Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA134357 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series: GSE20680: Whole Blood Cell Gene Expression Profiling in Patients with Coronary Artery Disease from the Cathgen Registry GSE20681: Whole Blood Cell Gene Expression Profiling in Patients with Coronary Artery Disease from the PREDICT Trial Refer to individual Series
2011-03-01 | E-GEOD-20686 | biostudies-arrayexpress
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2012-12-31 | GSE40165 | GEO
Project description:Dengue is the most important arboviral infection of humans. A host pro-inflammatory immune response is widely believed to contribute to the clinical complications that occur in some patients with dengue. Here, immune correlates of early prednisolone therapy were defined in Vietnamese dengue patients enrolled in a randomized controlled trial, comparing a three day regimen of high (2mg/kg) or low (0.5mg/kg) dose prednisolone with placebo. Prednisolone conferred a small change in the whole blood gene expression profile, with 81 transcripts from 64 genes differentially abundant between high-dose prednisolone and placebo treated patients. A prominent theme in the prednisolone gene expression signature was the under-abundance of transcripts from genes associated with T and NK cell cytolytic effector functions. Surprisingly, prednisolone therapy was not associated with attenuation of early-convalescent T cell responses or plasma cytokine levels. Collectively, these findings are consistent with a remarkably benign influence of prednisolone on immune response parameters in dengue patients, and are in line with the trial evidence showing lack of impact on clinical laboratory endpoints and clinical phenotype. The gene expression microarray assay was conducted on samples from the first 123 consecutive patients (placebo, 40; 0.5mg/kg prednisolone, 42; 2.0mg/kg prednisolone, 41).
2012-12-31 | E-GEOD-40165 | biostudies-arrayexpress
Project description:Homo sapiens fresh whole blood was infected with Candida parapsilosis. RNA-pool of both species extracted at 0min (control), 15, 30, 60, 120, 240 min. Samples are rRNA depleted. Measurement of Homo sapiens gene expression.
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Project description:Homo sapiens fresh whole blood was infected with Candida glabrata. RNA-pool of both species extracted at 0min (control), 15, 30, 60, 120, 240 min. Samples are rRNA depleted. Measurement of Candida glabrata gene expression.
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Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
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