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10.1016/j.gene.2021.145665 http://scihub22266oqcxt.onion/10.1016/j.gene.2021.145665 33887367!8054526!33887367     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33887367&cmd=llinks): Failed to open stream: HTTP request failed! 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Inferring molecular mechanisms of dexamethasone therapy in severe COVID-19 from existing transcriptomic data |pdf=|usr=}}{{33887367}} gab.com Text Inferring molecular mechanisms of dexamethasone therapy in severe COVID-19 from existing transcriptomic data JO: Gene http://www.kidney.de/pget.php?&tw=1&pmid=33887367 #FOAvip Dexamethasone, a synthetic glucocorticoid, has previously shown mortality benefit in severe coronavirus disease 2019 (COVID-19) in a randomized controlled trial. As the illness is considered to reflect a hyperinflammatory state, this therapeutic effectiveness is presumably ascribed to broad anti-inflammatory activities of glucocorticoids. Here, an unbiased analysis of available transcriptomic data on lung and blood immune cells from severe COVID-19 patients and matching cellular models of dexamethasone treatment is presented that supports this presumption. Comparison of differentially expressed genes in severe COVID-19 with that in dexamethasone treated cells reveals a small set of genes that are regulated in opposite direction between the disease and the drug, and are enriched for genes and processes related to glucocorticoid pathway and receptor binding. This expression signature differentiates as a whole various cytokines from a set of anti-cytokine/anti-inflammatory agents, with the former resembling COVID-19 and the latter dexamethasone in gene regulation. The signature apparently relates to TNF- alpha, IL-1alpha, IL-1beta, IFN-alpha, IFN-beta, and IFN-gamma signaling, but not IL-6 signaling, suggesting that therapeutic effect of dexamethasone in COVID-19 does not involve IL-6 pathway. However, as all these observations are purely based on bioinformatic analysis, experimental evidence will be required to validate the inferences drawn. In conclusion, the present analysis seems to provide a proof of concept for therapeutic mechanisms of dexamethasone in COVID-19. Twit Text FOAVip Inferring molecular mechanisms of dexamethasone therapy in severe COVID-19 from existing transcriptomic data ????Gene http://www.kidney.de/pget.php?&tw=1&pmid=33887367 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33887367 #FOAvip English Wikipedia <ref>{{Cite pmid|33887367}}</ref> Inferring molecular mechanisms of dexamethasone therapy in severe COVID-19 from existing transcriptomic data #MMPMID33887367 Sharma A Gene 2021[Jul]; 788 (ä): 145665 PMID33887367show ga Dexamethasone, a synthetic glucocorticoid, has previously shown mortality benefit in severe coronavirus disease 2019 (COVID-19) in a randomized controlled trial. As the illness is considered to reflect a hyperinflammatory state, this therapeutic effectiveness is presumably ascribed to broad anti-inflammatory activities of glucocorticoids. Here, an unbiased analysis of available transcriptomic data on lung and blood immune cells from severe COVID-19 patients and matching cellular models of dexamethasone treatment is presented that supports this presumption. Comparison of differentially expressed genes in severe COVID-19 with that in dexamethasone treated cells reveals a small set of genes that are regulated in opposite direction between the disease and the drug, and are enriched for genes and processes related to glucocorticoid pathway and receptor binding. This expression signature differentiates as a whole various cytokines from a set of anti-cytokine/anti-inflammatory agents, with the former resembling COVID-19 and the latter dexamethasone in gene regulation. The signature apparently relates to TNF- alpha, IL-1alpha, IL-1beta, IFN-alpha, IFN-beta, and IFN-gamma signaling, but not IL-6 signaling, suggesting that therapeutic effect of dexamethasone in COVID-19 does not involve IL-6 pathway. However, as all these observations are purely based on bioinformatic analysis, experimental evidence will be required to validate the inferences drawn. In conclusion, the present analysis seems to provide a proof of concept for therapeutic mechanisms of dexamethasone in COVID-19. |*COVID-19 Drug Treatment[MESH] |Anti-Inflammatory Agents/*therapeutic use[MESH] |Antiviral Agents/*therapeutic use[MESH] |Cell Line, Tumor[MESH] |Cytokines/immunology[MESH] |Dexamethasone[MESH] |Gene Expression Regulation/drug effects[MESH] |Glucocorticoids/*therapeutic use[MESH] |Humans[MESH]Inferring molecular mechanisms of dexamethasone therapy in severe COVI(epmc).pdf DeepDyve Pubget Overpricing