45 Samples
#> 854                      GPL6947                      36 Samples
#> 855                      GPL8490                     100 Samples
#> 856                       GPL570                       9 Samples
#> 857                     GPL16597                      60 Samples
#> 858                      GPL6102                     410 Samples
#> 859                      GPL6244                     128 Samples
#> 860                       GPL571                     378 Samples
#> 861                     GPL13667                     356 Samples
#> 862     GPL13667 GPL6947 GPL6102                     724 Samples
#> 863                      GPL6947                     247 Samples
#> 864                      GPL6102                      58 Samples
#> 865                      GPL6102                      63 Samples
#> 866                     GPL17346                       4 Samples
#> 867          GPL10558 12 Samples                            5167
#> 868                     GPL16686                      38 Samples
#> 869                     GPL15018                      40 Samples
#> 870                      GPL9115                      10 Samples
#> 871                      GPL6480                      16 Samples
#> 872                      GPL6480                      10 Samples
#> 873              GPL570 GPL11162                     130 Samples
#> 874                     GPL11162                      65 Samples
#> 875                       GPL570                      65 Samples
#> 876                      GPL4133                      28 Samples
#> 877                     GPL15802                     300 Samples
#> 878                     GPL16311                      90 Samples
#> 879                      GPL2507                      12 Samples
#> 880                       GPL570                      13 Samples
#> 881            GPL11154 GPL10999                      12 Samples
#> 882                     GPL13534                      47 Samples
#> 883                     GPL17938                       3 Samples
#> 884                     GPL11154                       2 Samples
#> 885                      GPL8786                      12 Samples
#> 886                      GPL9115                       9 Samples
#> 887                     GPL11154                       4 Samples
#> 888                      GPL6480                      15 Samples
#> 889                       GPL570                     150 Samples
#> 890                      GPL6244                      26 Samples
#> 891                     GPL11532                      18 Samples
#> 892                      GPL6244                      17 Samples
#> 893                     GPL13534                      10 Samples
#> 894                      GPL6480                      79 Samples
#> 895            GPL10999 GPL11154                      44 Samples
#> 896                      GPL5175                       9 Samples
#> 897                      GPL4133                      12 Samples
#> 898                      GPL7020                       6 Samples
#> 899                      GPL8300                       9 Samples
#> 900                      GPL8300                      10 Samples
#> 901            GPL11670 GPL14663                     229 Samples
#> 902            GPL14663 GPL11670                     107 Samples
#> 903            GPL11670 GPL14663                     122 Samples
#> 904                     GPL10558                       6 Samples
#> 905             GPL6884 GPL10558                      12 Samples
#> 906                      GPL6884                       6 Samples
#> 907                       GPL570                      52 Samples
#> 908                     GPL17232                       6 Samples
#> 909               GPL570 GPL1355                      39 Samples
#> 910                       GPL570                       6 Samples
#> 911                      GPL6480                      44 Samples
#> 912                      GPL6480                      62 Samples
#> 913                      GPL6884                     229 Samples
#> 914                     GPL13376                     298 Samples
#> 915                      GPL6883                       5 Samples
#> 916                      GPL6244                      10 Samples
#> 917                     GPL16548                      15 Samples
#> 918                     GPL16548                      12 Samples
#> 919                     GPL16548                       3 Samples
#> 920                     GPL10379                      14 Samples
#> 921                      GPL6884                     180 Samples
#> 922             GPL570 6 Samples                            5178
#> 923                      GPL8490                      32 Samples
#> 924                      GPL6883                      12 Samples
#> 925                      GPL8882                      76 Samples
#> 926                      GPL6480                      28 Samples
#> 927                      GPL6480                      24 Samples
#> 928                      GPL6480                      24 Samples
#> 929                      GPL6947                      24 Samples
#> 930                      GPL6947                      24 Samples
#> 931                      GPL6947                      24 Samples
#> 932                     GPL13607                      24 Samples
#> 933                     GPL10558                      23 Samples
#> 934                      GPL8179                      23 Samples
#> 935            GPL570 10 Samples                            4399
#> 936                       GPL570                     114 Samples
#> 937                       GPL570                      28 Samples
#> 938                       GPL570                     203 Samples
#> 939                       GPL570                      12 Samples
#> 940                       GPL570                      49 Samples
#> 941                      GPL9460                      19 Samples
#> 942                       GPL570                      58 Samples
#> 943                      GPL8179                      35 Samples
#> 944                  GPL96 GPL97                      26 Samples
#> 945           GPL6244 63 Samples                            4337
#> 946              GPL6480 GPL9128                     248 Samples
#> 947                      GPL6480                     124 Samples
#> 948                     GPL11154                       9 Samples
#> 949                       GPL570                       8 Samples
#> 950      GPL6244 GPL7583 GPL7408                      25 Samples
#> 951                      GPL7408                      10 Samples
#> 952                      GPL7583                      11 Samples
#> 953                      GPL6244                       4 Samples
#> 954                      GPL6947                      22 Samples
#> 955                      GPL7363                      34 Samples
#> 956                      GPL6102                      48 Samples
#> 957                     GPL11432                      15 Samples
#> 958                      GPL4372                     249 Samples
#> 959                       GPL570                       4 Samples
#> 960              GPL6947 GPL6887                      58 Samples
#> 961                       GPL570                      32 Samples
#> 962                      GPL6884                       2 Samples
#> 963                      GPL8490                      16 Samples
#> 964            GPL570 18 Samples                            4354
#> 965                      GPL6947                     204 Samples
#> 966                      GPL9052                       5 Samples
#> 967                      GPL6244                      54 Samples
#> 968           GPL6244 24 Samples                            4314
#> 969             GPL9052 GPL10999                      25 Samples
#> 970                     GPL14689                      37 Samples
#> 971                      GPL9115                      10 Samples
#> 972           GPL6244 56 Samples                            4412
#> 973                       GPL570                      18 Samples
#> 974                     GPL10335                      26 Samples
#> 975            GPL14644 GPL14638                     118 Samples
#> 976                      GPL9946                       6 Samples
#> 977            GPL570 40 Samples                            4521
#> 978            GPL571 21 Samples                            3980
#> 979          GPL11532 20 Samples                            3981
#> 980                      GPL6480                      40 Samples
#> 981                      GPL6801                      20 Samples
#> 982             GPL6883 GPL14951                      37 Samples
#> 983                      GPL6883                      15 Samples
#> 984                      GPL6883                      14 Samples
#> 985                     GPL11097                      32 Samples
#> 986                      GPL6947                      30 Samples
#> 987                      GPL8490                     168 Samples
#> 988                      GPL6480                     141 Samples
#> 989          GPL10526 96 Samples                            4562
#> 990                       GPL571                      25 Samples
#> 991                       GPL571                      22 Samples
#> 992                       GPL571                      22 Samples
#> 993                       GPL571                      69 Samples
#> 994                      GPL6947                      36 Samples
#> 995             GPL96 33 Samples                            3983
#> 996           GPL6244 11 Samples                            3984
#> 997          GPL9392 166 Samples                            4228
#> 998                       GPL570                       9 Samples
#> 999   GPL13273 GPL570 45 Samples                            3961
#> 1000          GPL6244 20 Samples                            4276
#> 1001                      GPL570                      33 Samples
#> 1002                     GPL9115                       5 Samples
#> 1003                      GPL571                       9 Samples
#> 1004                    GPL10850                      15 Samples
#> 1005                    GPL13507                      29 Samples
#> 1006            GPL570 4 Samples                            4798
#> 1007           GPL570 50 Samples                            3884
#> 1008                     GPL9052                       2 Samples
#> 1009             GPL96 8 Samples                            3889
#> 1010                    GPL11624                      48 Samples
#> 1011          GPL6102 22 Samples                            3881
#> 1012                     GPL6947                      11 Samples
#> 1013                     GPL7350                       5 Samples
#> 1014 GPL6883 GPL10322 60 Samples                            3963
#> 1015                    GPL10322                      10 Samples
#> 1016                     GPL5082                      16 Samples
#> 1017                     GPL6984                      12 Samples
#> 1018            GPL96 13 Samples                            3882
#> 1019                    GPL10113                      60 Samples
#> 1020                      GPL570                      24 Samples
#> 1021           GPL570 42 Samples                            3880
#> 1022                     GPL9052                      15 Samples
#> 1023                     GPL9115                      24 Samples
#> 1024                     GPL9052                      25 Samples
#> 1025                     GPL6254                       8 Samples
#> 1026            GPL570 7 Samples                            4011
#> 1027         GPL10526 35 Samples                            4012
#> 1028                     GPL6480                      60 Samples
#> 1029                      GPL570                      42 Samples
#> 1030                     GPL9275                     112 Samples
#> 1031                    GPL10775                      35 Samples
#> 1032                     GPL2725                      15 Samples
#> 1033                     GPL9053                      56 Samples
#> 1034                     GPL4133                      36 Samples
#> 1035                     GPL4133                      24 Samples
#> 1036           GPL570 17 Samples                            3883
#> 1037                       GPL96                      12 Samples
#> 1038           GPL91 110 Samples                            3715
#> 1039                      GPL570                      12 Samples
#> 1040                     GPL7731                      28 Samples
#> 1041            GPL6883 GPL10322                      50 Samples
#> 1042                     GPL9188                      49 Samples
#> 1043                       GPL80                      20 Samples
#> 1044          GPL570 224 Samples                            4130
#> 1045          GPL1352 20 Samples                            3782
#> 1046                     GPL8490                     195 Samples
#> 1047                     GPL9057                      10 Samples
#> 1048          GPL6884 18 Samples                            3649
#> 1049                     GPL9486                     118 Samples
#> 1050                     GPL9081                      19 Samples
#> 1051                        <NA> 5 related Platforms 758 Samples
#> 1052                     GPL8450                      40 Samples
#> 1053          GPL2700 32 Samples                            3656
#> 1054                     GPL7274                      26 Samples
#> 1055                GPL96 GPL570                      34 Samples
#> 1056                     GPL7397                     161 Samples
#> 1057                     GPL9268                       2 Samples
#> 1058                      GPL571                       2 Samples
#> 1059                     GPL6244                      18 Samples
#> 1060                        <NA> 6 related Platforms 878 Samples
#> 1061           GPL570 33 Samples                            4027
#> 1062             GPL6101 GPL8843                      25 Samples
#> 1063                     GPL8843                       8 Samples
#> 1064                     GPL5106                      71 Samples
#> 1065             GPL6947 GPL6106                     106 Samples
#> 1066                      GPL571                       4 Samples
#> 1067          GPL2986 10 Samples                            3665
#> 1068            GPL96 18 Samples                            3876
#> 1069           GPL570 12 Samples                            4030
#> 1070               GPL887 GPL890                      33 Samples
#> 1071                     GPL7166                       4 Samples
#> 1072                      GPL570                     247 Samples
#> 1073          GPL5104 57 Samples                            3658
#> 1074           GPL570 43 Samples                            4133
#> 1075          GPL8300 20 Samples                            3681
#> 1076                 GPL96 GPL97                     471 Samples
#> 1077                 GPL96 GPL97                     546 Samples
#> 1078                     GPL2986                      10 Samples
#> 1079                     GPL4372                     427 Samples
#> 1080           GPL570 12 Samples                            4037
#> 1081                GPL571 GPL96                      54 Samples
#> 1082           GPL570 59 Samples                            3326
#> 1083                      GPL571                      24 Samples
#> 1084           GPL570 29 Samples                            3104
#> 1085                        <NA>  9 related Platforms 59 Samples
#> 1086             GPL5834 GPL5835                       8 Samples
#> 1087            GPL96 36 Samples                            3181
#> 1088     GPL96 GPL97 234 Samples                            3875
#> 1089                        <NA>  4 related Platforms 44 Samples
#> 1090                     GPL5166                       4 Samples
#> 1091      GPL80 GPL96 24 Samples                            2791
#> 1092                     GPL4779                       3 Samples
#> 1093            GPL570 6 Samples                            2548
#> 1094                     GPL1708                       4 Samples
#> 1095                     GPL2750                       3 Samples
#> 1096                     GPL1708                       8 Samples
#> 1097            GPL96 17 Samples                            2084
#> 1098                     GPL3271                       6 Samples
#> 1099            GPL96 12 Samples                            1499
#> 1100                      GPL538                      67 Samples
#> 1101     GPL97 GPL96 242 Samples                            2855
#> 1102                 GPL96 GPL97                      40 Samples
#> 1103                      GPL310                        1 Sample
#> 1104                      GPL887                      21 Samples
#> 1105           GPL8300 6 Samples                             961
#> 1106                      GPL120                       4 Samples
#> 1107                        <NA>  5 related Platforms 50 Samples
#>                                                                                   FTP download
#> 1                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE197nnn/GSE197881/
#> 2                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE191nnn/GSE191210/
#> 3                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE207nnn/GSE207901/
#> 4                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE205nnn/GSE205668/
#> 5                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173735/
#> 6                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173734/
#> 7                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE202nnn/GSE202295/
#> 8                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE207nnn/GSE207122/
#> 9                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE197nnn/GSE197850/
#> 10                  GEO (PAIR, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188395/
#> 11                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153315/
#> 12                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE200nnn/GSE200678/
#> 13                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE206nnn/GSE206528/
#> 14                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE200nnn/GSE200659/
#> 15                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE201nnn/GSE201908/
#> 16                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE199nnn/GSE199437/
#> 17                       GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE199nnn/GSE199852/
#> 18                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE198nnn/GSE198520/
#> 19            GEO (NARROWPEAK, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185728/
#> 20                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE176nnn/GSE176145/
#> 21                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133666/
#> 22                   GEO (TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE203nnn/GSE203346/
#> 23            GEO (BEDGRAPH, RDATA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE203nnn/GSE203169/
#> 24              GEO (BEDGRAPH, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE203nnn/GSE203353/
#> 25                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135076/
#> 26                        GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE192nnn/GSE192541/
#> 27                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE202nnn/GSE202151/
#> 28                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE194nnn/GSE194156/
#> 29                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE194nnn/GSE194155/
#> 30                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE194nnn/GSE194154/
#> 31                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE175nnn/GSE175759/
#> 32                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE201nnn/GSE201543/
#> 33               GEO (BIGWIG, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181478/
#> 34                     GEO (BIGWIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181412/
#> 35                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180521/
#> 36                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE200nnn/GSE200983/
#> 37                        GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE200nnn/GSE200477/
#> 38                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE186nnn/GSE186883/
#> 39                        GEO (RCC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185845/
#> 40                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE199nnn/GSE199939/
#> 41                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188827/
#> 42                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE186nnn/GSE186021/
#> 43                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182138/
#> 44                  GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE199nnn/GSE199700/
#> 45                   GEO (TXT, XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE199nnn/GSE199148/
#> 46                    GEO (FA, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185052/
#> 47                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185191/
#> 48                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185190/
#> 49                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185189/
#> 50                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193161/
#> 51                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162622/
#> 52                 GEO (CSV, FASTA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE197nnn/GSE197456/
#> 53                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE197nnn/GSE197285/
#> 54                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162273/
#> 55                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE126nnn/GSE126803/
#> 56                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE196nnn/GSE196900/
#> 57                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193436/
#> 58              GEO (CSV, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166641/
#> 59                   GEO (CSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE167nnn/GSE167199/
#> 60                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159586/
#> 61                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159554/
#> 62                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166640/
#> 63                   GEO (CSV, TAR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185038/
#> 64                   GEO (CSV, TAR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185036/
#> 65                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185035/
#> 66                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE189nnn/GSE189849/
#> 67                       GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE186nnn/GSE186766/
#> 68                       GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE113nnn/GSE113409/
#> 69                       GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE113nnn/GSE113392/
#> 70                   GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163947/
#> 71                   GEO (TAR, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165784/
#> 72                   GEO (TXT, XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE176nnn/GSE176230/
#> 73                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166822/
#> 74                         GEO (H5) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE194nnn/GSE194061/
#> 75                  GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE194nnn/GSE194119/
#> 76                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193974/
#> 77                  GEO (GTF, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182259/
#> 78                  GEO (XLS, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE172nnn/GSE172148/
#> 79                   GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE167nnn/GSE167269/
#> 80                        GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193510/
#> 81                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193626/
#> 82                   GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE176nnn/GSE176171/
#> 83                        GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE176nnn/GSE176067/
#> 84                   GEO (TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE174nnn/GSE174475/
#> 85                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE193nnn/GSE193273/
#> 86                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156035/
#> 87                   GEO (BEDGRAPH) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154415/
#> 88                       GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154414/
#> 89                   GEO (BEDGRAPH) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154413/
#> 90                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE113nnn/GSE113199/
#> 91                   GEO (CSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181143/
#> 92                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142178/
#> 93                       GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162166/
#> 94                              GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE190nnn/GSE190973/
#> 95                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE190nnn/GSE190972/
#> 96                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE190nnn/GSE190971/
#> 97                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE184nnn/GSE184831/
#> 98                  GEO (CSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182870/
#> 99                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE190nnn/GSE190832/
#> 100                 GEO (CSV, IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180355/
#> 101                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE174nnn/GSE174481/
#> 102                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188235/
#> 103                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188234/
#> 104                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE189nnn/GSE189923/
#> 105                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185430/
#> 106                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181328/
#> 107                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159955/
#> 108                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123088/
#> 109                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123086/
#> 110                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE189nnn/GSE189107/
#> 111                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140842/
#> 112                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162135/
#> 113                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162133/
#> 114                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161989/
#> 115                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE188nnn/GSE188799/
#> 116             GEO (CEL, CHP, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE189nnn/GSE189007/
#> 117                 GEO (CSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162837/
#> 118                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE137nnn/GSE137766/
#> 119                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136887/
#> 120                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98887/
#> 121                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE186nnn/GSE186524/
#> 122                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165816/
#> 123                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE179nnn/GSE179568/
#> 124                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182494/
#> 125                  GEO (DCC, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166120/
#> 126                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE186nnn/GSE186432/
#> 127                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180470/
#> 128                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185598/
#> 129                       GEO (RCC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163211/
#> 130                 GEO (CSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE185nnn/GSE185749/
