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10.1016/j.compbiolchem.2021.107482 http://scihub22266oqcxt.onion/10.1016/j.compbiolchem.2021.107482 33845430!8020607!33845430     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Comput+Biol+Chem 2021 ; 92 (ä): 107482 Nephropedia Template TP {{tp|p=33845430|t=2021. The role of human C5a as a non-genomic target in corticosteroid therapy for management of severe COVID19 |pdf=|usr=}}{{33845430}} gab.com Text The role of human C5a as a non-genomic target in corticosteroid therapy for management of severe COVID19 JO: Comput Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33845430 #FOAvip Complement system plays a dual role; physiological as well as pathophysiological. While physiological role protects the host, pathophysiological role can substantially harm the host, by triggering several hyper-inflammatory pathways, referred as "hypercytokinaemia". Emerging clinical evidence suggests that exposure to severe acute respiratory syndrome coronavirus-2 (SARS-CoV2), tricks the complement to aberrantly activate the "hypercytokinaemia" loop, which significantly contributes to the severity of the COVID19. The pathophysiological response of the complement is usually amplified by the over production of potent chemoattractants and inflammatory modulators, like C3a and C5a. Therefore, it is logical that neutralizing the harmful effects of the inflammatory modulators of the complement system can be beneficial for the management of COVID19. While the hunt for safe and efficacious vaccines were underway, polypharmacology based combination therapies were fairly successful in reducing both the morbidity and mortality of COVID19 across the globe. Repurposing of small molecule drugs as "neutraligands" of C5a appears to be an alternative for modulating the hyper-inflammatory signals, triggered by the C5a-C5aR signaling axes. Thus, in the current study, few specific and non-specific immunomodulators (azithromycin, colchicine, famotidine, fluvoxamine, dexamethasone and prednisone) generally prescribed for prophylactic usage for management of COVID19 were subjected to computational and biophysical studies to probe whether any of the above drugs can act as "neutraligands", by selectively binding to C5a over C3a. The data presented in this study indicates that corticosteroids, like prednisone can have potentially better selectively (K(d) approximately 0.38 muM) toward C5a than C3a, suggesting the positive modulatory role of C5a in the general success of the corticosteroid therapy in moderate to severe COVID19. Twit Text FOAVip The role of human C5a as a non-genomic target in corticosteroid therapy for management of severe COVID19 ????Comput Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33845430 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33845430 #FOAvip English Wikipedia <ref>{{Cite pmid|33845430}}</ref> The role of human C5a as a non-genomic target in corticosteroid therapy for management of severe COVID19 #MMPMID33845430 Das A; Rana S Comput Biol Chem 2021[Jun]; 92 (ä): 107482 PMID33845430show ga Complement system plays a dual role; physiological as well as pathophysiological. While physiological role protects the host, pathophysiological role can substantially harm the host, by triggering several hyper-inflammatory pathways, referred as "hypercytokinaemia". Emerging clinical evidence suggests that exposure to severe acute respiratory syndrome coronavirus-2 (SARS-CoV2), tricks the complement to aberrantly activate the "hypercytokinaemia" loop, which significantly contributes to the severity of the COVID19. The pathophysiological response of the complement is usually amplified by the over production of potent chemoattractants and inflammatory modulators, like C3a and C5a. Therefore, it is logical that neutralizing the harmful effects of the inflammatory modulators of the complement system can be beneficial for the management of COVID19. While the hunt for safe and efficacious vaccines were underway, polypharmacology based combination therapies were fairly successful in reducing both the morbidity and mortality of COVID19 across the globe. Repurposing of small molecule drugs as "neutraligands" of C5a appears to be an alternative for modulating the hyper-inflammatory signals, triggered by the C5a-C5aR signaling axes. Thus, in the current study, few specific and non-specific immunomodulators (azithromycin, colchicine, famotidine, fluvoxamine, dexamethasone and prednisone) generally prescribed for prophylactic usage for management of COVID19 were subjected to computational and biophysical studies to probe whether any of the above drugs can act as "neutraligands", by selectively binding to C5a over C3a. The data presented in this study indicates that corticosteroids, like prednisone can have potentially better selectively (K(d) approximately 0.38 muM) toward C5a than C3a, suggesting the positive modulatory role of C5a in the general success of the corticosteroid therapy in moderate to severe COVID19. |*COVID-19 Drug Treatment[MESH] |*Molecular Docking Simulation[MESH] |*SARS-CoV-2[MESH] |Binding Sites[MESH] |COVID-19/pathology[MESH] |Complement C5a/*antagonists & inhibitors/chemistry[MESH] |Gene Expression Regulation/drug effects[MESH] |Humans[MESH] |Prednisone/*chemistry[MESH] |Protein Binding[MESH]The role of human C5a as a non-genomic target in corticosteroid therap(epmc).pdf DeepDyve Pubget Overpricing