This SuperSeries is composed of the SubSeries listed below.
Targeted expression profiling by RNA-Seq improves detection of cellular dynamics during pregnancy and identifies a role for T cells in term parturition.
Subject
View SamplesMaternal plasama colected longitudinally were profiled using paired-end Illumina RNA-Seq with globin reduction to evaluate changes with gestational age and with labor in normal pregnancy. Overall design: The study included normal pregnancies with (n=8) and without (n=8) spontaneous labor at term. Half of the women in each group had 3 longitudinal samples taken from 12.1-40.3 weeks of gestation, while the other half of women had only one sample taken at term before delivery, for a total of 32 samples.
Targeted expression profiling by RNA-Seq improves detection of cellular dynamics during pregnancy and identifies a role for T cells in term parturition.
Subject
View SamplesMaternal plasama colected longitudinally were profiled using Affymetrix Human Transcriptome Arrays to evaluate changes with gestational age and with labor in normal pregnancy.
Targeted expression profiling by RNA-Seq improves detection of cellular dynamics during pregnancy and identifies a role for T cells in term parturition.
Subject
View SamplesThis is the expression dataset for two studies: 1) Characterization of visceral and subcutaneous adipose tissue transcriptome and biological pathways in pregnant and non-pregnant women: Evidence for pregnancy-related regional-specific differences in adipose tissue and 2) Characterization of visceral and subcutaneous adipose tissue transcriptome in pregnant women with and without spontaneous labor at term: Implication of alternative splicing in the metabolic adaptations of adipose tissue to parturition.
Characterization of visceral and subcutaneous adipose tissue transcriptome in pregnant women with and without spontaneous labor at term: implication of alternative splicing in the metabolic adaptations of adipose tissue to parturition.
Specimen part, Disease stage, Subject
View SamplesMaternal plasama colected longitudinally were profiled using targeted sequencing (DriverMapâ„¢) (https://www.cellecta.com) to evaluate changes with gestational age and with labor in normal pregnancy. Overall design: The study included normal pregnancies with (TIL) (n=8) and without (TNL) (n=8) spontaneous labor at term. Half of the women in each group had 3 longitudinal samples taken from 12.1-40.3 weeks of gestation, while the other half of women had only one sample taken at term before delivery, for a total of 32 samples. Note that Sample_26 was considered contaminated and hence data for that sample was not included in downstream analyses.
Single cell transcriptional signatures of the human placenta in term and preterm parturition.
Subject
View SamplesHumoral responses of mice specifically deleted for Moz (a histone acetyltransferase) or c-Myb (a transcription factor) in B cells were aberrant. RNA-sequencing analysis was performed to assess gene expression differences compared to wild-type controls in germinal center B cells or plasmablasts. Overall design: Moz f/f Aicda1-Cre, Aicda1-Cre, Myb f/f Cd23-Cre, Mybf/f (no cre) mice were immunized with NP-KLH precipitated in alum and germinal center B cells were sort-purified. Secondary plasmablasts were sort-purified from immunized mice boosted with NP-KLH in PBS (Myb experiment). Two independent experiments were conducted.
Regulation of germinal center responses and B-cell memory by the chromatin modifier MOZ.
Specimen part, Subject
View SamplesC.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr/ mice. We discovered that C.pn-induced extracellular IL-1 triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux leading to accumulation of intracellular cholesterol and foam cell formation. Gpr109a and Abca1 were both upregulated in plaque lesions in Nlrp3/ mice in both hyperlipidemic and C.pn infection models.
Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.
Specimen part, Treatment
View SamplesThis 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). The classifier could be built by using any publicly available gene expression data with related histopathological information and was tested on the independent dataset described here.
Strengths and limitations of microarray-based phenotype prediction: lessons learned from the IMPROVER Diagnostic Signature Challenge.
Sex, Specimen part, Disease stage, Race
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MAFG is a transcriptional repressor of bile acid synthesis and metabolism.
Treatment
View SamplesSpecific bile acids are potent signaling molecules that modulate metabolic pathways affecting lipid, glucose and bile acid homeostasis, and the microbiota. Bile acids are synthesized from cholesterol in the liver, and the key enzymes involved in bile acid synthesis (Cyp7a1, Cyp8b1) are regulated transcriptionally by the nuclear receptor FXR. We have identified an FXR-regulated pathway upstream of a transcriptional repressor that controls multiple bile acid metabolism genes. We identify MafG as an FXR target gene and show that hepatic MAFG overexpression represses genes of the bile acid synthetic pathway and modifies the biliary bile acid composition. In contrast, loss-of-function studies using MafG(+/-) mice causes de-repression of the same genes with concordant changes in biliary bile acid levels. Finally, we identify functional MafG response elements in bile acid metabolism genes using ChIP-seq analysis. Our studies identify a molecular mechanism for the complex feedback regulation of bile acid synthesis controlled by FXR
MAFG is a transcriptional repressor of bile acid synthesis and metabolism.
Treatment
View Samples