#> 131                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142290/
#> 132                       GEO (ZIP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE175nnn/GSE175477/
#> 133                        GEO (H5) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141319/
#> 134                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182923/
#> 135                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180504/
#> 136                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159924/
#> 137                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139947/
#> 138                      GEO (H5AD) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE178nnn/GSE178991/
#> 139                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156911/
#> 140                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE169nnn/GSE169514/
#> 141                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE184nnn/GSE184050/
#> 142                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE184nnn/GSE184016/
#> 143                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE183nnn/GSE183965/
#> 144                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE183nnn/GSE183701/
#> 145                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE183nnn/GSE183568/
#> 146                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72991/
#> 147            GEO (BW, NARROWPEAK) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173277/
#> 148                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173228/
#> 149                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165709/
#> 150                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165708/
#> 151                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165703/
#> 152                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182737/
#> 153                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE122nnn/GSE122279/
#> 154                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159337/
#> 155                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182121/
#> 156                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182120/
#> 157                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182117/
#> 158                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE182nnn/GSE182053/
#> 159                  GEO (BED, TAB) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159867/
#> 160                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181881/
#> 161                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144414/
#> 162                 GEO (XLS, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE181nnn/GSE181674/
#> 163                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE118nnn/GSE118139/
#> 164                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173276/
#> 165                 GEO (TAR, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168071/
#> 166                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE179nnn/GSE179921/
#> 167                  GEO (BED, TDF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE179nnn/GSE179762/
#> 168                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168996/
#> 169                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163773/
#> 170                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180083/
#> 171                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE180nnn/GSE180081/
#> 172                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150212/
#> 173                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153837/
#> 174                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156411/
#> 175                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153834/
#> 176             GEO (H5, JSON, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE179nnn/GSE179143/
#> 177                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150724/
#> 178                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE178nnn/GSE178828/
#> 179                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE178nnn/GSE178721/
#> 180                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173983/
#> 181                   GEO (BED, BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE178nnn/GSE178734/
#> 182        GEO (BED, BROADPEAK, BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE178nnn/GSE178733/
#> 183                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156122/
#> 184                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156121/
#> 185                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156061/
#> 186                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE122nnn/GSE122086/
#> 187                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE176nnn/GSE176324/
#> 188                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173669/
#> 189                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165385/
#> 190                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE175nnn/GSE175745/
#> 191                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE175nnn/GSE175735/
#> 192                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114860/
#> 193                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE174nnn/GSE174502/
#> 194                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173613/
#> 195                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136344/
#> 196                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE173nnn/GSE173193/
#> 197                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE157nnn/GSE157988/
#> 198                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159556/
#> 199                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160310/
#> 200                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160308/
#> 201                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160306/
#> 202                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153410/
#> 203                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE164nnn/GSE164416/
#> 204               GEO (BW, H5, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151426/
#> 205                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141432/
#> 206                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136395/
#> 207                   GEO (BED, BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151405/
#> 208                        GEO (H5) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148073/
#> 209                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148642/
#> 210                  GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148640/
#> 211                  GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148639/
#> 212                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168437/
#> 213                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166785/
#> 214                   GEO (BW, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE167nnn/GSE167250/
#> 215                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112168/
#> 216                      GEO (DATA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162521/
#> 217                  GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163160/
#> 218                       GEO (DAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166047/
#> 219                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151497/
#> 220                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151496/
#> 221                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151495/
#> 222                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168492/
#> 223                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168072/
#> 224                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE168nnn/GSE168327/
#> 225             GEO (CSV, MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE167nnn/GSE167976/
#> 226                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE167nnn/GSE167914/
#> 227                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162689/
#> 228                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE165nnn/GSE165121/
#> 229                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166847/
#> 230                 GEO (CSV, IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166845/
#> 231                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166787/
#> 232                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166652/
#> 233                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166502/
#> 234                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE166nnn/GSE166467/
#> 235                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110829/
#> 236                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110828/
#> 237       GEO (CSV, MTX, TSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE158nnn/GSE158055/
#> 238                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE157nnn/GSE157640/
#> 239                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159717/
#> 240                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE147nnn/GSE147890/
#> 241                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153221/
#> 242                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153220/
#> 243                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153219/
#> 244                    GEO (BIGWIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE149nnn/GSE149148/
#> 245                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE164nnn/GSE164934/
#> 246                       GEO (HIC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163610/
#> 247                       GEO (HIC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160474/
#> 248                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160473/
#> 249                  GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160472/
#> 250                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161355/
#> 251                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE164nnn/GSE164338/
#> 252                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25194/
#> 253                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139577/
#> 254                  GEO (TXT, XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE118nnn/GSE118103/
#> 255                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163980/
#> 256                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163744/
#> 257                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163732/
#> 258                        GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150172/
#> 259                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163603/
#> 260                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE163nnn/GSE163510/
#> 261                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE158nnn/GSE158292/
#> 262                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162830/
#> 263                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE157nnn/GSE157515/
#> 264                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE162nnn/GSE162557/
#> 265                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE147nnn/GSE147965/
#> 266                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142401/
#> 267                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142153/
#> 268                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE149nnn/GSE149568/
#> 269                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE157nnn/GSE157859/
#> 270                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161914/
#> 271                  GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161721/
#> 272                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161720/
#> 273                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE161nnn/GSE161719/
#> 274                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154306/
#> 275                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144348/
#> 276                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141065/
#> 277     GEO (IDAT, NARROWPEAK, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145747/
#> 278           GEO (NARROWPEAK, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145746/
#> 279                 GEO (CSV, IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145745/
#> 280                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE160nnn/GSE160005/
#> 281             GEO (CSV, TAB, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159984/
#> 282                 GEO (CSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159759/
#> 283                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154378/
#> 284                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154377/
#> 285                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154348/
#> 286                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE132nnn/GSE132831/
#> 287                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE159nnn/GSE159467/
#> 288                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154609/
#> 289                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154126/
#> 290                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143783/
#> 291                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE152nnn/GSE152615/
#> 292                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE134nnn/GSE134431/
#> 293                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151764/
#> 294                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE157nnn/GSE157177/
#> 295                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154554/
#> 296                       GEO (RCC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143690/
#> 297                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156993/
#> 298                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140308/
#> 299                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156903/
#> 300                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148061/
#> 301                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148060/
#> 302                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148059/
#> 303                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE146nnn/GSE146028/
#> 304                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156249/
#> 305                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156248/
#> 306                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156247/
#> 307                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156341/
#> 308                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156340/
#> 309                     GEO (BEDPE) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156339/
#> 310      GEO (BEDPE, MTX, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135357/
#> 311                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135356/
#> 312                     GEO (BEDPE) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135355/
#> 313                     GEO (BEDPE) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135354/
#> 314            GEO (GTF, TSV, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE156nnn/GSE156109/
#> 315                      GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143209/
#> 316                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102485/
#> 317                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151683/
#> 318                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE155nnn/GSE155713/
#> 319                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144682/
#> 320                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143735/
#> 321           GEO (NARROWPEAK, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131169/
#> 322                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138781/
#> 323                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE155nnn/GSE155188/
#> 324                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151588/
#> 325                       GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109163/
#> 326                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153565/
#> 327                       GEO (RCC) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148961/
#> 328                  GEO (RCC, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154647/
#> 329                 GEO (CEL, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154629/
#> 330                 GEO (CEL, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE154nnn/GSE154628/
#> 331                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114192/
#> 332                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153792/
#> 333                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE153nnn/GSE153555/
#> 334                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE134nnn/GSE134594/
#> 335                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140959/
#> 336                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133225/
#> 337                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133217/
#> 338                GEO (CSV, FASTA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150060/
#> 339                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151889/
#> 340                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE121nnn/GSE121221/
#> 341                GEO (DOCX, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE151nnn/GSE151610/
#> 342                       GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145593/
#> 343                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123658/
#> 344                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115221/
#> 345                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE146nnn/GSE146338/
#> 346                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144605/
#> 347                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE147nnn/GSE147740/
#> 348                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145284/
#> 349                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE113nnn/GSE113969/
#> 350                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150586/
#> 351                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150621/
#> 352                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE150nnn/GSE150119/
#> 353                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139535/
#> 354                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148896/
#> 355                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148812/
#> 356                       GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148058/
#> 357                       GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133219/
#> 358                       GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133218/
#> 359                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143319/
#> 360                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE148nnn/GSE148375/
#> 361             GEO (BED, MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144693/
#> 362             GEO (BED, MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144692/
#> 363                       GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144691/
#> 364                 GEO (CEL, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE146nnn/GSE146108/
#> 365                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142385/
#> 366                 GEO (CSV, IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112652/
#> 367                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138323/
#> 368                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE126nnn/GSE126101/
#> 369                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE126nnn/GSE126100/
#> 370              GEO (BED, BW, CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE126nnn/GSE126099/
#> 371                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE145nnn/GSE145347/
#> 372                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139157/
#> 373                  GEO (MTX, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138857/
#> 374                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE146nnn/GSE146615/
#> 375                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142512/
#> 376        GEO (CSV, MTX, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139949/
#> 377                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95078/
#> 378                       GEO (TAB) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124742/
#> 379                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144908/
#> 380                    GEO (BEDGRAPH) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94729/
#> 381                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138598/
#> 382                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131528/
#> 383                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131526/
#> 384                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE125nnn/GSE125929/
#> 385                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144441/
#> 386                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE119nnn/GSE119296/
#> 387                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144169/
#> 388                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141639/
#> 389                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141309/
#> 390                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143979/
#> 391                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135155/
#> 392                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143495/
#> 393                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE143nnn/GSE143143/
#> 394                    GEO (BIGWIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142009/
#> 395       GEO (CEL, CHP, TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE121nnn/GSE121820/
#> 396                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124534/
#> 397                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139932/
#> 398                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133264/
#> 399                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131065/
#> 400                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE130nnn/GSE130279/
#> 401                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE122nnn/GSE122429/
#> 402                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94846/
#> 403                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142553/
#> 404                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141126/
#> 405                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE121nnn/GSE121346/
#> 406                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE121nnn/GSE121344/
#> 407                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE142nnn/GSE142025/
#> 408                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141512/
#> 409                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141410/
#> 410                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124272/
#> 411                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE141nnn/GSE141193/
#> 412                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140627/
#> 413                       GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140404/
#> 414                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140403/
#> 415             GEO (BED, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140065/
#> 416                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE140nnn/GSE140064/
#> 417                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139929/
#> 418                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135197/
#> 419                  GEO (BED, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124264/
#> 420                       GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115326/
#> 421                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115312/
#> 422                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115306/
#> 423                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135453/
#> 424                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135776/
#> 425             GEO (MTX, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129363/
#> 426                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE139nnn/GSE139073/
#> 427                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138885/
#> 428                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE138nnn/GSE138856/
#> 429                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131320/
#> 430                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112893/
#> 431                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114569/
#> 432                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114248/
#> 433                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114236/
#> 434                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE88nnn/GSE88839/
#> 435                  GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136048/
#> 436                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96971/
#> 437                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE137nnn/GSE137803/
#> 438                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136053/
#> 439                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE137nnn/GSE137136/
#> 440                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136865/
#> 441                        GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133135/
#> 442                        GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123404/
#> 443                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE137nnn/GSE137684/
#> 444                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE130nnn/GSE130672/
#> 445                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE137nnn/GSE137317/
#> 446                       GEO (RDS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE131nnn/GSE131882/
#> 447                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133910/
#> 448                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136353/
#> 449                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE136nnn/GSE136277/
#> 450            GEO (COV, TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE128nnn/GSE128289/
#> 451                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51674/
#> 452                  GEO (CSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE135nnn/GSE135944/
#> 453                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129935/
#> 454                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE132nnn/GSE132306/
#> 455                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE132nnn/GSE132111/
#> 456                  GEO (TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE120nnn/GSE120024/
#> 457                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE132nnn/GSE132187/
#> 458                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE88nnn/GSE88794/
#> 459                  GEO (CSV, TAB) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE133nnn/GSE133099/
