Septic shock is the most severe complication of sepsis, associated with high mortality. The patient's response to supportive therapy is very heterogeneous and the underlying mechanisms are still elusive. In order to identify which are the actors (genes and pathways) that play a role in establishing the response, we investigate the whole blood transcriptome in septic shock patients with positive and negative responses to early supportive hemodynamic therapy, assessed by changes in SOFA scores within the first 48 hours from ICU admission. We pinpointed genes and pathways that are differently modulated and enriched respectively within 48hrs between responders and non-responders. Overall design: We analyzed 31 patients (17 Responders and 14 Not Responders to early therapy). For each patient, 2 samples were collected. In particular the first sample (T1) collected within 16 hours from ICU admission whereas the second (T2) collected within 48 hours from ICU admission. Experimental groups (Responders and Not Responders) are defined accordingly with SOFA scores improvements within 48 hours.
Identification of a transcriptome profile associated with improvement of organ function in septic shock patients after early supportive therapy.
Specimen part, Subject, Time
View SamplesWe used RNA-seq to monitor mRNA levels of all genes in response to hypoxia of wild-type yeast, S. cerevisiae (strain yMH914 with wildtype HAP1). To gain insights into how gene expression changes over time, cells were subjected to 100% nitrogen gas and collected after 0,5,10,30,60,120,180, and 240 minutes. Total RNA was extracted and mRNAs were enriched by polyA selection. The cDNA was prepared into a sequencing library, multiplexed and single-end sequenced by an Illumina HiSeq 2500 sequencer. After mapping with Tophat2, the number of reads per feature was calculated using HTSeq. Overall design: RNA-seq analysis of eight time points of a yeast strain grown in hypoxia. There are three biological replicates of the time course.
Time-Course Analysis of Gene Expression During the Saccharomyces cerevisiae Hypoxic Response.
Subject
View SamplesComparing the mRNA expression profiles of c-Myb deficient and c-Myb sufficient Tcra-/- DP thymocytes.
c-Myb promotes the survival of CD4+CD8+ double-positive thymocytes through upregulation of Bcl-xL.
No sample metadata fields
View SamplesLeptin binding to the leptin receptor (LepR) causes rapid signaling to the nucleus. We investigated the early (2 hr) transcriptional response to acute leptin injection (intracerebroventricular)
Leptin Induces Mitosis and Activates the Canonical Wnt/β-Catenin Signaling Pathway in Neurogenic Regions of <i>Xenopus</i> Tadpole Brain.
Treatment
View SamplesMicroarray analysis was performed to determine the transcriptional profiles of NKT, CD1d-aGC+ Va24-, and CD4 T cells.
A naive-like population of human CD1d-restricted T cells expressing intermediate levels of promyelocytic leukemia zinc finger.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Multiple layers of transcriptional regulation by PLZF in NKT-cell development.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Egr2-dependent gene expression profiling and ChIP-Seq reveal novel biologic targets in T cell anergy.
Specimen part, Treatment
View SamplesT cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.
Egr2-dependent gene expression profiling and ChIP-Seq reveal novel biologic targets in T cell anergy.
Specimen part, Treatment
View SamplesComparative analyses of Mex67 and Npl3 binding to mRNA at normal growth condition (25째C) and upon shift to heat stress (30 min, 42째C). Overall design: Examination of two biological RNA Co-IP replicates of Mex67, Npl3 and no tag control at 25째C and upon shift to 30 min at 42째C (Heat stress) and subsequent Illumina RNA deep-sequencing
mRNA quality control is bypassed for immediate export of stress-responsive transcripts.
Cell line, Subject
View SamplesTo identify genes that require PLZF for their regulation in NKT cells, we compared the developmental stages of thymic NKT cells from wildtype and PLZF-deficient mice
Multiple layers of transcriptional regulation by PLZF in NKT-cell development.
Specimen part
View Samples