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accession-icon GSE51669
Expression data from the stomach of mice treated with dexamethasone.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Glucocorticoids are used for the treatment of inflammatory conditions but they also cause many side-effects.

Publication Title

Glucocorticoids induce gastroparesis in mice through depletion of l-arginine.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE67297
Cold acclimation improves insulin sensitivity in patients with type 2 diabetes mellitus.
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

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. Methods: Eight type 2 diabetic patients (age 59.35.8 years, BMI 29.83.2 kg/m2) followed a cold acclimation protocol, consisting of intermittent cold exposure (6 hours/day, 14-14.5 C) for 12 consecutive days. Before and after cold acclimation, cold-induced BAT activity was assessed by [18F]FDG-PET/CT scanning, insulin sensitivity at thermoneutrality by a hyperinsulinemic-euglycemic clamp, and muscle and WAT biopsies were taken. Results: Cold-induced BAT activity was low, but increased in all patients upon cold acclimation (SUV from 0.400.29 to 0.630.78, p<0.05). Interestingly, insulin sensitivity showed a very pronounced 40% increase upon cold acclimation (glucose rate of disappearance from 14.94.1 to 20.56.9 mol kg-1 min-1, p<0.05). A 40% increase in insulin sensitivity cannot be explained by BAT glucose uptake, in fact basal skeletal muscle GLUT4 content and translocation was markedly increased after cold acclimation, without effects on insulin signaling or AMPk activation. Conclusions: Regular mild cold exposure has marked effects on insulin sensitivity, which are accompanied by small increases in BAT activity and more pronounced effects on skeletal muscle. These data suggest a novel therapeutic option for the treatment of type 2 diabetes.

Publication Title

Short-term cold acclimation improves insulin sensitivity in patients with type 2 diabetes mellitus.

Sample Metadata Fields

Subject

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accession-icon GSE51952
Expression Profiles of HepG2 cells treated with 22 compounds and solvent controls
  • organism-icon Homo sapiens
  • sample-icon 97 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcriptomics changes induced in the human liver cell line HepG2 by 17 hepatotoxic compounds, 5 non-hepatotoxic compounds and solvent controls after treatment for 24h

Publication Title

Classification of hepatotoxicants using HepG2 cells: A proof of principle study.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE55883
Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative cross-omics analysis in primary mouse hepatocytes unravels mechanisms of cyclosporin A-induced hepatotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE55881
Expression Profiles of Primary Mouse Hepatocytes treated with Cyclosporin A and solvent control [RNA]
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The transcriptomics changes induced in Primary Mouse Hepatocytes by Cyclosporin A after treatment for 24h and 48h

Publication Title

Integrative cross-omics analysis in primary mouse hepatocytes unravels mechanisms of cyclosporin A-induced hepatotoxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE45802
Expression Profiles of mRNAs and microRNAs in HepG2 cells treated with Cyclosporin A and solvent control
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro.

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE45635
Expression Profiles of HepG2 cells treated with Cyclosporin A and solvent control
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcriptomics changes induced in the human liver cell line HepG2 by Cyclosporin A after treatment for 12h, 24h, 48h and 72h

Publication Title

Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro.

Sample Metadata Fields

Specimen part, Cell line, Time

View Samples
accession-icon GSE97010
The Impact of Acute Exposure to Cigarette Smoke on Airway Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 126 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

BACKGROUND: We have previously reported gene expression changes in the bronchial airway epithelium of active chronic smokers. In this study, we investigate the effects of Acute Smoke Exposure (ASE) from cigarettes on airway epithelial gene expression. METHODS: Bronchial airway epithelial cell brushings were collected via fiberoptic bronchoscopy from 63 individuals without recent exposure to cigarette smoke (> 2 days), at baseline and at 24 hours after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Differential gene expression was assessed using linear modeling and compared to previous smoking-related gene-expression signatures using Gene Set Enrichment Analysis (GSEA). RESULTS: We identified 91 genes differentially expressed 24-hours after exposure to three cigarettes (FDR < 0.25). ASE induces genes involved in xenobiotic metabolism, oxidative stress, and inflammation; and represses genes involved in cilium morphogenesis, and cell cycle. Genes induced by in vivo ASE are concordantly altered by ASE in vitro. While many genes altered by ASE are altered similarly in the airway of chronic smokers, metallothionein genes were induced by ASE and suppressed among chronic smokers. Metallothioneins were also suppressed in the bronchial airway of current and former chronic smokers with lung cancer relative to those with benign disease. CONCLUSIONS: Acute exposure to as little as three cigarettes alters gene-expression in bronchial airway epithelium in a manner that largely resembles the changes seen in chronic active smokers. The difference in the short-term and long-term effects of smoking on metallothionein expression and its relationship to lung cancer requires further study given these enzymes role in responding to oxidative stress.

Publication Title

Impact of acute exposure to cigarette smoke on airway gene expression.

Sample Metadata Fields

Sex

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accession-icon SRP059610
GATA1-deficient dendritic cells display impaired CCL21-dependent migration towards lymph nodes due to reduced levels of polysialic acid
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Dendritic cells (DCs) play a pivotal role in the regulation of the immune response. DC development and activation is finely orchestrated through transcriptional programs. GATA1 transcription factor is required for murine DC development and data suggests that it might be involved in the fine-tuning of the life span and function of activated DCs. We generated DC-specific Gata1 knockout mice (Gata1-KODC), which presented a 20% reduction of splenic DCs, partially explained by enhanced apoptosis. RNA-Seq analysis revealed a number of deregulated genes involved in cell survival, migration and function. DC migration towards peripheral lymph nodes was impaired in Gata1-KODC mice. Migration assays performed in vitro showed that this defect was selective for CCL21, but not CCL19. Interestingly, we show that Gata1-KODC DCs have reduced polysialic acid levels on their surface, which is a known determinant for the proper migration of DCs towards CCL21. Overall design: Dendritic cells from Gata1 knock-out or wild-type mice were stimulated with LPS of unstimulated (under steady state), 2 biological replicates each

Publication Title

GATA1-Deficient Dendritic Cells Display Impaired CCL21-Dependent Migration toward Lymph Nodes Due to Reduced Levels of Polysialic Acid.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP201917
Bcl6 neurogenic activity in in vitro cortical progenitors [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Transcriptome analysis following Bcl6 induction (24h doxycycline) in mouse ES-cell-derived cortical progenitors (differentiation day 12) shows that Bcl6 promotes a neurogenic transcription program and represses selective genes of the main proliferative pathways. Overall design: RNA-seq screen for Bcl6-elicited gene expression changes in in vitro cortical progenitors (n=4)

Publication Title

Cortical Neurogenesis Requires Bcl6-Mediated Transcriptional Repression of Multiple Self-Renewal-Promoting Extrinsic Pathways.

Sample Metadata Fields

Treatment, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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