#> 460                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE125nnn/GSE125769/
#> 461                       GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE125nnn/GSE125768/
#> 462                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE125nnn/GSE125590/
#> 463                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102677/
#> 464                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102633/
#> 465                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129112/
#> 466                  GEO (CSV, TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE121nnn/GSE121862/
#> 467                GEO (CEL, CYCHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE122nnn/GSE122584/
#> 468                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE130nnn/GSE130991/
#> 469                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114412/
#> 470                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129042/
#> 471                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129841/
#> 472                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE126nnn/GSE126169/
#> 473                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE101nnn/GSE101702/
#> 474                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129666/
#> 475                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129653/
#> 476                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129604/
#> 477                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129091/
#> 478                  GEO (BEDGRAPH) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE129nnn/GSE129383/
#> 479                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115020/
#> 480                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112690/
#> 481                  GEO (BED, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112342/
#> 482                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112341/
#> 483                  GEO (BED, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112337/
#> 484                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE128nnn/GSE128381/
#> 485                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE128nnn/GSE128331/
#> 486                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124811/
#> 487                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124810/
#> 488                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124809/
#> 489                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45515/
#> 490                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE127nnn/GSE127045/
#> 491                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE127nnn/GSE127042/
#> 492                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE127nnn/GSE127033/
#> 493                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124400/
#> 494                       GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE124nnn/GSE124284/
#> 495                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE127nnn/GSE127170/
#> 496                  GEO (TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115828/
#> 497                  GEO (RCC, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110786/
#> 498                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE103nnn/GSE103682/
#> 499                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77522/
#> 500                         GEO (WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77268/
#> 501                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104674/
#> 502                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115329/
#> 503                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115313/
#> 504               GEO (BIGWIG, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115421/
#> 505                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102295/
#> 506                  GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE118nnn/GSE118588/
#> 507                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109022/
#> 508                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104297/
#> 509                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71799/
#> 510                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE107nnn/GSE107375/
#> 511                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE78nnn/GSE78721/
#> 512                           GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9707/
#> 513                      GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE7nnn/GSE7319/
#> 514                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97554/
#> 515                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE108nnn/GSE108403/
#> 516    GEO (FA, GTF, MTX, TSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE120nnn/GSE120522/
#> 517                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123844/
#> 518                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE108nnn/GSE108056/
#> 519                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE117nnn/GSE117454/
#> 520                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116726/
#> 521                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE112nnn/GSE112594/
#> 522                  GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE123nnn/GSE123279/
#> 523                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE115nnn/GSE115257/
#> 524                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE107nnn/GSE107943/
#> 525                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110914/
#> 526                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116761/
#> 527                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE117nnn/GSE117469/
#> 528                             GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106181/
#> 529                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106177/
#> 530                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE105nnn/GSE105167/
#> 531                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE120nnn/GSE120904/
#> 532                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE120nnn/GSE120299/
#> 533                   GEO (BW, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE101nnn/GSE101207/
#> 534                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116559/
#> 535                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE118nnn/GSE118230/
#> 536                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE118nnn/GSE118481/
#> 537                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106800/
#> 538                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102498/
#> 539                       GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE108nnn/GSE108413/
#> 540                GEO (IDAT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106099/
#> 541                 GEO (CEL, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE103nnn/GSE103552/
#> 542                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE89nnn/GSE89475/
#> 543                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96804/
#> 544                       GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102371/
#> 545                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102234/
#> 546   GEO (BEDGRAPH, CEL, NARROWPEAK) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86376/
#> 547                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85990/
#> 548                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106953/
#> 549                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116497/
#> 550                  GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE111nnn/GSE111154/
#> 551                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116369/
#> 552                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83782/
#> 553                         GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83781/
#> 554                         GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83699/
#> 555                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE116nnn/GSE116029/
#> 556                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114477/
#> 557                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104815/
#> 558                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99853/
#> 559                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70365/
#> 560                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114908/
#> 561                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE114nnn/GSE114051/
#> 562                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110935/
#> 563                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84453/
#> 564                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37785/
#> 565                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE12nnn/GSE12844/
#> 566                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97205/
#> 567                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE113nnn/GSE113080/
#> 568                       GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109266/
#> 569                       GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109265/
#> 570                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE111nnn/GSE111876/
#> 571         GEO (CEL, CSV, IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98224/
#> 572                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106813/
#> 573                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95243/
#> 574                         GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98675/
#> 575                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE110nnn/GSE110552/
#> 576                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104423/
#> 577                         GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98485/
#> 578                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104195/
#> 579                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104190/
#> 580            GEO (GPR, XLS, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE105nnn/GSE105096/
#> 581                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102080/
#> 582                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102079/
#> 583                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104954/
#> 584                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE104nnn/GSE104948/
#> 585                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE93nnn/GSE93709/
#> 586                       GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109178/
#> 587                       GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE109nnn/GSE109140/
#> 588                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE92nnn/GSE92724/
#> 589                         GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE92nnn/GSE92772/
#> 590               GEO (CEL, CHP, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE80nnn/GSE80178/
#> 591                      GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106148/
#> 592                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76896/
#> 593                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76895/
#> 594                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76894/
#> 595                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77108/
#> 596                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE106nnn/GSE106520/
#> 597                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84814/
#> 598                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63992/
#> 599               GEO (CEL, CHP, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90076/
#> 600                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90074/
#> 601                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90073/
#> 602                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE105nnn/GSE105052/
#> 603                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81547/
#> 604                 GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE103nnn/GSE103931/
#> 605                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE103nnn/GSE103393/
#> 606                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75062/
#> 607                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE103nnn/GSE103657/
#> 608                    GEO (RCC, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97123/
#> 609                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE93nnn/GSE93032/
#> 610                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85192/
#> 611                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90999/
#> 612                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE74nnn/GSE74240/
#> 613                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87005/
#> 614                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99340/
#> 615                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99339/
#> 616                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99325/
#> 617                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86069/
#> 618                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97655/
#> 619                 GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE102nnn/GSE102177/
#> 620                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95368/
#> 621                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE101nnn/GSE101931/
#> 622                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94497/
#> 623                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94496/
#> 624                  GEO (GPR, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE101nnn/GSE101461/
#> 625                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86298/
#> 626                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83452/
#> 627              GEO (TXT, XLS, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE99nnn/GSE99068/
#> 628                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97647/
#> 629                         GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97591/
#> 630                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE100nnn/GSE100271/
#> 631                       GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE100nnn/GSE100185/
#> 632                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90028/
#> 633                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96569/
#> 634                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96568/
#> 635                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96564/
#> 636                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96563/
#> 637                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE96nnn/GSE96562/
#> 638                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98501/
#> 639                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98399/
#> 640                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57362/
#> 641                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97530/
#> 642                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE90nnn/GSE90117/
#> 643                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68475/
#> 644                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE98nnn/GSE98043/
#> 645                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81965/
#> 646                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94019/
#> 647                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE88nnn/GSE88929/
#> 648                         GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE97nnn/GSE97084/
#> 649                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84823/
#> 650                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84821/
#> 651                        GEO (DIFF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87626/
#> 652                          GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83345/
#> 653                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72490/
#> 654                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95849/
#> 655                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95675/
#> 656                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE95nnn/GSE95674/
#> 657                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE89nnn/GSE89360/
#> 658                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE78nnn/GSE78840/
#> 659                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE94nnn/GSE94649/
#> 660                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85226/
#> 661                    GEO (CEL, PDF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77962/
#> 662                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE89nnn/GSE89552/
#> 663                         GEO (TSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84714/
#> 664                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87893/
#> 665                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70318/
#> 666                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24555/
#> 667                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE64nnn/GSE64605/
#> 668                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87000/
#> 669                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85527/
#> 670                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84934/
#> 671                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87340/
#> 672                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85573/
#> 673                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85531/
#> 674                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85530/
#> 675                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE89nnn/GSE89022/
#> 676                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86473/
#> 677                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86469/
#> 678                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86468/
#> 679                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE89nnn/GSE89632/
#> 680                          GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65319/
#> 681                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87530/
#> 682                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63117/
#> 683                         GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67740/
#> 684             GEO (IDAT, TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87571/
#> 685                    GEO (CSV, PDF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85241/
#> 686                          GEO (BW) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE85nnn/GSE85928/
#> 687                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84971/
#> 688                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84133/
#> 689                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE87nnn/GSE87295/
#> 690                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE78nnn/GSE78922/
#> 691                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86884/
#> 692                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86611/
#> 693                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE86nnn/GSE86544/
#> 694                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81608/
#> 695                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72377/
#> 696                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72376/
#> 697                    GEO (TXT, XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67566/
#> 698                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE84nnn/GSE84908/
#> 699                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76398/
#> 700                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76394/
#> 701                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76285/
#> 702                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71301/
#> 703                    GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69705/
#> 704                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE58nnn/GSE58557/
#> 705                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67141/
#> 706                         GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76308/
#> 707                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE83nnn/GSE83139/
#> 708                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71678/
#> 709                   GEO (GPR, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63492/
#> 710                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72462/
#> 711               GEO (CSV, RTF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81076/
#> 712                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE79nnn/GSE79670/
#> 713                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE79nnn/GSE79668/
#> 714                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75248/
#> 715                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE74nnn/GSE74296/
#> 716                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE80nnn/GSE80569/
#> 717                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76171/
#> 718                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76170/
#> 719                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76169/
#> 720                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81258/
#> 721     GEO (BED, BROADPEAK, BW, CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE81nnn/GSE81255/
#> 722                         GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75941/
#> 723                   GEO (TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE78nnn/GSE78805/
#> 724                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65793/
#> 725                    GEO (TXT, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57628/
#> 726                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67705/
#> 727                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70901/
#> 728                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65057/
#> 729                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE64nnn/GSE64998/
#> 730                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE78nnn/GSE78891/
#> 731                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67775/
#> 732                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67774/
#> 733                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67773/
#> 734                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77350/
#> 735                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55311/
#> 736                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76161/
#> 737                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE77nnn/GSE77114/
#> 738                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76899/
#> 739                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51546/
#> 740                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62761/
#> 741                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60861/
#> 742                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60860/
#> 743                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45980/
#> 744                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44639/
#> 745                    GEO (BED, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76268/
#> 746                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76189/
#> 747                    GEO (CSV, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE76nnn/GSE76065/
#> 748                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE73nnn/GSE73034/
#> 749                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69438/
#> 750                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75685/
#> 751                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75678/
#> 752                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE75nnn/GSE75669/
#> 753                  GEO (BED, BEDPE) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69600/
#> 754                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE73nnn/GSE73408/
#> 755                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68526/
#> 756                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE74nnn/GSE74782/
#> 757                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70961/
#> 758                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69889/
#> 759                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65561/
#> 760                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE74nnn/GSE74629/
#> 761                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE74nnn/GSE74559/
#> 762                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE72nnn/GSE72492/
#> 763                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE41nnn/GSE41767/
#> 764                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE73nnn/GSE73418/
#> 765                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71730/
#> 766                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68049/
#> 767                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37025/
#> 768                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63423/
#> 769                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70752/
#> 770                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70494/
#> 771                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70493/
#> 772                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70453/
#> 773         GEO (CEL, CHP, TXT, XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21891/
#> 774                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71416/
#> 775                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69658/
#> 776                       GEO (RDATA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71102/
#> 777                       GEO (RDATA) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE71nnn/GSE71099/
#> 778                         GEO (TAB) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69595/
#> 779                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE70nnn/GSE70528/
#> 780                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65682/
#> 781                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67297/
#> 782                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE59nnn/GSE59363/
#> 783                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE59nnn/GSE59421/
#> 784                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE49nnn/GSE49885/
#> 785                        GEO (XLSX) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67543/
#> 786                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69528/
#> 787                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE69nnn/GSE69421/
#> 788                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE66nnn/GSE66785/
#> 789                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67279/
#> 790                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE48nnn/GSE48278/
#> 791                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68571/
