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10.3390/ijms22136764 http://scihub22266oqcxt.onion/10.3390/ijms22136764 34201797!8269070!34201797     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34201797&cmd=llinks): Failed to open stream: HTTP request failed! 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Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Molecular Levels?|pdf=|usr=}}{{34201797}} gab.com Text Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Molecular Levels JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34201797 #FOAvip The coronavirus disease 2019 (COVID-19) caused by infection of the severe respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly impacted human society. Recently, the synthetic pure glucocorticoid dexamethasone was identified as an effective compound for treatment of severe COVID-19. However, glucocorticoids are generally harmful for infectious diseases, such as bacterial sepsis and severe influenza pneumonia, which can develop respiratory failure and systemic inflammation similar to COVID-19. This apparent inconsistency suggests the presence of pathologic mechanism(s) unique to COVID-19 that renders this steroid effective. We review plausible mechanisms and advance the hypothesis that SARS-CoV-2 infection is accompanied by infected cell-specific glucocorticoid insensitivity as reported for some other viruses. This alteration in local glucocorticoid actions interferes with undesired glucocorticoid to facilitate viral replication but does not affect desired anti-inflammatory properties in non-infected organs/tissues. We postulate that the virus coincidentally causes glucocorticoid insensitivity in the process of modulating host cell activities for promoting its replication in infected cells. We explore this tenet focusing on SARS-CoV-2-encoding proteins and potential molecular mechanisms supporting this hypothetical glucocorticoid insensitivity unique to COVID-19 but not characteristic of other life-threatening viral diseases, probably due to a difference in specific virally-encoded molecules and host cell activities modulated by them. Twit Text FOAVip Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Molecular Levels ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34201797 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34201797 #FOAvip English Wikipedia <ref>{{Cite pmid|34201797}}</ref> Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Molecular Levels? #MMPMID34201797 Kino T; Burd I; Segars JH Int J Mol Sci 2021[Jun]; 22 (13): ä PMID34201797show ga The coronavirus disease 2019 (COVID-19) caused by infection of the severe respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly impacted human society. Recently, the synthetic pure glucocorticoid dexamethasone was identified as an effective compound for treatment of severe COVID-19. However, glucocorticoids are generally harmful for infectious diseases, such as bacterial sepsis and severe influenza pneumonia, which can develop respiratory failure and systemic inflammation similar to COVID-19. This apparent inconsistency suggests the presence of pathologic mechanism(s) unique to COVID-19 that renders this steroid effective. We review plausible mechanisms and advance the hypothesis that SARS-CoV-2 infection is accompanied by infected cell-specific glucocorticoid insensitivity as reported for some other viruses. This alteration in local glucocorticoid actions interferes with undesired glucocorticoid to facilitate viral replication but does not affect desired anti-inflammatory properties in non-infected organs/tissues. We postulate that the virus coincidentally causes glucocorticoid insensitivity in the process of modulating host cell activities for promoting its replication in infected cells. We explore this tenet focusing on SARS-CoV-2-encoding proteins and potential molecular mechanisms supporting this hypothetical glucocorticoid insensitivity unique to COVID-19 but not characteristic of other life-threatening viral diseases, probably due to a difference in specific virally-encoded molecules and host cell activities modulated by them. |*COVID-19 Drug Treatment[MESH] |Antiviral Agents/*pharmacology[MESH] |Dexamethasone/*pharmacology[MESH] |Host Microbial Interactions[MESH] |Humans[MESH] |Hypothalamo-Hypophyseal System/*physiology[MESH] |Immunity, Innate[MESH] |Inflammation/*drug therapy[MESH] |SARS-CoV-2/drug effects/physiology[MESH] |Severity of Illness Index[MESH]Dexamethasone for Severe COVID-19: How Does It Work at Cellular and Mo(epmc).pdf DeepDyve Pubget Overpricing