To evaluate and characterize gene expression changes and toxicity following oral gavage administration of AMG A & AMG B in male Sprague Dawley rats.
Application of genomics for identification of systemic toxicity triggers associated with VEGF-R inhibitors.
No sample metadata fields
View SamplesMyelin-reactive T cells have been identified in patients with multiple sclerosis (MS) and healthy subjects with comparable frequencies, but the contribution of these autoreactive T cells to disease pathology remains unknown. A total of 13,324 T cell libraries generated from blood of 23 patients and 22 healthy controls were interrogated for reactivity to myelin antigens. Libraries derived from CCR6+ myelin-reactive T cells from patients with MS exhibited significantly enhanced production of IFN-?, IL-17, and GM-CSF compared to healthy controls. Single-cell clones isolated by MHC/peptide tetramers from CCR6+ T cell libraries also secreted more pro-inflammatory cytokines while clones isolated from controls secreted more IL-10. The transcriptomes of myelin-specific CCR6+ T cells from patients with MS were distinct from those derived from healthy controls, and of note, were enriched in Th17-induced experimental autoimmune encephalitis (EAE) gene signatures and gene signatures derived from Th17 cells isolated other human autoimmune diseases. These data, although not casual, imply that functional differences between antigen specific T cells from MS and healthy controls is fundamental to disease development and support the notion that IL-10 production from myelin-reactive T cells may act to limit disease progression, or even pathogenesis. Overall design: Four conditions of purified T cells with between 3 and 5 replicates per condition
Functional inflammatory profiles distinguish myelin-reactive T cells from patients with multiple sclerosis.
No sample metadata fields
View SamplesWe hypothesized that altered extracellular osmolality per se could affect the transcriptome of the kidney inner medullary collecting duct (IMCD) cells, and hence it might change renal tubular function. The data sets of transcriptomics were incorporated into the "omic" data sets of metabolomics. Primary cultured IMCD cells of rat kidney were grown in hyperosmolar culture medium (640 mOsm/KgH2O) for 4 d, and then the cells were cultured in the medium with either reduced (300 mOsm/KgH2O) or the same osmolality for 1 or 2 d more.
Patterns of gene and metabolite define the effects of extracellular osmolality on kidney collecting duct.
Sex, Age, Specimen part, Treatment
View SamplesWe are investigating the transcriptional response of changes in RNA steady-state levels between normal and DM1.
RNA steady-state defects in myotonic dystrophy are linked to nuclear exclusion of SHARP.
Specimen part
View SamplesEmbryonic CNS neurons can differentiate in culture and provide a model for maturation-related changes. A transcriptome profile over the course of maturation was perform to investigate the underlying molecular mechanism that drives maturation and its related changes such as developmental loss of intrinsic regenerative capacity. Overall design: Primary cortical neurons were excised from E18 rat embryos and were co-cultured with primary rat astrocytes from P0-2 rats. RNA were then extracted on day 1, 4, 8, 16, and 24 after plating.
Selective rab11 transport and the intrinsic regenerative ability of CNS axons.
No sample metadata fields
View SamplesAnalysis of DNA methylation and gene expression changes during regulated endothelial progenitor cells (EPCs) to outgrowth endothelial cells (OECs). Results provide information of DNA methylation and gene expression pattern during cord-blood derived EPCs differentiation. Taken together, we discovered specific set of genes regulated by hyper- and hypo-methylation during differentiation. Overall design: mRNA and MeDIP seq using total RNA and genomic DNA isolated from cord blood-derived EPCs and OECs.
Integrative analysis of DNA methylation and mRNA expression during differentiation of umbilical cord blood derived mononuclear cells to endothelial cells.
Specimen part, Subject
View SamplesChemotherapeutic use of cisplatin is limited by its severe side effects. In this study, we demonstrated that cisplatin induces cell death in a proximal tubular cell line by suppressing glycolysis- and tricarboxylic acid (TCA)/mitochondria-related genes. HK-2 cells were cultured to confluence in 100mm dishes. Total RNA was extracted (QIAGEN, Valencia, CA, USA), and the concentration in the samples was measured using a Micro UV-Vis fluorescence spectrophotometer (Malcom, Tokyo, JAPAN). Sample of 10g of Total RNA from HK-2 cells were labeled with biotin (3'IVT Labeling Kit, Affymetrix, USA) and hybridized (GeneAtlas Hybridization, Wash, and Stain Kit for 3' IVT Arrays, Affymetrix).
Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation.
Specimen part, Cell line, Treatment
View SamplesGene expression profiles during the differentiation of EPCs into OECs were analyzed.
Endothelial progenitor cell homing: prominent role of the IGF2-IGF2R-PLCbeta2 axis.
No sample metadata fields
View SamplesWe 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).
Molecular signatures of human induced pluripotent stem cells highlight sex differences and cancer genes.
Specimen part
View SamplesWe compared the gene expression of A549 cells following 24 and 48 hours of treatment with a no-observed-effect level dose of cisplatin. The objective of the study is to identify genes that are differentially expressed in response to sub-lethal doses of cisplatin. This study helps identify not only treatment responses but also changes in gene expression that may confer cytoprotective mechanisms that allow these cells to survive treatment and to develop treatment resistance.
Combined Use of Gene Expression Modeling and siRNA Screening Identifies Genes and Pathways Which Enhance the Activity of Cisplatin When Added at No Effect Levels to Non-Small Cell Lung Cancer Cells In Vitro.
Cell line, Treatment, Time
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