#> 792                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60760/
#> 793                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68186/
#> 794                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68185/
#> 795                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68184/
#> 796                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68183/
#> 797                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68226/
#> 798                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE68nnn/GSE68224/
#> 799                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62117/
#> 800                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67738/
#> 801                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63887/
#> 802                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37084/
#> 803              GEO (GPR, TIFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE67nnn/GSE67567/
#> 804                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE53nnn/GSE53257/
#> 805                   GEO (IDAT, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62219/
#> 806                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE66nnn/GSE66413/
#> 807                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE66nnn/GSE66360/
#> 808                         GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62003/
#> 809                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55645/
#> 810                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE65nnn/GSE65737/
#> 811                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE66nnn/GSE66175/
#> 812                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62372/
#> 813                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62370/
#> 814                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62832/
#> 815                    GEO (TXT, XYS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE63nnn/GSE63981/
#> 816                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60424/
#> 817                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45856/
#> 818                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38267/
#> 819                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE34nnn/GSE34198/
#> 820                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55650/
#> 821                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38835/
#> 822                   GEO (TIFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE56nnn/GSE56081/
#> 823                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57896/
#> 824                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55465/
#> 825                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55464/
#> 826                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62523/
#> 827                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62500/
#> 828                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE62nnn/GSE62499/
#> 829               GEO (CEL, CHP, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE61nnn/GSE61769/
#> 830                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE61nnn/GSE61714/
#> 831                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE61nnn/GSE61166/
#> 832                        GEO (IDAT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE61nnn/GSE61129/
#> 833                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE56nnn/GSE56781/
#> 834                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE56nnn/GSE56685/
#> 835                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60803/
#> 836                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE52nnn/GSE52376/
#> 837                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55567/
#> 838                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55566/
#> 839                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42902/
#> 840                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE60nnn/GSE60436/
#> 841                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55100/
#> 842                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55099/
#> 843                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE55nnn/GSE55098/
#> 844                    GEO (GPR, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50866/
#> 845                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50397/
#> 846                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30575/
#> 847                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE58nnn/GSE58634/
#> 848                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44558/
#> 849                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57928/
#> 850                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57880/
#> 851                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE52nnn/GSE52724/
#> 852                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE57nnn/GSE57484/
#> 853                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50005/
#> 854                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51058/
#> 855                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE56nnn/GSE56606/
#> 856                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE48nnn/GSE48101/
#> 857                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44093/
#> 858                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29536/
#> 859                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE54nnn/GSE54279/
#> 860                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE46nnn/GSE46097/
#> 861                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43488/
#> 862                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30211/
#> 863                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30210/
#> 864                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30209/
#> 865                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30208/
#> 866                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE48nnn/GSE48318/
#> 867                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE54nnn/GSE54350/
#> 868                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE48nnn/GSE48354/
#> 869                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE48nnn/GSE48353/
#> 870                         GEO (GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE53nnn/GSE53949/
#> 871                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44314/
#> 872                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44313/
#> 873                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29623/
#> 874                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29622/
#> 875                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29621/
#> 876                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE28nnn/GSE28038/
#> 877                   GEO (GFF, PAIR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47385/
#> 878                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE53nnn/GSE53454/
#> 879                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE40nnn/GSE40878/
#> 880                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE36nnn/GSE36233/
#> 881                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE52nnn/GSE52314/
#> 882                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE40nnn/GSE40360/
#> 883                         GEO (LSR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE52nnn/GSE52422/
#> 884                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51924/
#> 885                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE52nnn/GSE52233/
#> 886                         GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51311/
#> 887                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE51nnn/GSE51310/
#> 888                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50800/
#> 889                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43580/
#> 890                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE33nnn/GSE33070/
#> 891                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42432/
#> 892                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50892/
#> 893                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE49nnn/GSE49667/
#> 894                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35279/
#> 895                         GEO (BED) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE50nnn/GSE50386/
#> 896                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42715/
#> 897                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE41nnn/GSE41744/
#> 898                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE49nnn/GSE49524/
#> 899                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE49nnn/GSE49566/
#> 900                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE39nnn/GSE39825/
#> 901                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47185/
#> 902                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47184/
#> 903                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47183/
#> 904                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE46nnn/GSE46899/
#> 905                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE46nnn/GSE46900/
#> 906                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE46nnn/GSE46897/
#> 907                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47874/
#> 908                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE47nnn/GSE47720/
#> 909                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE40nnn/GSE40498/
#> 910                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE40nnn/GSE40496/
#> 911                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42507/
#> 912                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE40nnn/GSE40234/
#> 913                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45986/
#> 914                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45792/
#> 915                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE45nnn/GSE45777/
#> 916                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE44nnn/GSE44035/
#> 917                    GEO (GFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43752/
#> 918                    GEO (GFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43751/
#> 919                    GEO (GFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43750/
#> 920                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE43nnn/GSE43950/
#> 921                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32909/
#> 922                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE34nnn/GSE34512/
#> 923                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38291/
#> 924                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE14nnn/GSE14368/
#> 925                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42487/
#> 926                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42229/
#> 927                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42228/
#> 928                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42227/
#> 929                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29231/
#> 930                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29226/
#> 931                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29221/
#> 932                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42148/
#> 933                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42094/
#> 934                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE42nnn/GSE42093/
#> 935                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE34nnn/GSE34526/
#> 936                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35725/
#> 937                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35716/
#> 938                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35713/
#> 939                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35712/
#> 940                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35711/
#> 941                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37794/
#> 942                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30161/
#> 943                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35851/
#> 944                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30802/
#> 945                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38642/
#> 946                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35191/
#> 947                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35186/
#> 948                    GEO (GFF, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38447/
#> 949                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE38nnn/GSE38396/
#> 950              GEO (CEL, GFF, PAIR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE36nnn/GSE36403/
#> 951                   GEO (GFF, PAIR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE36nnn/GSE36402/
#> 952                   GEO (GFF, PAIR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE36nnn/GSE36397/
#> 953                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE36nnn/GSE36084/
#> 954                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE33nnn/GSE33440/
#> 955                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19637/
#> 956                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32575/
#> 957                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE34nnn/GSE34223/
#> 958                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37824/
#> 959                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37901/
#> 960                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE28nnn/GSE28384/
#> 961                    GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE15nnn/GSE15932/
#> 962                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE37nnn/GSE37639/
#> 963                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21232/
#> 964                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30159/
#> 965                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32512/
#> 966                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29660/
#> 967                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26244/
#> 968                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26887/
#> 969                         GEO (BAM) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32874/
#> 970                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32691/
#> 971                    GEO (BED, GTF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35296/
#> 972                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE31nnn/GSE31901/
#> 973                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29908/
#> 974                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE35nnn/GSE35411/
#> 975                         GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32544/
#> 976                    GEO (GPR, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19943/
#> 977                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE22nnn/GSE22255/
#> 978                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13760/
#> 979                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32357/
#> 980                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24818/
#> 981                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE33nnn/GSE33032/
#> 982                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE28nnn/GSE28024/
#> 983                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE28nnn/GSE28022/
#> 984                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE27nnn/GSE27507/
#> 985                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE32nnn/GSE32553/
#> 986                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE27nnn/GSE27175/
#> 987                               GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE27nnn/GSE27317/
#> 988                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21815/
#> 989                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE31nnn/GSE31056/
#> 990                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30566/
#> 991                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30529/
#> 992                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30528/
#> 993                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30122/
#> 994                         GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23506/
#> 995                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30803/
#> 996                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30732/
#> 997                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE30nnn/GSE30310/
#> 998                         GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE28nnn/GSE28059/
#> 999                    GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE27nnn/GSE27951/
#> 1000                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29718/
#> 1001                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE27nnn/GSE27949/
#> 1002                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24326/
#> 1003                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23338/
#> 1004                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29190/
#> 1005                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29142/
#> 1006                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE29nnn/GSE29084/
#> 1007                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25462/
#> 1008                 GEO (BED, GRAPH) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25862/
#> 1009                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24193/
#> 1010                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26744/
#> 1011                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19790/
#> 1012                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21980/
#> 1013                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19649/
#> 1014                              GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26168/
#> 1015                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26167/
#> 1016                   GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE26nnn/GSE26073/
#> 1017                  GEO (IDAT, PDF) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25826/
#> 1018                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25724/
#> 1019                       GEO (PAIR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE20nnn/GSE20553/
#> 1020                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24422/
#> 1021                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19420/
#> 1022 GEO (BAM, BED, BIGWIG, TAGALIGN) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24685/
#> 1023                   GEO (BED, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE25nnn/GSE25249/
#> 1024                        GEO (WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23784/
#> 1025                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE16nnn/GSE16804/
#> 1026                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE14nnn/GSE14503/
#> 1027                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24290/
#> 1028                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24215/
#> 1029                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE24nnn/GSE24147/
#> 1030                        GEO (XYS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23858/
#> 1031                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23561/
#> 1032                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE18nnn/GSE18821/
#> 1033                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17710/
#> 1034                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE12nnn/GSE12385/
#> 1035                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE12nnn/GSE12384/
#> 1036                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE23nnn/GSE23343/
#> 1037                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21785/
#> 1038                   GEO (CEL, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE22nnn/GSE22309/
#> 1039                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21989/
#> 1040                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE18nnn/GSE18470/
#> 1041                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21321/
#> 1042                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17941/
#> 1043                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE21nnn/GSE21340/
#> 1044                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19519/
#> 1045                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE20nnn/GSE20966/
#> 1046                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE20nnn/GSE20067/
#> 1047                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17727/
#> 1048                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE20nnn/GSE20247/
#> 1049                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE18nnn/GSE18732/
#> 1050                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19769/
#> 1051    GEO (BAM, BED, CEL, TXT, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE18nnn/GSE18927/
#> 1052                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE15nnn/GSE15790/
#> 1053                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17635/
#> 1054                        GEO (LSR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13840/
#> 1055                   GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE15nnn/GSE15072/
#> 1056                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE12nnn/GSE12959/
#> 1057                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE18nnn/GSE18212/
#> 1058                     GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE8nnn/GSE8908/
#> 1059                   GEO (CEL, CHP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17556/
#> 1060              GEO (BAM, BED, WIG) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE16nnn/GSE16256/
#> 1061                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE15nnn/GSE15543/
#> 1062                   GEO (GPR, TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17060/
#> 1063                        GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE17nnn/GSE17058/
#> 1064                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE16nnn/GSE16025/
#> 1065                        GEO (XLS) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13015/
#> 1066                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE5nnn/GSE5903/
#> 1067                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE16nnn/GSE16415/
#> 1068                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE15nnn/GSE15653/
#> 1069                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13736/
#> 1070                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13465/
#> 1071                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13920/
#> 1072                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE10nnn/GSE10334/
#> 1073                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE13nnn/GSE13290/
#> 1074                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE8nnn/GSE8157/
#> 1075                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE12nnn/GSE12643/
#> 1076                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE11nnn/GSE11908/
#> 1077                        GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE11nnn/GSE11907/
#> 1078                        GEO (TXT) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE10nnn/GSE10540/
#> 1079                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9588/
#> 1080                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9984/
#> 1081                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9939/
#> 1082                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6751/
#> 1083                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6599/
#> 1084                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6798/
#> 1085                          GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9157/
#> 1086                          GEO (GPR) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9017/
#> 1087                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9105/
#> 1088                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE9nnn/GSE9006/
#> 1089                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE4nnn/GSE4704/
#> 1090                          GEO (CSV) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE7nnn/GSE7818/
#> 1091                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE7nnn/GSE7146/
#> 1092                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6862/
#> 1093                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE6nnn/GSE6573/
#> 1094                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE4nnn/GSE4901/
#> 1095                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE3nnn/GSE3118/
#> 1096                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE4nnn/GSE4117/
#> 1097                     GEO (CEL, EXP) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE5nnn/GSE5090/
#> 1098                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE3nnn/GSE3881/
#> 1099                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE3nnn/GSE3308/
#> 1100                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE3nnn/GSE3447/
#> 1101                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE3nnn/GSE3307/
#> 1102                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE2nnn/GSE2138/
#> 1103                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE2nnn/GSE2956/
#> 1104                                GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE1nnn/GSE1322/
#> 1105                          GEO (CEL) ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE1nnn/GSE1009/
#> 1106                                  GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSEnnn/GSE634/
#> 1107                                  GEO ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSEnnn/GSE121/
#>      Series Accession        ID
#> 1           GSE197881 200197881
#> 2           GSE191210 200191210
#> 3           GSE207901 200207901
#> 4           GSE205668 200205668
#> 5           GSE173735 200173735
#> 6           GSE173734 200173734
#> 7           GSE202295 200202295
#> 8           GSE207122 200207122
#> 9           GSE197850 200197850
#> 10          GSE188395 200188395
#> 11          GSE153315 200153315
#> 12          GSE200678 200200678
#> 13          GSE206528 200206528
#> 14          GSE200659 200200659
#> 15          GSE201908 200201908
#> 16          GSE199437 200199437
#> 17          GSE199852 200199852
#> 18          GSE198520 200198520
#> 19          GSE185728 200185728
#> 20          GSE176145 200176145
#> 21          GSE133666 200133666
#> 22          GSE203346 200203346
#> 23          GSE203169 200203169
#> 24          GSE203353 200203353
#> 25          GSE135076 200135076
#> 26          GSE192541 200192541
#> 27          GSE202151 200202151
#> 28          GSE194156 200194156
#> 29          GSE194155 200194155
