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accession-icon GSE38783
Acute venous hypertension induces local release of inflammatory cytokines and endothelial activation in humans
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Venous hypertension is often present in advanced and in acute decompensated heart failure (HF). However, it is unclear whether high intravenous pressure can cause alterations in homeostasis by promoting inflammation and endothelial cell (EC) activation. We used an experimental model of acute, local venous hypertension to study the changes in circulating inflammatory mediators and EC phenotype that occur in response to biomechanical stress. Methods and Results: Twenty-four healthy subjects (14 men, age 352 years) were studied. Venous arm pressure was increased to ~30 mmHg above baseline level by inflating a tourniquet cuff around the dominant arm (test arm). Blood and endothelial cells (ECs) were sampled from test and control arm (lacking an inflated cuff) before and after 75 minutes of venous hypertension, using angiocatheters and endovascular wires. Magnetic beads coated with EC specific antibodies were used for EC separation; amplified mRNA was analyzed by Affymetrix HG-U133 2.0 Microarray. Plasma endothelin-1 (ET-1), interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1) and chemokine (C-X-C motif) ligand 2 (CXCL2) were significantly increased in the congested arm. 5,332 probe sets were differentially expressed in venous ECs before vs. after testing. Among the 143 probe sets that exhibited a significant absolute fold change >2, we identified several inflammatory mediators including ET-1, VCAM-1, and CXCL2. Conclusions: Acute experimental venous hypertension is sufficient to cause local increase in circulating inflammatory mediators and to activate venous ECs in healthy human subjects. Additional work is needed to determine the effect of venous hypertension in patients with established HF.

Publication Title

Peripheral venous congestion causes inflammation, neurohormonal, and endothelial cell activation.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon SRP069101
The effect of Abl kinases on non-small cell carcinoma global transcriptome
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

To gain insight into the signaling pathway(s) required for ABL1/ABL2-dependent non-small cell carcinoma cells metastasis Overall design: Samples were analyzed by pair of either control versus ABL Kinase inhibitor GNF5, Or using scrambled shRNA versus ABL1/ABL2-specific shRNAs.

Publication Title

Inactivation of ABL kinases suppresses non-small cell lung cancer metastasis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15724
Gene expression in mouse tracheal basal cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Epithelial basal cells (BCs) are an important stem cell population of the airways. We purified BCs from a KRT5-GFP transgenic mouse line and used Affymetrix arrays to compare there gene expression to that of non-BC epithelium.

Publication Title

Basal cells as stem cells of the mouse trachea and human airway epithelium.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE86171
Transcriptional Dynamics of Cultured Human Villous Cytotrophoblasts
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Transcriptomic characterization of cultured primary human cytrophoblasts (2nd trimester) undergoing differentiation/invasion in vitro.

Publication Title

Transcriptional Dynamics of Cultured Human Villous Cytotrophoblasts.

Sample Metadata Fields

Specimen part

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accession-icon GSE24206
Validated Gene Expression Signatures of Idiopathic Pulmonary Fibrosis
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease that is difficult to diagnose and follows an unpredictable clinical course. The object of this study was to develop a predictive gene signature model of IPF from whole lung tissue. We collected whole lung samples from 11 IPF patients undergoing diagnostic surgical biopsy or transplantation. Whenever possible, samples were obtained from different lobes. Normals consisted of healthy organs donated for transplantation. We measured gene expression on microarrays. Data were analyzed by hierarchical clustering and Principal Component Analysis. By this approach, we found that gene expression was similar in the upper and lower lobes of individuals with IPF. We also found that biopsied and explanted specimens contained different patterns of gene expression; therefore, we analyzed biopsies and explants separately. Signatures were derived by fitting top genes to a Bayesian probit regression model. We developed a 153-gene signature that discriminates IPF biopsies from normal. We also developed a 70-gene signature that discriminates IPF explants from normal. Both signatures were validated on an independent cohort. The IPF Biopsy signature correctly diagnosed 76% of the validation cases (p < 0.01), while IPF Explant correctly diagnosed 78% (p < 0.001). Examination of differentially expressed genes revealed partial overlap between IPF Biopsy and IPF Explant and almost no overlap with previously reported IPF gene lists. However, several overlapping genes may provide a basis for developing therapeutic targets.

Publication Title

Bayesian probit regression model for the diagnosis of pulmonary fibrosis: proof-of-principle.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE104896
BDE-47 Transcriptomic Alterations in Human Primary Villous Cytrophoblasts
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Transcriptomic characterization of BDE-47 exposed cultured primary human cytrophoblasts (2nd trimester) undergoing differentiation in vitro.

Publication Title

Genomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE94644
Defective Decidualization During and After Severe Preeclampsia
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st), Agilent-026652 Whole Human Genome Microarray 4x44K v2 (Probe Name version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP103786
Human Oral and Cutaneous Wound Healing Transcriptomes
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Comparative analysis between oral and cutaneous wound healing in humans using paired and sequential biopsies during the repair process. Overall design: mRNA profiles of Oral/Skin Wound Healing human sample were generated by sequencing using Illumina

Publication Title

Transcriptional signature primes human oral mucosa for rapid wound healing.

Sample Metadata Fields

Specimen part, Disease stage, Subject

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accession-icon GSE94643
Defective Decidualization During and After Severe Preeclampsia Reveals a Possible Maternal Contribution to the Etiology
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

In preeclampsia (PE), cytotrophoblast (CTB) invasion of the uterus and spiral arteries is often shallow. Thus, the placentas role has been a focus. We hypothesized that decidual defects are an important determinant of the placental phenotype. We isolated (human) endometrial stromal cells (hESCs) from non-pregnant donors with a prior pregnancy that was complicated by severe PE (sPE). Versus controls, they failed to decidualize as demonstrated by morphological criteria and the analysis of stage-specific antigens. These results were bolstered by showing that they were transcriptionally inert. Additionally, we used laser microdissection to isolate the decidua from tissue sections of the maternal-fetal interface. Transcriptional profiling revealed sPE-associated defects in gene expression. Also, decidual cells from sPE patients, which de-differentiated in vitro, failed to re-decidualize in culture. Immediately following isolation they released factors that inhibited CTB invasion, linking a possible cause to a known effect. These data suggested that failed decidualization is an important contributor to down regulated CTB invasion in sPE. Diagnosis of this defect prior to pregnancy would enable therapies that are designed to improve decidualization, a novel strategy for prevention.

Publication Title

Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE26576
Genome-wide Analyses of Diffuse Intrinsic Pontine Gliomas
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Purpose: More than 90% of children with diffuse intrinsic pontine glioma (DIPG) die within 2 years of diagnosis. There is a dire need to identify therapeutic targets, however lack of patient material for research has limited progress. We evaluated a large cohort of diffuse intrinsic pontine gliomas (DIPGs) to identify recurrent genomic abnormalities and gene expression signatures underlying DIPG.

Publication Title

Genome-wide analyses identify recurrent amplifications of receptor tyrosine kinases and cell-cycle regulatory genes in diffuse intrinsic pontine glioma.

Sample Metadata Fields

Age, Specimen part, Disease

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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