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10.1080/08830185.2021.1884248 http://scihub22266oqcxt.onion/10.1080/08830185.2021.1884248 33616462!7919105!33616462     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+Rev+Immunol 2022 ; 41 (2): 217-230 Nephropedia Template TP {{tp|p=33616462|t=2022. Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality |pdf=|usr=}}{{33616462}} gab.com Text Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality JO: Int Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33616462 #FOAvip The coronavirus disease 2019 (COVID-19) triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) erupted in Hubei Province of China in December 2019 and has become a pandemic. Severe COVID-19 patients who suffer from acute respiratory distress syndrome (ARDS) and multi-organ dysfunction have high mortality. Several studies have shown that this is closely related to the cytokine release syndrome (CRS), often loosely referred to as cytokine storm. IL-6 is one of the key factors and its level is positively correlated with the severity of the disease. The molecular mechanisms for CRS in COVID-19 are related to the effects of the S-protein and N-protein of the virus and its ability to trigger NF-kappaB activation by disabling the inhibitory component IkappaB. This leads to activation of immune cells and the secretion of proinflammatory cytokines such as IL-6 and TNF-alpha. Other mechanisms related to IL-6 include its interaction with GM-CSF and interferon responses. The pivotal role of IL-6 makes it a target for therapeutic agents and studies on tocilizumab are already ongoing. Other possible targets of treating CRS in COVID-19 include IL-1beta and TNF-alpha. Recently, reports of a CRS like illness called multisystem inflammatory syndrome in children (MIS-C) in children have surfaced, with a variable presentation which in some cases resembles Kawasaki disease. It is likely that the immunological derangement and cytokine release occurring in COVID-19 cases is variable, or on a spectrum, that can potentially be governed by genetic factors. Currently, there are no approved biological modulators for the treatment of COVID-19, but the urgency of the pandemic has led to numerous clinical trials worldwide. Ultimately, there is great promise that an anti-inflammatory modulator targeting a cytokine storm effect may prove to be very beneficial in reducing morbidity and mortality in COVID-19 patients. Twit Text FOAVip Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality ????Int Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33616462 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33616462 #FOAvip English Wikipedia <ref>{{Cite pmid|33616462}}</ref> Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality #MMPMID33616462 Que Y; Hu C; Wan K; Hu P; Wang R; Luo J; Li T; Ping R; Hu Q; Sun Y; Wu X; Tu L; Du Y; Chang C; Xu G Int Rev Immunol 2022[]; 41 (2): 217-230 PMID33616462show ga The coronavirus disease 2019 (COVID-19) triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) erupted in Hubei Province of China in December 2019 and has become a pandemic. Severe COVID-19 patients who suffer from acute respiratory distress syndrome (ARDS) and multi-organ dysfunction have high mortality. Several studies have shown that this is closely related to the cytokine release syndrome (CRS), often loosely referred to as cytokine storm. IL-6 is one of the key factors and its level is positively correlated with the severity of the disease. The molecular mechanisms for CRS in COVID-19 are related to the effects of the S-protein and N-protein of the virus and its ability to trigger NF-kappaB activation by disabling the inhibitory component IkappaB. This leads to activation of immune cells and the secretion of proinflammatory cytokines such as IL-6 and TNF-alpha. Other mechanisms related to IL-6 include its interaction with GM-CSF and interferon responses. The pivotal role of IL-6 makes it a target for therapeutic agents and studies on tocilizumab are already ongoing. Other possible targets of treating CRS in COVID-19 include IL-1beta and TNF-alpha. Recently, reports of a CRS like illness called multisystem inflammatory syndrome in children (MIS-C) in children have surfaced, with a variable presentation which in some cases resembles Kawasaki disease. It is likely that the immunological derangement and cytokine release occurring in COVID-19 cases is variable, or on a spectrum, that can potentially be governed by genetic factors. Currently, there are no approved biological modulators for the treatment of COVID-19, but the urgency of the pandemic has led to numerous clinical trials worldwide. Ultimately, there is great promise that an anti-inflammatory modulator targeting a cytokine storm effect may prove to be very beneficial in reducing morbidity and mortality in COVID-19 patients. |*COVID-19/complications[MESH] |*Cytokine Release Syndrome[MESH] |Humans[MESH] |Morbidity[MESH] |SARS-CoV-2[MESH]Cytokine release syndrome in COVID-19: a major mechanism of morbidity (epmc).pdf DeepDyve Pubget Overpricing