#> 30          GSE194154 200194154
#> 31          GSE175759 200175759
#> 32          GSE201543 200201543
#> 33          GSE181478 200181478
#> 34          GSE181412 200181412
#> 35          GSE180521 200180521
#> 36          GSE200983 200200983
#> 37          GSE200477 200200477
#> 38          GSE186883 200186883
#> 39          GSE185845 200185845
#> 40          GSE199939 200199939
#> 41          GSE188827 200188827
#> 42          GSE186021 200186021
#> 43          GSE182138 200182138
#> 44          GSE199700 200199700
#> 45          GSE199148 200199148
#> 46          GSE185052 200185052
#> 47          GSE185191 200185191
#> 48          GSE185190 200185190
#> 49          GSE185189 200185189
#> 50          GSE193161 200193161
#> 51          GSE162622 200162622
#> 52          GSE197456 200197456
#> 53          GSE197285 200197285
#> 54          GSE162273 200162273
#> 55          GSE126803 200126803
#> 56          GSE196900 200196900
#> 57          GSE193436 200193436
#> 58          GSE166641 200166641
#> 59          GSE167199 200167199
#> 60          GSE159586 200159586
#> 61          GSE159554 200159554
#> 62          GSE166640 200166640
#> 63          GSE185038 200185038
#> 64          GSE185036 200185036
#> 65          GSE185035 200185035
#> 66          GSE189849 200189849
#> 67          GSE186766 200186766
#> 68          GSE113409 200113409
#> 69          GSE113392 200113392
#> 70          GSE163947 200163947
#> 71          GSE165784 200165784
#> 72          GSE176230 200176230
#> 73          GSE166822 200166822
#> 74          GSE194061 200194061
#> 75          GSE194119 200194119
#> 76          GSE193974 200193974
#> 77          GSE182259 200182259
#> 78          GSE172148 200172148
#> 79          GSE167269 200167269
#> 80          GSE193510 200193510
#> 81          GSE193626 200193626
#> 82          GSE176171 200176171
#> 83          GSE176067 200176067
#> 84          GSE174475 200174475
#> 85          GSE193273 200193273
#> 86          GSE156035 200156035
#> 87          GSE154415 200154415
#> 88          GSE154414 200154414
#> 89          GSE154413 200154413
#> 90          GSE113199 200113199
#> 91          GSE181143 200181143
#> 92          GSE142178 200142178
#> 93          GSE162166 200162166
#> 94          GSE190973 200190973
#> 95          GSE190972 200190972
#> 96          GSE190971 200190971
#> 97          GSE184831 200184831
#> 98          GSE182870 200182870
#> 99          GSE190832 200190832
#> 100         GSE180355 200180355
#> 101         GSE174481 200174481
#> 102         GSE188235 200188235
#> 103         GSE188234 200188234
#> 104         GSE189923 200189923
#> 105         GSE185430 200185430
#> 106         GSE181328 200181328
#> 107         GSE159955 200159955
#> 108         GSE123088 200123088
#> 109         GSE123086 200123086
#> 110         GSE189107 200189107
#> 111         GSE140842 200140842
#> 112         GSE162135 200162135
#> 113         GSE162133 200162133
#> 114         GSE161989 200161989
#> 115         GSE188799 200188799
#> 116         GSE189007 200189007
#> 117         GSE162837 200162837
#> 118         GSE137766 200137766
#> 119         GSE136887 200136887
#> 120          GSE98887 200098887
#> 121         GSE186524 200186524
#> 122         GSE165816 200165816
#> 123         GSE179568 200179568
#> 124         GSE182494 200182494
#> 125         GSE166120 200166120
#> 126         GSE186432 200186432
#> 127         GSE180470 200180470
#> 128         GSE185598 200185598
#> 129         GSE163211 200163211
#> 130         GSE185749 200185749
#> 131         GSE142290 200142290
#> 132         GSE175477 200175477
#> 133         GSE141319 200141319
#> 134         GSE182923 200182923
#> 135         GSE180504 200180504
#> 136         GSE159924 200159924
#> 137         GSE139947 200139947
#> 138         GSE178991 200178991
#> 139         GSE156911 200156911
#> 140         GSE169514 200169514
#> 141         GSE184050 200184050
#> 142         GSE184016 200184016
#> 143         GSE183965 200183965
#> 144         GSE183701 200183701
#> 145         GSE183568 200183568
#> 146          GSE72991 200072991
#> 147         GSE173277 200173277
#> 148         GSE173228 200173228
#> 149         GSE165709 200165709
#> 150         GSE165708 200165708
#> 151         GSE165703 200165703
#> 152         GSE182737 200182737
#> 153         GSE122279 200122279
#> 154         GSE159337 200159337
#> 155         GSE182121 200182121
#> 156         GSE182120 200182120
#> 157         GSE182117 200182117
#> 158         GSE182053 200182053
#> 159         GSE159867 200159867
#> 160         GSE181881 200181881
#> 161         GSE144414 200144414
#> 162         GSE181674 200181674
#> 163         GSE118139 200118139
#> 164         GSE173276 200173276
#> 165         GSE168071 200168071
#> 166         GSE179921 200179921
#> 167         GSE179762 200179762
#> 168         GSE168996 200168996
#> 169         GSE163773 200163773
#> 170         GSE180083 200180083
#> 171         GSE180081 200180081
#> 172         GSE150212 200150212
#> 173         GSE153837 200153837
#> 174         GSE156411 200156411
#> 175         GSE153834 200153834
#> 176         GSE179143 200179143
#> 177         GSE150724 200150724
#> 178         GSE178828 200178828
#> 179         GSE178721 200178721
#> 180         GSE173983 200173983
#> 181         GSE178734 200178734
#> 182         GSE178733 200178733
#> 183         GSE156122 200156122
#> 184         GSE156121 200156121
#> 185         GSE156061 200156061
#> 186         GSE122086 200122086
#> 187         GSE176324 200176324
#> 188         GSE173669 200173669
#> 189         GSE165385 200165385
#> 190         GSE175745 200175745
#> 191         GSE175735 200175735
#> 192         GSE114860 200114860
#> 193         GSE174502 200174502
#> 194         GSE173613 200173613
#> 195         GSE136344 200136344
#> 196         GSE173193 200173193
#> 197         GSE157988 200157988
#> 198         GSE159556 200159556
#> 199         GSE160310 200160310
#> 200         GSE160308 200160308
#> 201         GSE160306 200160306
#> 202         GSE153410 200153410
#> 203         GSE164416 200164416
#> 204         GSE151426 200151426
#> 205         GSE141432 200141432
#> 206         GSE136395 200136395
#> 207         GSE151405 200151405
#> 208         GSE148073 200148073
#> 209         GSE148642 200148642
#> 210         GSE148640 200148640
#> 211         GSE148639 200148639
#> 212         GSE168437 200168437
#> 213         GSE166785 200166785
#> 214         GSE167250 200167250
#> 215         GSE112168 200112168
#> 216         GSE162521 200162521
#> 217         GSE163160 200163160
#> 218         GSE166047 200166047
#> 219         GSE151497 200151497
#> 220         GSE151496 200151496
#> 221         GSE151495 200151495
#> 222         GSE168492 200168492
#> 223         GSE168072 200168072
#> 224         GSE168327 200168327
#> 225         GSE167976 200167976
#> 226         GSE167914 200167914
#> 227         GSE162689 200162689
#> 228         GSE165121 200165121
#> 229         GSE166847 200166847
#> 230         GSE166845 200166845
#> 231         GSE166787 200166787
#> 232         GSE166652 200166652
#> 233         GSE166502 200166502
#> 234         GSE166467 200166467
#> 235         GSE110829 200110829
#> 236         GSE110828 200110828
#> 237         GSE158055 200158055
#> 238         GSE157640 200157640
#> 239         GSE159717 200159717
#> 240         GSE147890 200147890
#> 241         GSE153221 200153221
#> 242         GSE153220 200153220
#> 243         GSE153219 200153219
#> 244         GSE149148 200149148
#> 245         GSE164934 200164934
#> 246         GSE163610 200163610
#> 247         GSE160474 200160474
#> 248         GSE160473 200160473
#> 249         GSE160472 200160472
#> 250         GSE161355 200161355
#> 251         GSE164338 200164338
#> 252          GSE25194 200025194
#> 253         GSE139577 200139577
#> 254         GSE118103 200118103
#> 255         GSE163980 200163980
#> 256         GSE163744 200163744
#> 257         GSE163732 200163732
#> 258         GSE150172 200150172
#> 259         GSE163603 200163603
#> 260         GSE163510 200163510
#> 261         GSE158292 200158292
#> 262         GSE162830 200162830
#> 263         GSE157515 200157515
#> 264         GSE162557 200162557
#> 265         GSE147965 200147965
#> 266         GSE142401 200142401
#> 267         GSE142153 200142153
#> 268         GSE149568 200149568
#> 269         GSE157859 200157859
#> 270         GSE161914 200161914
#> 271         GSE161721 200161721
#> 272         GSE161720 200161720
#> 273         GSE161719 200161719
#> 274         GSE154306 200154306
#> 275         GSE144348 200144348
#> 276         GSE141065 200141065
#> 277         GSE145747 200145747
#> 278         GSE145746 200145746
#> 279         GSE145745 200145745
#> 280         GSE160005 200160005
#> 281         GSE159984 200159984
#> 282         GSE159759 200159759
#> 283         GSE154378 200154378
#> 284         GSE154377 200154377
#> 285         GSE154348 200154348
#> 286         GSE132831 200132831
#> 287         GSE159467 200159467
#> 288         GSE154609 200154609
#> 289         GSE154126 200154126
#> 290         GSE143783 200143783
#> 291         GSE152615 200152615
#> 292         GSE134431 200134431
#> 293         GSE151764 200151764
#> 294         GSE157177 200157177
#> 295         GSE154554 200154554
#> 296         GSE143690 200143690
#> 297         GSE156993 200156993
#> 298         GSE140308 200140308
#> 299         GSE156903 200156903
#> 300         GSE148061 200148061
#> 301         GSE148060 200148060
#> 302         GSE148059 200148059
#> 303         GSE146028 200146028
#> 304         GSE156249 200156249
#> 305         GSE156248 200156248
#> 306         GSE156247 200156247
#> 307         GSE156341 200156341
#> 308         GSE156340 200156340
#> 309         GSE156339 200156339
#> 310         GSE135357 200135357
#> 311         GSE135356 200135356
#> 312         GSE135355 200135355
#> 313         GSE135354 200135354
#> 314         GSE156109 200156109
#> 315         GSE143209 200143209
#> 316         GSE102485 200102485
#> 317         GSE151683 200151683
#> 318         GSE155713 200155713
#> 319         GSE144682 200144682
#> 320         GSE143735 200143735
#> 321         GSE131169 200131169
#> 322         GSE138781 200138781
#> 323         GSE155188 200155188
#> 324         GSE151588 200151588
#> 325         GSE109163 200109163
#> 326         GSE153565 200153565
#> 327         GSE148961 200148961
#> 328         GSE154647 200154647
#> 329         GSE154629 200154629
#> 330         GSE154628 200154628
#> 331         GSE114192 200114192
#> 332         GSE153792 200153792
#> 333         GSE153555 200153555
#> 334         GSE134594 200134594
#> 335         GSE140959 200140959
#> 336         GSE133225 200133225
#> 337         GSE133217 200133217
#> 338         GSE150060 200150060
#> 339         GSE151889 200151889
#> 340         GSE121221 200121221
#> 341         GSE151610 200151610
#> 342         GSE145593 200145593
#> 343         GSE123658 200123658
#> 344         GSE115221 200115221
#> 345         GSE146338 200146338
#> 346         GSE144605 200144605
#> 347         GSE147740 200147740
#> 348         GSE145284 200145284
#> 349         GSE113969 200113969
#> 350         GSE150586 200150586
#> 351         GSE150621 200150621
#> 352         GSE150119 200150119
#> 353         GSE139535 200139535
#> 354         GSE148896 200148896
#> 355         GSE148812 200148812
#> 356         GSE148058 200148058
#> 357         GSE133219 200133219
#> 358         GSE133218 200133218
#> 359         GSE143319 200143319
#> 360         GSE148375 200148375
#> 361         GSE144693 200144693
#> 362         GSE144692 200144692
#> 363         GSE144691 200144691
#> 364         GSE146108 200146108
#> 365         GSE142385 200142385
#> 366         GSE112652 200112652
#> 367         GSE138323 200138323
#> 368         GSE126101 200126101
#> 369         GSE126100 200126100
#> 370         GSE126099 200126099
#> 371         GSE145347 200145347
#> 372         GSE139157 200139157
#> 373         GSE138857 200138857
#> 374         GSE146615 200146615
#> 375         GSE142512 200142512
#> 376         GSE139949 200139949
#> 377          GSE95078 200095078
#> 378         GSE124742 200124742
#> 379         GSE144908 200144908
#> 380          GSE94729 200094729
#> 381         GSE138598 200138598
#> 382         GSE131528 200131528
#> 383         GSE131526 200131526
#> 384         GSE125929 200125929
#> 385         GSE144441 200144441
#> 386         GSE119296 200119296
#> 387         GSE144169 200144169
#> 388         GSE141639 200141639
#> 389         GSE141309 200141309
#> 390         GSE143979 200143979
#> 391         GSE135155 200135155
#> 392         GSE143495 200143495
#> 393         GSE143143 200143143
#> 394         GSE142009 200142009
#> 395         GSE121820 200121820
#> 396         GSE124534 200124534
#> 397         GSE139932 200139932
#> 398         GSE133264 200133264
#> 399         GSE131065 200131065
#> 400         GSE130279 200130279
#> 401         GSE122429 200122429
#> 402          GSE94846 200094846
#> 403         GSE142553 200142553
#> 404         GSE141126 200141126
#> 405         GSE121346 200121346
#> 406         GSE121344 200121344
#> 407         GSE142025 200142025
#> 408         GSE141512 200141512
#> 409         GSE141410 200141410
#> 410         GSE124272 200124272
#> 411         GSE141193 200141193
#> 412         GSE140627 200140627
#> 413         GSE140404 200140404
#> 414         GSE140403 200140403
#> 415         GSE140065 200140065
#> 416         GSE140064 200140064
#> 417         GSE139929 200139929
#> 418         GSE135197 200135197
#> 419         GSE124264 200124264
#> 420         GSE115326 200115326
#> 421         GSE115312 200115312
#> 422         GSE115306 200115306
#> 423         GSE135453 200135453
#> 424         GSE135776 200135776
#> 425         GSE129363 200129363
#> 426         GSE139073 200139073
#> 427         GSE138885 200138885
#> 428         GSE138856 200138856
#> 429         GSE131320 200131320
#> 430         GSE112893 200112893
#> 431         GSE114569 200114569
#> 432         GSE114248 200114248
#> 433         GSE114236 200114236
#> 434          GSE88839 200088839
#> 435         GSE136048 200136048
#> 436          GSE96971 200096971
#> 437         GSE137803 200137803
#> 438         GSE136053 200136053
#> 439         GSE137136 200137136
#> 440         GSE136865 200136865
#> 441         GSE133135 200133135
#> 442         GSE123404 200123404
#> 443         GSE137684 200137684
#> 444         GSE130672 200130672
#> 445         GSE137317 200137317
#> 446         GSE131882 200131882
#> 447         GSE133910 200133910
#> 448         GSE136353 200136353
#> 449         GSE136277 200136277
#> 450         GSE128289 200128289
#> 451          GSE51674 200051674
#> 452         GSE135944 200135944
#> 453         GSE129935 200129935
#> 454         GSE132306 200132306
#> 455         GSE132111 200132111
#> 456         GSE120024 200120024
#> 457         GSE132187 200132187
#> 458          GSE88794 200088794
#> 459         GSE133099 200133099
#> 460         GSE125769 200125769
#> 461         GSE125768 200125768
#> 462         GSE125590 200125590
#> 463         GSE102677 200102677
#> 464         GSE102633 200102633
#> 465         GSE129112 200129112
#> 466         GSE121862 200121862
#> 467         GSE122584 200122584
#> 468         GSE130991 200130991
#> 469         GSE114412 200114412
#> 470         GSE129042 200129042
#> 471         GSE129841 200129841
#> 472         GSE126169 200126169
#> 473         GSE101702 200101702
#> 474         GSE129666 200129666
#> 475         GSE129653 200129653
#> 476         GSE129604 200129604
#> 477         GSE129091 200129091
#> 478         GSE129383 200129383
#> 479         GSE115020 200115020
#> 480         GSE112690 200112690
#> 481         GSE112342 200112342
#> 482         GSE112341 200112341
#> 483         GSE112337 200112337
#> 484         GSE128381 200128381
#> 485         GSE128331 200128331
#> 486         GSE124811 200124811
#> 487         GSE124810 200124810
#> 488         GSE124809 200124809
#> 489          GSE45515 200045515
#> 490         GSE127045 200127045
#> 491         GSE127042 200127042
#> 492         GSE127033 200127033
#> 493         GSE124400 200124400
#> 494         GSE124284 200124284
#> 495         GSE127170 200127170
#> 496         GSE115828 200115828
#> 497         GSE110786 200110786
#> 498         GSE103682 200103682
#> 499          GSE77522 200077522
#> 500          GSE77268 200077268
#> 501         GSE104674 200104674
#> 502         GSE115329 200115329
#> 503         GSE115313 200115313
#> 504         GSE115421 200115421
#> 505         GSE102295 200102295
#> 506         GSE118588 200118588
#> 507         GSE109022 200109022
#> 508         GSE104297 200104297
#> 509          GSE71799 200071799
#> 510         GSE107375 200107375
#> 511          GSE78721 200078721
#> 512           GSE9707 200009707
#> 513           GSE7319 200007319
#> 514          GSE97554 200097554
#> 515         GSE108403 200108403
#> 516         GSE120522 200120522
#> 517         GSE123844 200123844
#> 518         GSE108056 200108056
#> 519         GSE117454 200117454
#> 520         GSE116726 200116726
#> 521         GSE112594 200112594
#> 522         GSE123279 200123279
#> 523         GSE115257 200115257
#> 524         GSE107943 200107943
#> 525         GSE110914 200110914
#> 526         GSE116761 200116761
#> 527         GSE117469 200117469
#> 528         GSE106181 200106181
#> 529         GSE106177 200106177
#> 530         GSE105167 200105167
#> 531         GSE120904 200120904
#> 532         GSE120299 200120299
#> 533         GSE101207 200101207
#> 534         GSE116559 200116559
#> 535         GSE118230 200118230
#> 536         GSE118481 200118481
#> 537         GSE106800 200106800
#> 538         GSE102498 200102498
#> 539         GSE108413 200108413
#> 540         GSE106099 200106099
#> 541         GSE103552 200103552
#> 542          GSE89475 200089475
#> 543          GSE96804 200096804
#> 544         GSE102371 200102371
#> 545         GSE102234 200102234
#> 546          GSE86376 200086376
#> 547          GSE85990 200085990
#> 548         GSE106953 200106953
#> 549         GSE116497 200116497
#> 550         GSE111154 200111154
#> 551         GSE116369 200116369
#> 552          GSE83782 200083782
#> 553          GSE83781 200083781
#> 554          GSE83699 200083699
#> 555         GSE116029 200116029
#> 556         GSE114477 200114477
#> 557         GSE104815 200104815
#> 558          GSE99853 200099853
#> 559          GSE70365 200070365
#> 560         GSE114908 200114908
#> 561         GSE114051 200114051
#> 562         GSE110935 200110935
#> 563          GSE84453 200084453
#> 564          GSE37785 200037785
#> 565          GSE12844 200012844
#> 566          GSE97205 200097205
#> 567         GSE113080 200113080
#> 568         GSE109266 200109266
#> 569         GSE109265 200109265
#> 570         GSE111876 200111876
#> 571          GSE98224 200098224
#> 572         GSE106813 200106813
#> 573          GSE95243 200095243
#> 574          GSE98675 200098675
#> 575         GSE110552 200110552
#> 576         GSE104423 200104423
#> 577          GSE98485 200098485
#> 578         GSE104195 200104195
#> 579         GSE104190 200104190
#> 580         GSE105096 200105096
#> 581         GSE102080 200102080
#> 582         GSE102079 200102079
#> 583         GSE104954 200104954
#> 584         GSE104948 200104948
#> 585          GSE93709 200093709
#> 586         GSE109178 200109178
#> 587         GSE109140 200109140
#> 588          GSE92724 200092724
#> 589          GSE92772 200092772
#> 590          GSE80178 200080178
#> 591         GSE106148 200106148
#> 592          GSE76896 200076896
#> 593          GSE76895 200076895
#> 594          GSE76894 200076894
#> 595          GSE77108 200077108
#> 596         GSE106520 200106520
#> 597          GSE84814 200084814
#> 598          GSE63992 200063992
#> 599          GSE90076 200090076
#> 600          GSE90074 200090074
#> 601          GSE90073 200090073
#> 602         GSE105052 200105052
#> 603          GSE81547 200081547
#> 604         GSE103931 200103931
#> 605         GSE103393 200103393
#> 606          GSE75062 200075062
#> 607         GSE103657 200103657
#> 608          GSE97123 200097123
#> 609          GSE93032 200093032
#> 610          GSE85192 200085192
#> 611          GSE90999 200090999
#> 612          GSE74240 200074240
#> 613          GSE87005 200087005
#> 614          GSE99340 200099340
#> 615          GSE99339 200099339
#> 616          GSE99325 200099325
#> 617          GSE86069 200086069
#> 618          GSE97655 200097655
#> 619         GSE102177 200102177
#> 620          GSE95368 200095368
#> 621         GSE101931 200101931
#> 622          GSE94497 200094497
#> 623          GSE94496 200094496
#> 624         GSE101461 200101461
#> 625          GSE86298 200086298
#> 626          GSE83452 200083452
#> 627          GSE99068 200099068
#> 628          GSE97647 200097647
#> 629          GSE97591 200097591
#> 630         GSE100271 200100271
#> 631         GSE100185 200100185
#> 632          GSE90028 200090028
#> 633          GSE96569 200096569
#> 634          GSE96568 200096568
#> 635          GSE96564 200096564
#> 636          GSE96563 200096563
#> 637          GSE96562 200096562
#> 638          GSE98501 200098501
#> 639          GSE98399 200098399
#> 640          GSE57362 200057362
#> 641          GSE97530 200097530
#> 642          GSE90117 200090117
#> 643          GSE68475 200068475
#> 644          GSE98043 200098043
#> 645          GSE81965 200081965
#> 646          GSE94019 200094019
#> 647          GSE88929 200088929
#> 648          GSE97084 200097084
#> 649          GSE84823 200084823
#> 650          GSE84821 200084821
#> 651          GSE87626 200087626
#> 652          GSE83345 200083345
#> 653          GSE72490 200072490
#> 654          GSE95849 200095849
#> 655          GSE95675 200095675
#> 656          GSE95674 200095674
#> 657          GSE89360 200089360
#> 658          GSE78840 200078840
#> 659          GSE94649 200094649
#> 660          GSE85226 200085226
#> 661          GSE77962 200077962
#> 662          GSE89552 200089552
#> 663          GSE84714 200084714
#> 664          GSE87893 200087893
#> 665          GSE70318 200070318
#> 666          GSE24555 200024555
#> 667          GSE64605 200064605
#> 668          GSE87000 200087000
#> 669          GSE85527 200085527
#> 670          GSE84934 200084934
#> 671          GSE87340 200087340
#> 672          GSE85573 200085573
#> 673          GSE85531 200085531
#> 674          GSE85530 200085530
#> 675          GSE89022 200089022
#> 676          GSE86473 200086473
#> 677          GSE86469 200086469
#> 678          GSE86468 200086468
#> 679          GSE89632 200089632
#> 680          GSE65319 200065319
#> 681          GSE87530 200087530
#> 682          GSE63117 200063117
#> 683          GSE67740 200067740
#> 684          GSE87571 200087571
#> 685          GSE85241 200085241
#> 686          GSE85928 200085928
#> 687          GSE84971 200084971
#> 688          GSE84133 200084133
#> 689          GSE87295 200087295
#> 690          GSE78922 200078922
#> 691          GSE86884 200086884
#> 692          GSE86611 200086611
#> 693          GSE86544 200086544
#> 694          GSE81608 200081608
#> 695          GSE72377 200072377
#> 696          GSE72376 200072376
#> 697          GSE67566 200067566
#> 698          GSE84908 200084908
#> 699          GSE76398 200076398
#> 700          GSE76394 200076394
#> 701          GSE76285 200076285
#> 702          GSE71301 200071301
#> 703          GSE69705 200069705
#> 704          GSE58557 200058557
#> 705          GSE67141 200067141
#> 706          GSE76308 200076308
#> 707          GSE83139 200083139
#> 708          GSE71678 200071678
#> 709          GSE63492 200063492
#> 710          GSE72462 200072462
#> 711          GSE81076 200081076
#> 712          GSE79670 200079670
#> 713          GSE79668 200079668
#> 714          GSE75248 200075248
#> 715          GSE74296 200074296
#> 716          GSE80569 200080569
#> 717          GSE76171 200076171
#> 718          GSE76170 200076170
#> 719          GSE76169 200076169
#> 720          GSE81258 200081258
#> 721          GSE81255 200081255
#> 722          GSE75941 200075941
#> 723          GSE78805 200078805
#> 724          GSE65793 200065793
#> 725          GSE57628 200057628
#> 726          GSE67705 200067705
#> 727          GSE70901 200070901
#> 728          GSE65057 200065057
#> 729          GSE64998 200064998
#> 730          GSE78891 200078891
#> 731          GSE67775 200067775
#> 732          GSE67774 200067774
#> 733          GSE67773 200067773
#> 734          GSE77350 200077350
#> 735          GSE55311 200055311
#> 736          GSE76161 200076161
#> 737          GSE77114 200077114
#> 738          GSE76899 200076899
#> 739          GSE51546 200051546
#> 740          GSE62761 200062761
#> 741          GSE60861 200060861
#> 742          GSE60860 200060860
#> 743          GSE45980 200045980
#> 744          GSE44639 200044639
#> 745          GSE76268 200076268
#> 746          GSE76189 200076189
#> 747          GSE76065 200076065
#> 748          GSE73034 200073034
#> 749          GSE69438 200069438
#> 750          GSE75685 200075685
#> 751          GSE75678 200075678
#> 752          GSE75669 200075669
#> 753          GSE69600 200069600
#> 754          GSE73408 200073408
#> 755          GSE68526 200068526
#> 756          GSE74782 200074782
#> 757          GSE70961 200070961
#> 758          GSE69889 200069889
#> 759          GSE65561 200065561
#> 760          GSE74629 200074629
#> 761          GSE74559 200074559
#> 762          GSE72492 200072492
#> 763          GSE41767 200041767
#> 764          GSE73418 200073418
#> 765          GSE71730 200071730
#> 766          GSE68049 200068049
#> 767          GSE37025 200037025
#> 768          GSE63423 200063423
#> 769          GSE70752 200070752
#> 770          GSE70494 200070494
#> 771          GSE70493 200070493
#> 772          GSE70453 200070453
#> 773          GSE21891 200021891
#> 774          GSE71416 200071416
#> 775          GSE69658 200069658
#> 776          GSE71102 200071102
#> 777          GSE71099 200071099
#> 778          GSE69595 200069595
#> 779          GSE70528 200070528
#> 780          GSE65682 200065682
#> 781          GSE67297 200067297
#> 782          GSE59363 200059363
#> 783          GSE59421 200059421
#> 784          GSE49885 200049885
#> 785          GSE67543 200067543
#> 786          GSE69528 200069528
#> 787          GSE69421 200069421
#> 788          GSE66785 200066785
#> 789          GSE67279 200067279
#> 790          GSE48278 200048278
#> 791          GSE68571 200068571
#> 792          GSE60760 200060760
#> 793          GSE68186 200068186
#> 794          GSE68185 200068185
#> 795          GSE68184 200068184
#> 796          GSE68183 200068183
#> 797          GSE68226 200068226
#> 798          GSE68224 200068224
#> 799          GSE62117 200062117
#> 800          GSE67738 200067738
#> 801          GSE63887 200063887
#> 802          GSE37084 200037084
#> 803          GSE67567 200067567
#> 804          GSE53257 200053257
#> 805          GSE62219 200062219
#> 806          GSE66413 200066413
#> 807          GSE66360 200066360
#> 808          GSE62003 200062003
#> 809          GSE55645 200055645
#> 810          GSE65737 200065737
#> 811          GSE66175 200066175
#> 812          GSE62372 200062372
#> 813          GSE62370 200062370
#> 814          GSE62832 200062832
#> 815          GSE63981 200063981
#> 816          GSE60424 200060424
#> 817          GSE45856 200045856
#> 818          GSE38267 200038267
#> 819          GSE34198 200034198
#> 820          GSE55650 200055650
#> 821          GSE38835 200038835
#> 822          GSE56081 200056081
#> 823          GSE57896 200057896
#> 824          GSE55465 200055465
#> 825          GSE55464 200055464
#> 826          GSE62523 200062523
#> 827          GSE62500 200062500
#> 828          GSE62499 200062499
#> 829          GSE61769 200061769
#> 830          GSE61714 200061714
#> 831          GSE61166 200061166
#> 832          GSE61129 200061129
#> 833          GSE56781 200056781
#> 834          GSE56685 200056685
#> 835          GSE60803 200060803
#> 836          GSE52376 200052376
#> 837          GSE55567 200055567
#> 838          GSE55566 200055566
#> 839          GSE42902 200042902
#> 840          GSE60436 200060436
#> 841          GSE55100 200055100
#> 842          GSE55099 200055099
#> 843          GSE55098 200055098
#> 844          GSE50866 200050866
#> 845          GSE50397 200050397
#> 846          GSE30575 200030575
#> 847          GSE58634 200058634
#> 848          GSE44558 200044558
#> 849          GSE57928 200057928
#> 850          GSE57880 200057880
#> 851          GSE52724 200052724
#> 852          GSE57484 200057484
#> 853          GSE50005 200050005
#> 854          GSE51058 200051058
#> 855          GSE56606 200056606
#> 856          GSE48101 200048101
#> 857          GSE44093 200044093
#> 858          GSE29536 200029536
#> 859          GSE54279 200054279
#> 860          GSE46097 200046097
#> 861          GSE43488 200043488
#> 862          GSE30211 200030211
#> 863          GSE30210 200030210
#> 864          GSE30209 200030209
#> 865          GSE30208 200030208
#> 866          GSE48318 200048318
#> 867          GSE54350 200054350
#> 868          GSE48354 200048354
#> 869          GSE48353 200048353
#> 870          GSE53949 200053949
#> 871          GSE44314 200044314
#> 872          GSE44313 200044313
#> 873          GSE29623 200029623
#> 874          GSE29622 200029622
#> 875          GSE29621 200029621
#> 876          GSE28038 200028038
#> 877          GSE47385 200047385
#> 878          GSE53454 200053454
#> 879          GSE40878 200040878
#> 880          GSE36233 200036233
#> 881          GSE52314 200052314
#> 882          GSE40360 200040360
#> 883          GSE52422 200052422
#> 884          GSE51924 200051924
#> 885          GSE52233 200052233
#> 886          GSE51311 200051311
#> 887          GSE51310 200051310
#> 888          GSE50800 200050800
#> 889          GSE43580 200043580
#> 890          GSE33070 200033070
#> 891          GSE42432 200042432
#> 892          GSE50892 200050892
#> 893          GSE49667 200049667
#> 894          GSE35279 200035279
#> 895          GSE50386 200050386
#> 896          GSE42715 200042715
#> 897          GSE41744 200041744
#> 898          GSE49524 200049524
#> 899          GSE49566 200049566
#> 900          GSE39825 200039825
#> 901          GSE47185 200047185
#> 902          GSE47184 200047184
#> 903          GSE47183 200047183
#> 904          GSE46899 200046899
#> 905          GSE46900 200046900
#> 906          GSE46897 200046897
#> 907          GSE47874 200047874
#> 908          GSE47720 200047720
#> 909          GSE40498 200040498
#> 910          GSE40496 200040496
#> 911          GSE42507 200042507
#> 912          GSE40234 200040234
#> 913          GSE45986 200045986
#> 914          GSE45792 200045792
#> 915          GSE45777 200045777
#> 916          GSE44035 200044035
#> 917          GSE43752 200043752
#> 918          GSE43751 200043751
#> 919          GSE43750 200043750
#> 920          GSE43950 200043950
#> 921          GSE32909 200032909
#> 922          GSE34512 200034512
#> 923          GSE38291 200038291
#> 924          GSE14368 200014368
#> 925          GSE42487 200042487
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#> 927          GSE42228 200042228
#> 928          GSE42227 200042227
#> 929          GSE29231 200029231
#> 930          GSE29226 200029226
#> 931          GSE29221 200029221
#> 932          GSE42148 200042148
#> 933          GSE42094 200042094
#> 934          GSE42093 200042093
#> 935          GSE34526 200034526
#> 936          GSE35725 200035725
#> 937          GSE35716 200035716
#> 938          GSE35713 200035713
#> 939          GSE35712 200035712
#> 940          GSE35711 200035711
#> 941          GSE37794 200037794
#> 942          GSE30161 200030161
#> 943          GSE35851 200035851
#> 944          GSE30802 200030802
#> 945          GSE38642 200038642
#> 946          GSE35191 200035191
#> 947          GSE35186 200035186
#> 948          GSE38447 200038447
#> 949          GSE38396 200038396
#> 950          GSE36403 200036403
#> 951          GSE36402 200036402
#> 952          GSE36397 200036397
#> 953          GSE36084 200036084
#> 954          GSE33440 200033440
#> 955          GSE19637 200019637
#> 956          GSE32575 200032575
#> 957          GSE34223 200034223
#> 958          GSE37824 200037824
#> 959          GSE37901 200037901
#> 960          GSE28384 200028384
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#> 962          GSE37639 200037639
#> 963          GSE21232 200021232
#> 964          GSE30159 200030159
#> 965          GSE32512 200032512
#> 966          GSE29660 200029660
#> 967          GSE26244 200026244
#> 968          GSE26887 200026887
#> 969          GSE32874 200032874
#> 970          GSE32691 200032691
#> 971          GSE35296 200035296
#> 972          GSE31901 200031901
#> 973          GSE29908 200029908
#> 974          GSE35411 200035411
#> 975          GSE32544 200032544
#> 976          GSE19943 200019943
#> 977          GSE22255 200022255
#> 978          GSE13760 200013760
#> 979          GSE32357 200032357
#> 980          GSE24818 200024818
#> 981          GSE33032 200033032
#> 982          GSE28024 200028024
#> 983          GSE28022 200028022
#> 984          GSE27507 200027507
#> 985          GSE32553 200032553
#> 986          GSE27175 200027175
#> 987          GSE27317 200027317
#> 988          GSE21815 200021815
#> 989          GSE31056 200031056
#> 990          GSE30566 200030566
#> 991          GSE30529 200030529
#> 992          GSE30528 200030528
#> 993          GSE30122 200030122
#> 994          GSE23506 200023506
#> 995          GSE30803 200030803
#> 996          GSE30732 200030732
#> 997          GSE30310 200030310
#> 998          GSE28059 200028059
#> 999          GSE27951 200027951
#> 1000         GSE29718 200029718
#> 1001         GSE27949 200027949
#> 1002         GSE24326 200024326
#> 1003         GSE23338 200023338
#> 1004         GSE29190 200029190
#> 1005         GSE29142 200029142
#> 1006         GSE29084 200029084
#> 1007         GSE25462 200025462
#> 1008         GSE25862 200025862
#> 1009         GSE24193 200024193
#> 1010         GSE26744 200026744
#> 1011         GSE19790 200019790
#> 1012         GSE21980 200021980
#> 1013         GSE19649 200019649
#> 1014         GSE26168 200026168
#> 1015         GSE26167 200026167
#> 1016         GSE26073 200026073
#> 1017         GSE25826 200025826
#> 1018         GSE25724 200025724
#> 1019         GSE20553 200020553
#> 1020         GSE24422 200024422
#> 1021         GSE19420 200019420
#> 1022         GSE24685 200024685
#> 1023         GSE25249 200025249
#> 1024         GSE23784 200023784
#> 1025         GSE16804 200016804
#> 1026         GSE14503 200014503
#> 1027         GSE24290 200024290
#> 1028         GSE24215 200024215
#> 1029         GSE24147 200024147
#> 1030         GSE23858 200023858
#> 1031         GSE23561 200023561
#> 1032         GSE18821 200018821
#> 1033         GSE17710 200017710
#> 1034         GSE12385 200012385
#> 1035         GSE12384 200012384
#> 1036         GSE23343 200023343
#> 1037         GSE21785 200021785
#> 1038         GSE22309 200022309
#> 1039         GSE21989 200021989
#> 1040         GSE18470 200018470
#> 1041         GSE21321 200021321
#> 1042         GSE17941 200017941
#> 1043         GSE21340 200021340
#> 1044         GSE19519 200019519
#> 1045         GSE20966 200020966
#> 1046         GSE20067 200020067
#> 1047         GSE17727 200017727
#> 1048         GSE20247 200020247
#> 1049         GSE18732 200018732
#> 1050         GSE19769 200019769
#> 1051         GSE18927 200018927
#> 1052         GSE15790 200015790
#> 1053         GSE17635 200017635
#> 1054         GSE13840 200013840
#> 1055         GSE15072 200015072
#> 1056         GSE12959 200012959
#> 1057         GSE18212 200018212
#> 1058          GSE8908 200008908
#> 1059         GSE17556 200017556
#> 1060         GSE16256 200016256
#> 1061         GSE15543 200015543
#> 1062         GSE17060 200017060
#> 1063         GSE17058 200017058
#> 1064         GSE16025 200016025
#> 1065         GSE13015 200013015
#> 1066          GSE5903 200005903
#> 1067         GSE16415 200016415
#> 1068         GSE15653 200015653
#> 1069         GSE13736 200013736
#> 1070         GSE13465 200013465
#> 1071         GSE13920 200013920
#> 1072         GSE10334 200010334
#> 1073         GSE13290 200013290
#> 1074          GSE8157 200008157
#> 1075         GSE12643 200012643
#> 1076         GSE11908 200011908
#> 1077         GSE11907 200011907
#> 1078         GSE10540 200010540
#> 1079          GSE9588 200009588
#> 1080          GSE9984 200009984
#> 1081          GSE9939 200009939
#> 1082          GSE6751 200006751
#> 1083          GSE6599 200006599
#> 1084          GSE6798 200006798
#> 1085          GSE9157 200009157
#> 1086          GSE9017 200009017
#> 1087          GSE9105 200009105
#> 1088          GSE9006 200009006
#> 1089          GSE4704 200004704
#> 1090          GSE7818 200007818
#> 1091          GSE7146 200007146
#> 1092          GSE6862 200006862
#> 1093          GSE6573 200006573
#> 1094          GSE4901 200004901
#> 1095          GSE3118 200003118
#> 1096          GSE4117 200004117
#> 1097          GSE5090 200005090
#> 1098          GSE3881 200003881
#> 1099          GSE3308 200003308
#> 1100          GSE3447 200003447
#> 1101          GSE3307 200003307
#> 1102          GSE2138 200002138
#> 1103          GSE2956 200002956
#> 1104          GSE1322 200001322
#> 1105          GSE1009 200001009
#> 1106           GSE634 200000634
#> 1107           GSE121 200000121
#>                                                SRA Run Selector
#> 1                                                          <NA>
#> 2                                                          <NA>
#> 3                                                          <NA>
#> 4                                                          <NA>
#> 5    https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA726931
#> 6    https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA726930
#> 7                                                          <NA>
#> 8                                                          <NA>
#> 9                                                          <NA>
#> 10                                                         <NA>
#> 11   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA642130
#> 12                                                         <NA>
#> 13                                                         <NA>
#> 14                                                         <NA>
#> 15                                                         <NA>
#> 16                                                         <NA>
#> 17                                                         <NA>
#> 18                                                         <NA>
#> 19   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA770632
#> 20   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA735124
#> 21                                                         <NA>
#> 22                                                         <NA>
#> 23                                                         <NA>
#> 24                                                         <NA>
#> 25   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA557351
#> 26                                                         <NA>
#> 27                                                         <NA>
#> 28                                                         <NA>
#> 29                                                         <NA>
#> 30                                                         <NA>
#> 31   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA733490
#> 32                                                         <NA>
#> 33   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA752137
#> 34   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA751907
#> 35   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA748583
#> 36                                                         <NA>
#> 37                                                         <NA>
#> 38   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA777441
#> 39                                                         <NA>
#> 40                                                         <NA>
#> 41   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA780478
#> 42   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA771705
#> 43   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA754770
#> 44                                                         <NA>
#> 45                                                         <NA>
#> 46   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA767536
#> 47                                                         <NA>
#> 48                                                         <NA>
#> 49                                                         <NA>
#> 50                                                         <NA>
#> 51                                                         <NA>
#> 52                                                         <NA>
#> 53                                                         <NA>
#> 54                                                         <NA>
#> 55   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA523368
#> 56                                                         <NA>
#> 57                                                         <NA>
#> 58   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA701465
#> 59   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA703847
#> 60   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA669838
#> 61   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA669691
#> 62   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA701460
#> 63                                                         <NA>
#> 64   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA767420
#> 65   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA767419
#> 66   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA784780
#> 67                                                         <NA>
#> 68                                                         <NA>
#> 69                                                         <NA>
#> 70   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA688302
#> 71   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA697911
#> 72   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA735526
#> 73   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA702073
#> 74                                                         <NA>
#> 75                                                         <NA>
#> 76                                                         <NA>
#> 77   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA755604
#> 78   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA722250
#> 79                                                         <NA>
#> 80                                                         <NA>
#> 81                                                         <NA>
#> 82   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA735210
#> 83                                                         <NA>
#> 84                                                         <NA>
#> 85                                                         <NA>
#> 86                                                         <NA>
#> 87                                                         <NA>
#> 88   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA646212
#> 89   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA646213
#> 90   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA450426
#> 91   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA750782
#> 92   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA596193
#> 93                                                         <NA>
#> 94                                                         <NA>
#> 95                                                         <NA>
#> 96                                                         <NA>
#> 97   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA766625
#> 98   https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA758093
#> 99                                                         <NA>
#> 100                                                        <NA>
#> 101  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA730026
#> 102  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA777955
#> 103  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA777956
#> 104                                                        <NA>
#> 105  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA769094
#> 106  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA751582
#> 107  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA670944
#> 108                                                        <NA>
#> 109                                                        <NA>
#> 110                                                        <NA>
#> 111  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA591150
#> 112                                                        <NA>
#> 113  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA680747
#> 114  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA680270
#> 115  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA780413
#> 116                                                        <NA>
#> 117  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA683224
#> 118  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA568200
#> 119  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA563923
#> 120  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA386507
#> 121  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA774285
#> 122                                                        <NA>
#> 123  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA744210
#> 124                                                        <NA>
#> 125  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA699294
#> 126                                                        <NA>
#> 127  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA748375
#> 128  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA769945
#> 129                                                        <NA>
#> 130  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA770660
#> 131  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA596473
#> 132  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA732455
#> 133  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA593046
#> 134  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA758362
#> 135  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA748427
#> 136  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA670900
#> 137  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA587715
#> 138  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA741804
#> 139  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA659500
#> 140  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA716957
#> 141  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA762935
#> 142  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA762859
#> 143  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA762540
#> 144  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA761711
#> 145  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA761336
#> 146  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA295525
#> 147  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA725009
#> 148  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA724727
#> 149                                                        <NA>
#> 150  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA695511
#> 151  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA695509
#> 152                                                        <NA>
#> 153                                                        <NA>
#> 154  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA662421
#> 155                                                        <NA>
#> 156                                                        <NA>
#> 157  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA754599
#> 158  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA754377
#> 159  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA670712
#> 160  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA753798
#> 161  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA603578
#> 162  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA752997
#> 163                                                        <NA>
#> 164  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA725008
#> 165  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA705983
#> 166  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA745682
#> 167  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA744913
#> 168                                                        <NA>
#> 169  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA687512
#> 170                                                        <NA>
#> 171                                                        <NA>
#> 172  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA631512
#> 173                                                        <NA>
#> 174                                                        <NA>
#> 175  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA644333
#> 176  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA742406
#> 177  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA633387
#> 178                                                        <NA>
#> 179  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA740192
#> 180  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA727801
#> 181                                                        <NA>
#> 182                                                        <NA>
#> 183                                                        <NA>
#> 184  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA656806
#> 185  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA656558
#> 186                                                        <NA>
#> 187  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA735767
#> 188  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA726564
#> 189  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA694301
#> 190                                                        <NA>
#> 191                                                        <NA>
#> 192  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA472881
#> 193  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA730290
#> 194                                                        <NA>
#> 195                                                        <NA>
#> 196  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA724666
#> 197  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA663592
#> 198  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA669693
#> 199                                                        <NA>
#> 200                                                        <NA>
#> 201                                                        <NA>
#> 202  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA642363
#> 203  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA690574
#> 204                                                        <NA>
#> 205  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA593449
#> 206                                                        <NA>
#> 207  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA635687
#> 208  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA623002
#> 209                                                        <NA>
#> 210                                                        <NA>
#> 211                                                        <NA>
#> 212                                                        <NA>
#> 213  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA701954
#> 214  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA703993
#> 215  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA442026
#> 216                                                        <NA>
#> 217  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA685127
#> 218  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA699024
#> 219                                                        <NA>
#> 220  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA636082
#> 221  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA636079
#> 222                                                        <NA>
#> 223                                                        <NA>
#> 224                                                        <NA>
#> 225  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA705698
#> 226                                                        <NA>
#> 227  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA682616
#> 228                                                        <NA>
#> 229  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA702119
#> 230                                                        <NA>
#> 231                                                        <NA>
#> 232                                                        <NA>
#> 233                                                        <NA>
#> 234                                                        <NA>
#> 235                                                        <NA>
#> 236                                                        <NA>
#> 237                                                        <NA>
#> 238  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA662313
#> 239  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA670242
#> 240                                                        <NA>
#> 241                                                        <NA>
#> 242                                                        <NA>
#> 243                                                        <NA>
#> 244  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA627460
#> 245                                                        <NA>
#> 246  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA686946
#> 247                                                        <NA>
#> 248  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA673283
#> 249  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA673284
#> 250                                                        <NA>
#> 251                                                        <NA>
#> 252                                                        <NA>
#> 253  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA580290
#> 254                                                        <NA>
#> 255                                                        <NA>
#> 256  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA687419
#> 257                                                        <NA>
#> 258  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA631368
#> 259  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA686939
#> 260  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA686410
#> 261  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA664761
#> 262  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA683217
#> 263                                                        <NA>
#> 264                                                        <NA>
#> 265  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA622680
#> 266                                                        <NA>
#> 267                                                        <NA>
#> 268                                                        <NA>
#> 269  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA662985
#> 270  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA679891
#> 271                                                        <NA>
#> 272                                                        <NA>
#> 273                                                        <NA>
#> 274  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA645833
#> 275  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA603462
#> 276                                                        <NA>
#> 277                                                        <NA>
#> 278  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA608119
#> 279                                                        <NA>
#> 280                                                        <NA>
#> 281  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA671458
#> 282  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA670431
#> 283                                                        <NA>
#> 284  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA646066
#> 285  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA645920
#> 286  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA549248
#> 287  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA669014
#> 288                                                        <NA>
#> 289  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA666806
#> 290  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA601667
#> 291  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA639829
#> 292  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA555081
#> 293  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA637143
#> 294  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA660402
#> 295                                                        <NA>
#> 296                                                        <NA>
#> 297                                                        <NA>
#> 298  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA589266
#> 299  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA659488
#> 300                                                        <NA>
#> 301  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA622976
#> 302  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA622977
#> 303  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA552427
#> 304                                                        <NA>
#> 305                                                        <NA>
#> 306                                                        <NA>
#> 307  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA657567
#> 308  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA657560
#> 309  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA657559
#> 310                                                        <NA>
#> 311  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA558555
#> 312  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA558556
#> 313  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA558553
#> 314  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA656788
#> 315                                                        <NA>
#> 316  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA397857
#> 317                                                        <NA>
#> 318  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA655260
#> 319  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA604580
#> 320  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA601464
#> 321  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA542809
#> 322  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA577123
#> 323                                                        <NA>
#> 324  https://www.ncbi.nlm.nih.gov/Traces/study/?acc=PRJNA636404
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#> 326                                                        <NA>
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#> 202                 <NA>                               <NA>
#> 203                 <NA>                               <NA>
#> 204                 <NA>                               <NA>
#> 205                 <NA>                               <NA>
#> 206                 <NA>                               <NA>
#> 207                 <NA>                               <NA>
#> 208                 <NA>                               <NA>
#> 209                 <NA>                               <NA>
#> 210                 <NA>                               <NA>
#> 211                 <NA>                               <NA>
#> 212                 <NA>                               <NA>
#> 213                 <NA>                               <NA>
#> 214                 <NA>                               <NA>
#> 215                 <NA>                               <NA>
#> 216                 <NA>                               <NA>
#> 217                 <NA>                               <NA>
#> 218                 <NA>                               <NA>
#> 219                 <NA>                               <NA>
#> 220                 <NA>                               <NA>
#> 221                 <NA>                               <NA>
#> 222                 <NA>                               <NA>
#> 223                 <NA>                               <NA>
#> 224                 <NA>                               <NA>
#> 225                 <NA>                               <NA>
#> 226                 <NA>                               <NA>
#> 227                 <NA>                               <NA>
#> 228                 <NA>                               <NA>
#> 229                 <NA>                               <NA>
#> 230                 <NA>                               <NA>
#> 231                 <NA>                               <NA>
#> 232                 <NA>                               <NA>
#> 233                 <NA>                               <NA>
#> 234                 <NA>                               <NA>
#> 235                 <NA>                               <NA>
#> 236                 <NA>                               <NA>
#> 237                 <NA>                               <NA>
#> 238                 <NA>                               <NA>
#> 239                 <NA>                               <NA>
#> 240                 <NA>                               <NA>
#> 241                 <NA>                               <NA>
#> 242                 <NA>                               <NA>
#> 243                 <NA>                               <NA>
#> 244                 <NA>                               <NA>
#> 245                 <NA>                               <NA>
#> 246                 <NA>                               <NA>
#> 247                 <NA>                               <NA>
#> 248                 <NA>                               <NA>
#> 249                 <NA>                               <NA>
#> 250                 <NA>                               <NA>
#> 251                 <NA>                               <NA>
#> 252                 <NA>                               <NA>
#> 253                 <NA>                               <NA>
#> 254                 <NA>                               <NA>
#> 255                 <NA>                               <NA>
#> 256                 <NA>                               <NA>
#> 257                 <NA>                               <NA>
#> 258                 <NA>                               <NA>
#> 259                 <NA>                               <NA>
#> 260                 <NA>                               <NA>
#> 261                 <NA>                               <NA>
#> 262                 <NA>                               <NA>
#> 263                 <NA>                               <NA>
#> 264                 <NA>                               <NA>
#> 265                 <NA>                               <NA>
#> 266                 <NA>                               <NA>
#> 267                 <NA>                               <NA>
#> 268                 <NA>                               <NA>
#> 269                 <NA>                               <NA>
#> 270                 <NA>                               <NA>
#> 271                 <NA>                               <NA>
#> 272                 <NA>                               <NA>
#> 273                 <NA>                               <NA>
#> 274                 <NA>                               <NA>
#> 275                 <NA>                               <NA>
#> 276                 <NA>                               <NA>
#> 277                 <NA>                               <NA>
#> 278                 <NA>                               <NA>
#> 279                 <NA>                               <NA>
#> 280                 <NA>                               <NA>
#> 281                 <NA>                               <NA>
#> 282                 <NA>                               <NA>
#> 283                 <NA>                               <NA>
#> 284                 <NA>                               <NA>
#> 285                 <NA>                               <NA>
#> 286                 <NA>                               <NA>
#> 287                 <NA>                               <NA>
#> 288                 <NA>                               <NA>
#> 289                 <NA>                               <NA>
#> 290                 <NA>                               <NA>
#> 291                 <NA>                               <NA>
#> 292                 <NA>                               <NA>
#> 293                 <NA>                               <NA>
#> 294                 <NA>                               <NA>
#> 295                 <NA>                               <NA>
#> 296                 <NA>                               <NA>
#> 297                 <NA>                               <NA>
#> 298                 <NA>                               <NA>
#> 299                 <NA>                               <NA>
#> 300                 <NA>                               <NA>
#> 301                 <NA>                               <NA>
#> 302                 <NA>                               <NA>
#> 303                 <NA>                               <NA>
#> 304                 <NA>                               <NA>
#> 305                 <NA>                               <NA>
#> 306                 <NA>                               <NA>
#> 307                 <NA>                               <NA>
#> 308                 <NA>                               <NA>
#> 309                 <NA>                               <NA>
#> 310                 <NA>                               <NA>
#> 311                 <NA>                               <NA>
#> 312                 <NA>                               <NA>
#> 313                 <NA>                               <NA>
#> 314                 <NA>                               <NA>
#> 315                 <NA>                               <NA>
#> 316                 <NA>                               <NA>
#> 317                 <NA>                               <NA>
#> 318                 <NA>                               <NA>
#> 319                 <NA>                               <NA>
#> 320                 <NA>                               <NA>
#> 321                 <NA>                               <NA>
#> 322                 <NA>                               <NA>
#> 323                 <NA>                               <NA>
#> 324                 <NA>                               <NA>
#> 325                 <NA>                               <NA>
#> 326                 <NA>                               <NA>
#> 327                 <NA>                               <NA>
#> 328                 <NA>                               <NA>
#> 329                 <NA>                               <NA>
#> 330                 <NA>                               <NA>
#> 331                 <NA>                               <NA>
#> 332                 <NA>                               <NA>
#> 333                 <NA>                               <NA>
#> 334                 <NA>                               <NA>
#> 335                 <NA>                               <NA>
#> 336                 <NA>                               <NA>
#> 337                 <NA>                               <NA>
#> 338                 <NA>                               <NA>
#> 339                 <NA>                               <NA>
#> 340                 <NA>                               <NA>
#> 341                 <NA>                               <NA>
#> 342                 <NA>                               <NA>
#> 343                 <NA>                               <NA>
#> 344                 <NA>                               <NA>
#> 345                 <NA>                               <NA>
#> 346                 <NA>                               <NA>
#> 347                 <NA>                               <NA>
#> 348                 <NA>                               <NA>
#> 349                 <NA>                               <NA>
#> 350                 <NA>                               <NA>
#> 351                 <NA>                               <NA>
#> 352                 <NA>                               <NA>
#> 353                 <NA>                               <NA>
#> 354                 <NA>                               <NA>
#> 355                 <NA>                               <NA>
#> 356                 <NA>                               <NA>
#> 357                 <NA>                               <NA>
#> 358                 <NA>                               <NA>
#> 359                 <NA>                               <NA>
#> 360                 <NA>                               <NA>
#> 361                 <NA>                               <NA>
#> 362                 <NA>                               <NA>
#> 363                 <NA>                               <NA>
#> 364                 <NA>                               <NA>
#> 365                 <NA>                               <NA>
#> 366                 <NA>                               <NA>
#> 367                 <NA>                               <NA>
#> 368                 <NA>                               <NA>
#> 369                 <NA>                               <NA>
#> 370                 <NA>                               <NA>
#> 371                 <NA>                               <NA>
#> 372                 <NA>                               <NA>
#> 373                 <NA>                               <NA>
#> 374                 <NA>                               <NA>
#> 375                 <NA>                               <NA>
#> 376                 <NA>                               <NA>
#> 377                 <NA>                               <NA>
#> 378                 <NA>                               <NA>
#> 379                 <NA>                               <NA>
#> 380                 <NA>                               <NA>
#> 381                 <NA>                               <NA>
#> 382                 <NA>                               <NA>
#> 383                 <NA>                               <NA>
#> 384                 <NA>                               <NA>
#> 385                 <NA>                               <NA>
#> 386                 <NA>                               <NA>
#> 387                 <NA>                               <NA>
#> 388                 <NA>                               <NA>
#> 389                 <NA>                               <NA>
#> 390                 <NA>                               <NA>
#> 391                 <NA>                               <NA>
#> 392                 <NA>                               <NA>
#> 393                 <NA>                               <NA>
#> 394                 <NA>                               <NA>
#> 395                 <NA>                               <NA>
#> 396                 <NA>                               <NA>
#> 397                 <NA>                               <NA>
#> 398                 <NA>                               <NA>
#> 399                 <NA>                               <NA>
#> 400                 <NA>                               <NA>
#> 401                 <NA>                               <NA>
#> 402                 <NA>                               <NA>
#> 403                 <NA>                               <NA>
#> 404                 <NA>                               <NA>
#> 405                 <NA>                               <NA>
#> 406                 <NA>                               <NA>
#> 407                 <NA>                               <NA>
#> 408                 <NA>                               <NA>
#> 409                 <NA>                               <NA>
#> 410                 <NA>                               <NA>
#> 411                 <NA>                               <NA>
#> 412                 <NA>                               <NA>
#> 413                 <NA>                               <NA>
#> 414                 <NA>                               <NA>
#> 415                 <NA>                               <NA>
#> 416                 <NA>                               <NA>
#> 417                 <NA>                               <NA>
#> 418                 <NA>                               <NA>
#> 419                 <NA>                               <NA>
#> 420                 <NA>                               <NA>
#> 421                 <NA>                               <NA>
#> 422                 <NA>                               <NA>
#> 423                 <NA>                               <NA>
#> 424                 <NA>                               <NA>
#> 425                 <NA>                               <NA>
#> 426                 <NA>                               <NA>
#> 427                 <NA>                               <NA>
#> 428                 <NA>                               <NA>
#> 429                 <NA>                               <NA>
#> 430                 <NA>                               <NA>
#> 431                 <NA>                               <NA>
#> 432                 <NA>                               <NA>
#> 433                 <NA>                               <NA>
#> 434                 <NA>                               <NA>
#> 435                 <NA>                               <NA>
#> 436                 <NA>                               <NA>
#> 437                 <NA>                               <NA>
#> 438                 <NA>                               <NA>
#> 439                 <NA>                               <NA>
#> 440                 <NA>                               <NA>
#> 441                 <NA>                               <NA>
#> 442                 <NA>                               <NA>
#> 443                 <NA>                               <NA>
#> 444                 <NA>                               <NA>
#> 445                 <NA>                               <NA>
#> 446                 <NA>                               <NA>
#> 447                 <NA>                               <NA>
#> 448                 <NA>                               <NA>
#> 449                 <NA>                               <NA>
#> 450                 <NA>                               <NA>
#> 451                 <NA>                               <NA>
#> 452                 <NA>                               <NA>
#> 453                 <NA>                               <NA>
#> 454                 <NA>                               <NA>
#> 455                 <NA>                               <NA>
#> 456                 <NA>                               <NA>
#> 457                 <NA>                               <NA>
#> 458                 <NA>                               <NA>
#> 459                 <NA>                               <NA>
#> 460                 <NA>                               <NA>
#> 461                 <NA>                               <NA>
#> 462                 <NA>                               <NA>
#> 463                 <NA>                               <NA>
#> 464                 <NA>                               <NA>
#> 465                 <NA>                               <NA>
#> 466                 <NA>                               <NA>
#> 467                 <NA>                               <NA>
#> 468                 <NA>                               <NA>
#> 469                 <NA>                               <NA>
#> 470                 <NA>                               <NA>
#> 471                 <NA>                               <NA>
#> 472                 <NA>                               <NA>
#> 473                 <NA>                               <NA>
#> 474                 <NA>                               <NA>
#> 475                 <NA>                               <NA>
#> 476                 <NA>                               <NA>
#> 477                 <NA>                               <NA>
#> 478                 <NA>                               <NA>
#> 479                 <NA>                               <NA>
#> 480                 <NA>                               <NA>
#> 481                 <NA>                               <NA>
#> 482                 <NA>                               <NA>
#> 483                 <NA>                               <NA>
#> 484                 <NA>                               <NA>
#> 485                 <NA>                               <NA>
#> 486                 <NA>                               <NA>
#> 487                 <NA>                               <NA>
#> 488                 <NA>                               <NA>
#> 489                 <NA>                               <NA>
#> 490               ENCODE                               <NA>
#> 491               ENCODE                               <NA>
#> 492               ENCODE                               <NA>
#> 493                 <NA>                               <NA>
#> 494                 <NA>                               <NA>
#> 495                 <NA>                               <NA>
#> 496                 <NA>                               <NA>
#> 497                 <NA>                               <NA>
#> 498                 <NA>                               <NA>
#> 499                 <NA>                               <NA>
#> 500                 <NA>                               <NA>
#> 501                 <NA>                               <NA>
#> 502                 <NA>                               <NA>
#> 503                 <NA>                               <NA>
#> 504                 <NA>                               <NA>
#> 505                 <NA>                               <NA>
#> 506                 <NA>                               <NA>
#> 507                 <NA>                               <NA>
#> 508                 <NA>                               <NA>
#> 509                 <NA>                               <NA>
#> 510                 <NA>                               <NA>
#> 511                 <NA>                               <NA>
#> 512                 <NA>                               <NA>
#> 513                 <NA>                               <NA>
#> 514                 <NA>                               <NA>
#> 515                 <NA>                               <NA>
#> 516                 <NA>                               <NA>
#> 517                 <NA>                               <NA>
#> 518                 <NA>                               <NA>
#> 519                 <NA>                               <NA>
#> 520                 <NA>                               <NA>
#> 521                 <NA>                               <NA>
#> 522                 <NA>                               <NA>
#> 523                 <NA>                               <NA>
#> 524                 <NA>                               <NA>
#> 525                 <NA>                               <NA>
#> 526                 <NA>                               <NA>
#> 527                 <NA>                               <NA>
#> 528                 <NA>                               <NA>
#> 529                 <NA>                               <NA>
#> 530                 <NA>                               <NA>
#> 531                 <NA>                               <NA>
#> 532                 <NA>                               <NA>
#> 533                 <NA>                               <NA>
#> 534                 <NA>                               <NA>
#> 535                 <NA>                               <NA>
#> 536                 <NA>                               <NA>
#> 537                 <NA>                               <NA>
#> 538                 <NA>                               <NA>
#> 539                 <NA>                               <NA>
#> 540                 <NA>                               <NA>
#> 541                 <NA>                               <NA>
#> 542                 <NA>                               <NA>
#> 543                 <NA>                               <NA>
#> 544                 <NA>                               <NA>
#> 545                 <NA>                               <NA>
#> 546                 <NA>                               <NA>
#> 547                 <NA>                               <NA>
#> 548                 <NA>                               <NA>
#> 549                 <NA>                               <NA>
#> 550                 <NA>                               <NA>
#> 551                 <NA>                               <NA>
#> 552                 <NA>                               <NA>
#> 553                 <NA>                               <NA>
#> 554                 <NA>                               <NA>
#> 555                 <NA>                               <NA>
#> 556                 <NA>                               <NA>
#> 557                 <NA>                               <NA>
#> 558                 <NA>                               <NA>
#> 559                 <NA>                               <NA>
#> 560                 <NA>                               <NA>
#> 561                 <NA>                               <NA>
#> 562                 <NA>                               <NA>
#> 563                 <NA>                               <NA>
#> 564                 <NA>                               <NA>
#> 565                 <NA>                               <NA>
#> 566                 <NA>                               <NA>
#> 567                 <NA>                               <NA>
#> 568                 <NA>                               <NA>
#> 569                 <NA>                               <NA>
#> 570                 <NA>                               <NA>
#> 571                 <NA>                               <NA>
#> 572                 <NA>                               <NA>
#> 573                 <NA>                               <NA>
#> 574                 <NA>                               <NA>
#> 575                 <NA>                               <NA>
#> 576                 <NA>                               <NA>
#> 577                 <NA>                               <NA>
#> 578                 <NA>                               <NA>
#> 579                 <NA>                               <NA>
#> 580                 <NA>                               <NA>
#> 581                 <NA>                               <NA>
#> 582                 <NA>                               <NA>
#> 583                 <NA>                               <NA>
#> 584                 <NA>                               <NA>
#> 585                 <NA>                               <NA>
#> 586                 <NA>                               <NA>
#> 587                 <NA>                               <NA>
#> 588                 <NA>                               <NA>
#> 589                 <NA>                               <NA>
#> 590                 <NA>                               <NA>
#> 591                 <NA>                               <NA>
#> 592                 <NA>                               <NA>
#> 593                 <NA>                               <NA>
#> 594                 <NA>                               <NA>
#> 595                 <NA>                               <NA>
#> 596                 <NA>                               <NA>
#> 597                 <NA>                               <NA>
#> 598                 <NA>                               <NA>
#> 599                 <NA>                               <NA>
#> 600                 <NA>                               <NA>
#> 601                 <NA>                               <NA>
#> 602                 <NA>                               <NA>
#> 603                 <NA>                               <NA>
#> 604                 <NA>                               <NA>
#> 605                 <NA>                               <NA>
#> 606                 <NA>                               <NA>
#> 607                 <NA>                               <NA>
#> 608                 <NA>                               <NA>
#> 609                 <NA>                               <NA>
#> 610                 <NA>                               <NA>
#> 611                 <NA>                               <NA>
#> 612                 <NA>                               <NA>
#> 613                 <NA>                               <NA>
#> 614                 <NA>                               <NA>
#> 615                 <NA>                               <NA>
#> 616                 <NA>                               <NA>
#> 617                 <NA>                               <NA>
#> 618                 <NA>                               <NA>
#> 619                 <NA>                               <NA>
#> 620                 <NA>                               <NA>
#> 621                 <NA>                               <NA>
#> 622                 <NA>                               <NA>
#> 623                 <NA>                               <NA>
#> 624                 <NA>                               <NA>
#> 625                 <NA>                               <NA>
#> 626                 <NA>                               <NA>
#> 627                 <NA>                               <NA>
#> 628                 <NA>                               <NA>
#> 629                 <NA>                               <NA>
#> 630                 <NA>                               <NA>
#> 631                 <NA>                               <NA>
#> 632                 <NA>                               <NA>
#> 633                 <NA>                               <NA>
#> 634                 <NA>                               <NA>
#> 635                 <NA>                               <NA>
#> 636                 <NA>                               <NA>
#> 637                 <NA>                               <NA>
#> 638                 <NA>                               <NA>
#> 639                 <NA>                               <NA>
#> 640                 <NA>                               <NA>
#> 641                 <NA>                               <NA>
#> 642                 <NA>                               <NA>
#> 643                 <NA>                               <NA>
#> 644                 <NA>                               <NA>
#> 645                 <NA>                               <NA>
#> 646                 <NA>                               <NA>
#> 647                 <NA>                               <NA>
#> 648                 <NA>                               <NA>
#> 649                 <NA>                               <NA>
#> 650                 <NA>                               <NA>
#> 651                 <NA>                               <NA>
#> 652                 <NA>                               <NA>
#> 653                 <NA>                               <NA>
#> 654                 <NA>                               <NA>
#> 655                 <NA>                               <NA>
#> 656                 <NA>                               <NA>
#> 657                 <NA>                               <NA>
#> 658                 <NA>                               <NA>
#> 659                 <NA>                               <NA>
#> 660                 <NA>                               <NA>
#> 661                 <NA>                               <NA>
#> 662                 <NA>                               <NA>
#> 663                 <NA>                               <NA>
#> 664                 <NA>                               <NA>
#> 665                 <NA>                               <NA>
#> 666                 <NA>                               <NA>
#> 667                 <NA>                               <NA>
#> 668                 <NA>                               <NA>
#> 669                 <NA>                               <NA>
#> 670                 <NA>                               <NA>
#> 671                 <NA>                               <NA>
#> 672                 <NA>                               <NA>
#> 673                 <NA>                               <NA>
#> 674                 <NA>                               <NA>
#> 675                 <NA>                               <NA>
#> 676                 <NA>                               <NA>
#> 677                 <NA>                               <NA>
#> 678                 <NA>                               <NA>
#> 679                 <NA>                               <NA>
#> 680                 <NA>                               <NA>
#> 681                 <NA>                               <NA>
#> 682                 <NA>                               <NA>
#> 683                 <NA>                               <NA>
#> 684                 <NA>                               <NA>
#> 685                 <NA>                               <NA>
#> 686                 <NA>                               <NA>
#> 687                 <NA>                               <NA>
#> 688                 <NA>                               <NA>
#> 689                 <NA>                               <NA>
#> 690                 <NA>                               <NA>
#> 691                 <NA>                               <NA>
#> 692                 <NA>                               <NA>
#> 693                 <NA>                               <NA>
#> 694                 <NA>                               <NA>
#> 695                 <NA>                               <NA>
#> 696                 <NA>                               <NA>
#> 697                 <NA>                               <NA>
#> 698                 <NA>                               <NA>
#> 699                 <NA>                               <NA>
#> 700                 <NA>                               <NA>
#> 701                 <NA>                               <NA>
#> 702                 <NA>                               <NA>
#> 703                 <NA>                               <NA>
#> 704                 <NA>                               <NA>
#> 705                 <NA>                               <NA>
#> 706                 <NA>                               <NA>
#> 707                 <NA>                               <NA>
#> 708                 <NA>                               <NA>
#> 709                 <NA>                               <NA>
#> 710                 <NA>                               <NA>
#> 711                 <NA>                               <NA>
#> 712                 <NA>                               <NA>
#> 713                 <NA>                               <NA>
#> 714                 <NA>                               <NA>
#> 715                 <NA>                               <NA>
#> 716                 <NA>                               <NA>
#> 717                 <NA>                               <NA>
#> 718                 <NA>                               <NA>
#> 719                 <NA>                               <NA>
#> 720                 <NA>                               <NA>
#> 721                 <NA>                               <NA>
#> 722                 <NA>                               <NA>
#> 723                 <NA>                               <NA>
#> 724                 <NA>                               <NA>
#> 725                 <NA>                               <NA>
#> 726                 <NA>                               <NA>
#> 727                 <NA>                               <NA>
#> 728                 <NA>                               <NA>
#> 729                 <NA>                               <NA>
#> 730                 <NA>                               <NA>
#> 731                 <NA>                               <NA>
#> 732                 <NA>                               <NA>
#> 733                 <NA>                               <NA>
#> 734                 <NA>                               <NA>
#> 735                 <NA>                               <NA>
#> 736                 <NA>                               <NA>
#> 737                 <NA>                               <NA>
#> 738                 <NA>                               <NA>
#> 739                 <NA>                               <NA>
#> 740                 <NA>                               <NA>
#> 741                 <NA>                               <NA>
#> 742                 <NA>                               <NA>
#> 743                 <NA>                               <NA>
#> 744                 <NA>                               <NA>
#> 745                 <NA>                               <NA>
#> 746                 <NA>                               <NA>
#> 747                 <NA>                               <NA>
#> 748                 <NA>                               <NA>
#> 749                 <NA>                               <NA>
#> 750                 <NA>                               <NA>
#> 751                 <NA>                               <NA>
#> 752                 <NA>                               <NA>
#> 753                 <NA>                               <NA>
#> 754                 <NA>                               <NA>
#> 755                 <NA>                               <NA>
#> 756                 <NA>                               <NA>
#> 757                 <NA>                               <NA>
#> 758                 <NA>                               <NA>
#> 759                 <NA>                               <NA>
#> 760                 <NA>                               <NA>
#> 761                 <NA>                               <NA>
#> 762                 <NA>                               <NA>
#> 763                 <NA>                               <NA>
#> 764                 <NA>                               <NA>
#> 765                 <NA>                               <NA>
#> 766                 <NA>                               <NA>
#> 767                 <NA>                               <NA>
#> 768                 <NA>                               <NA>
#> 769                 <NA>                               <NA>
#> 770                 <NA>                               <NA>
#> 771                 <NA>                               <NA>
#> 772                 <NA>                               <NA>
#> 773                 <NA>                               <NA>
#> 774                 <NA>                               <NA>
#> 775                 <NA>                               <NA>
#> 776                 <NA>                               <NA>
#> 777                 <NA>                               <NA>
#> 778                 <NA>                               <NA>
#> 779                 <NA>                               <NA>
#> 780                 <NA>                               <NA>
#> 781                 <NA>                               <NA>
#> 782                 <NA>                               <NA>
#> 783                 <NA>                               <NA>
#> 784                 <NA>                               <NA>
#> 785                 <NA>                               <NA>
#> 786                 <NA>                               <NA>
#> 787                 <NA>                               <NA>
#> 788                 <NA>                               <NA>
#> 789                 <NA>                               <NA>
#> 790                 <NA>                               <NA>
#> 791                 <NA>                               <NA>
#> 792                 <NA>                               <NA>
#> 793                 <NA>                               <NA>
#> 794                 <NA>                               <NA>
#> 795                 <NA>                               <NA>
#> 796                 <NA>                               <NA>
#> 797                 <NA>                               <NA>
#> 798                 <NA>                               <NA>
#> 799                 <NA>                               <NA>
#> 800                 <NA>                               <NA>
#> 801                 <NA>                               <NA>
#> 802                 <NA>                               <NA>
#> 803                 <NA>                               <NA>
#> 804                 <NA>                               <NA>
#> 805                 <NA>                               <NA>
#> 806                 <NA>                               <NA>
#> 807                 <NA>                               <NA>
#> 808                 <NA>                               <NA>
#> 809                 <NA>                               <NA>
#> 810                 <NA>                               <NA>
#> 811                 <NA>                               <NA>
#> 812                 <NA>                               <NA>
#> 813                 <NA>                               <NA>
#> 814                 <NA>                               <NA>
#> 815                 <NA>                               <NA>
#> 816                 <NA>                               <NA>
#> 817                 <NA>                               <NA>
#> 818                 <NA>                               <NA>
#> 819                 <NA>                               <NA>
#> 820                 <NA>                               <NA>
#> 821                 <NA>                               <NA>
#> 822                 <NA>                               <NA>
#> 823                 <NA>                               <NA>
#> 824                 <NA>                               <NA>
#> 825                 <NA>                               <NA>
#> 826                 <NA>                               <NA>
#> 827                 <NA>                               <NA>
#> 828                 <NA>                               <NA>
#> 829                 <NA>                               <NA>
#> 830                 <NA>                               <NA>
#> 831                 <NA>                               <NA>
#> 832                 <NA>                               <NA>
#> 833                 <NA>                               <NA>
#> 834                 <NA>                               <NA>
#> 835                 <NA>                               <NA>
#> 836                 <NA>                               <NA>
#> 837                 <NA>                               <NA>
#> 838                 <NA>                               <NA>
#> 839                 <NA>                               <NA>
#> 840                 <NA>                               <NA>
#> 841                 <NA>                               <NA>
#> 842                 <NA>                               <NA>
#> 843                 <NA>                               <NA>
#> 844                 <NA>                               <NA>
#> 845                 <NA>                               <NA>
#> 846                 <NA>                               <NA>
#> 847                 <NA>                               <NA>
#> 848                 <NA>                               <NA>
#> 849                 <NA>                               <NA>
#> 850                 <NA>                               <NA>
#> 851                 <NA>                               <NA>
#> 852                 <NA>                               <NA>
#> 853                 <NA>                               <NA>
#> 854                 <NA>                               <NA>
#> 855                 <NA>                               <NA>
#> 856                 <NA>                               <NA>
#> 857                 <NA>                               <NA>
#> 858                 <NA>                               <NA>
#> 859                 <NA>                               <NA>
#> 860                 <NA>                               <NA>
#> 861                 <NA>                               <NA>
#> 862                 <NA>                               <NA>
#> 863                 <NA>                               <NA>
#> 864                 <NA>                               <NA>
#> 865                 <NA>                               <NA>
#> 866                 <NA>                               <NA>
#> 867                 <NA>                                GDS
#> 868                 <NA>                               <NA>
#> 869                 <NA>                               <NA>
#> 870                 <NA>                               <NA>
#> 871                 <NA>                               <NA>
#> 872                 <NA>                               <NA>
#> 873                 <NA>                               <NA>
#> 874                 <NA>                               <NA>
#> 875                 <NA>                               <NA>
#> 876                 <NA>                               <NA>
#> 877                 <NA>                               <NA>
#> 878                 <NA>                               <NA>
#> 879                 <NA>                               <NA>
#> 880                 <NA>                               <NA>
#> 881                 <NA>                               <NA>
#> 882                 <NA>                               <NA>
#> 883                 <NA>                               <NA>
#> 884                 <NA>                               <NA>
#> 885                 <NA>                               <NA>
#> 886                 <NA>                               <NA>
#> 887                 <NA>                               <NA>
#> 888                 <NA>                               <NA>
#> 889                 <NA>                               <NA>
#> 890                 <NA>                               <NA>
#> 891                 <NA>                               <NA>
#> 892                 <NA>                               <NA>
#> 893                 <NA>                               <NA>
#> 894                 <NA>                               <NA>
#> 895                 <NA>                               <NA>
#> 896                 <NA>                               <NA>
#> 897                 <NA>                               <NA>
#> 898                 <NA>                               <NA>
#> 899                 <NA>                               <NA>
#> 900                 <NA>                               <NA>
#> 901                 <NA>                               <NA>
#> 902                 <NA>                               <NA>
#> 903                 <NA>                               <NA>
#> 904                 <NA>                               <NA>
#> 905                 <NA>                               <NA>
#> 906                 <NA>                               <NA>
#> 907                 <NA>                               <NA>
#> 908                 <NA>                               <NA>
#> 909                 <NA>                               <NA>
#> 910                 <NA>                               <NA>
#> 911                 <NA>                               <NA>
#> 912                 <NA>                               <NA>
#> 913                 <NA>                               <NA>
#> 914                 <NA>                               <NA>
#> 915                 <NA>                               <NA>
#> 916                 <NA>                               <NA>
#> 917                 <NA>                               <NA>
#> 918                 <NA>                               <NA>
#> 919                 <NA>                               <NA>
#> 920                 <NA>                               <NA>
#> 921                 <NA>                               <NA>
#> 922                 <NA>                                GDS
#> 923                 <NA>                               <NA>
#> 924                 <NA>                               <NA>
#> 925                 <NA>                               <NA>
#> 926                 <NA>                               <NA>
#> 927                 <NA>                               <NA>
#> 928                 <NA>                               <NA>
#> 929                 <NA>                               <NA>
#> 930                 <NA>                               <NA>
#> 931                 <NA>                               <NA>
#> 932                 <NA>                               <NA>
#> 933                 <NA>                               <NA>
#> 934                 <NA>                               <NA>
#> 935                 <NA>                                GDS
#> 936                 <NA>                               <NA>
#> 937                 <NA>                               <NA>
#> 938                 <NA>                               <NA>
#> 939                 <NA>                               <NA>
#> 940                 <NA>                               <NA>
#> 941                 <NA>                               <NA>
#> 942                 <NA>                               <NA>
#> 943                 <NA>                               <NA>
#> 944                 <NA>                               <NA>
#> 945                 <NA>                                GDS
#> 946                 <NA>                               <NA>
#> 947                 <NA>                               <NA>
#> 948                 <NA>                               <NA>
#> 949                 <NA>                               <NA>
#> 950                 <NA>                               <NA>
#> 951                 <NA>                               <NA>
#> 952                 <NA>                               <NA>
#> 953                 <NA>                               <NA>
#> 954                 <NA>                               <NA>
#> 955                 <NA>                               <NA>
#> 956                 <NA>                               <NA>
#> 957                 <NA>                               <NA>
#> 958                 <NA>                               <NA>
#> 959                 <NA>                               <NA>
#> 960                 <NA>                               <NA>
#> 961                 <NA>                               <NA>
#> 962                 <NA>                               <NA>
#> 963                 <NA>                               <NA>
#> 964                 <NA>                                GDS
#> 965                 <NA>                               <NA>
#> 966                 <NA>                               <NA>
#> 967                 <NA>                               <NA>
#> 968                 <NA>                                GDS
#> 969                 <NA>                               <NA>
#> 970                 <NA>                               <NA>
#> 971                 <NA>                               <NA>
#> 972                 <NA>                                GDS
#> 973                 <NA>                               <NA>
#> 974                 <NA>                               <NA>
#> 975                 <NA>                               <NA>
#> 976                 <NA>                               <NA>
#> 977                 <NA>                                GDS
#> 978                 <NA>                                GDS
#> 979                 <NA>                                GDS
#> 980                 <NA>                               <NA>
#> 981                 <NA>                               <NA>
#> 982                 <NA>                               <NA>
#> 983                 <NA>                               <NA>
#> 984                 <NA>                               <NA>
#> 985                 <NA>                               <NA>
#> 986                 <NA>                               <NA>
#> 987                 <NA>                               <NA>
#> 988                 <NA>                               <NA>
#> 989                 <NA>                                GDS
#> 990                 <NA>                               <NA>
#> 991                 <NA>                               <NA>
#> 992                 <NA>                               <NA>
#> 993                 <NA>                               <NA>
#> 994                 <NA>                               <NA>
#> 995                 <NA>                                GDS
#> 996                 <NA>                                GDS
#> 997                 <NA>                                GDS
#> 998                 <NA>                               <NA>
#> 999                 <NA>                                GDS
#> 1000                <NA>                                GDS
#> 1001                <NA>                               <NA>
#> 1002                <NA>                               <NA>
#> 1003                <NA>                               <NA>
#> 1004                <NA>                               <NA>
#> 1005                <NA>                               <NA>
#> 1006                <NA>                                GDS
#> 1007                <NA>                                GDS
#> 1008                <NA>                               <NA>
#> 1009                <NA>                                GDS
#> 1010                <NA>                               <NA>
#> 1011                <NA>                                GDS
#> 1012                <NA>                               <NA>
#> 1013                <NA>                               <NA>
#> 1014                <NA>                                GDS
#> 1015                <NA>                               <NA>
#> 1016                <NA>                               <NA>
#> 1017                <NA>                               <NA>
#> 1018                <NA>                                GDS
#> 1019                <NA>                               <NA>
#> 1020                <NA>                               <NA>
#> 1021                <NA>                                GDS
#> 1022              ENCODE                               <NA>
#> 1023 Roadmap Epigenomics                               <NA>
#> 1024                <NA>                               <NA>
#> 1025                <NA>                               <NA>
#> 1026                <NA>                                GDS
#> 1027                <NA>                                GDS
#> 1028                <NA>                               <NA>
#> 1029                <NA>                               <NA>
#> 1030                <NA>                               <NA>
#> 1031                <NA>                               <NA>
#> 1032                <NA>                               <NA>
#> 1033                <NA>                               <NA>
#> 1034                <NA>                               <NA>
#> 1035                <NA>                               <NA>
#> 1036                <NA>                                GDS
#> 1037                <NA>                               <NA>
#> 1038                <NA>                                GDS
#> 1039                <NA>                               <NA>
#> 1040                <NA>                               <NA>
#> 1041                <NA>                               <NA>
#> 1042                <NA>                               <NA>
#> 1043                <NA>                               <NA>
#> 1044                <NA>                        GDS4129 GDS
#> 1045                <NA>                                GDS
#> 1046                <NA>                               <NA>
#> 1047                <NA>                               <NA>
#> 1048                <NA>                                GDS
#> 1049                <NA>                               <NA>
#> 1050                <NA>                               <NA>
#> 1051 Roadmap Epigenomics                               <NA>
#> 1052                <NA>                               <NA>
#> 1053                <NA>                                GDS
#> 1054                <NA>                               <NA>
#> 1055                <NA>                               <NA>
#> 1056                <NA>                               <NA>
#> 1057                <NA>                               <NA>
#> 1058                <NA>                               <NA>
#> 1059                <NA>                               <NA>
#> 1060 Roadmap Epigenomics                               <NA>
#> 1061                <NA>                                GDS
#> 1062                <NA>                               <NA>
#> 1063                <NA>                               <NA>
#> 1064                <NA>                               <NA>
#> 1065                <NA>                               <NA>
#> 1066                <NA>                               <NA>
#> 1067                <NA>                                GDS
#> 1068                <NA>                                GDS
#> 1069                <NA>                                GDS
#> 1070                <NA>                               <NA>
#> 1071                <NA>                               <NA>
#> 1072                <NA>                               <NA>
#> 1073                <NA>                                GDS
#> 1074                <NA>                        GDS4132 GDS
#> 1075                <NA>                                GDS
#> 1076                <NA>                               <NA>
#> 1077                <NA>                               <NA>
#> 1078                <NA>                               <NA>
#> 1079                <NA>                               <NA>
#> 1080                <NA>                                GDS
#> 1081                <NA>                               <NA>
#> 1082                <NA>                                GDS
#> 1083                <NA>                               <NA>
#> 1084                <NA>                                GDS
#> 1085                <NA>                               <NA>
#> 1086                <NA>                               <NA>
#> 1087                <NA>                                GDS
#> 1088                <NA>                        GDS3874 GDS
#> 1089                <NA>                               <NA>
#> 1090                <NA>                               <NA>
#> 1091                <NA>                        GDS2790 GDS
#> 1092                <NA>                               <NA>
#> 1093                <NA>                                GDS
#> 1094                <NA>                               <NA>
#> 1095                <NA>                               <NA>
#> 1096                <NA>                               <NA>
#> 1097                <NA>                                GDS
#> 1098                <NA>                               <NA>
#> 1099                <NA>                                GDS
#> 1100                <NA>                               <NA>
#> 1101                <NA>                        GDS1956 GDS
#> 1102                <NA>                               <NA>
#> 1103                <NA>                               <NA>
#> 1104                <NA>                               <NA>
#> 1105                <NA>                                GDS
#> 1106                <NA>                               <NA>
#> 1107                <NA> GDS157 GDS158 GDS160 GDS161 GDS162