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10.1371/journal.pcbi.1008810 http://scihub22266oqcxt.onion/10.1371/journal.pcbi.1008810 33684134!7971900!33684134     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 302.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 302.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 302.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 302.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 302.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Comput+Biol 2021 ; 17 (3): e1008810 Nephropedia Template TP {{tp|p=33684134|t=2021. A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19 |pdf=|usr=}}{{33684134}} gab.com Text A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19 JO: PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=33684134 #FOAvip Abnormal coagulation and an increased risk of thrombosis are features of severe COVID-19, with parallels proposed with hemophagocytic lymphohistiocytosis (HLH), a life-threating condition associated with hyperinflammation. The presence of HLH was described in severely ill patients during the H1N1 influenza epidemic, presenting with pulmonary vascular thrombosis. We tested the hypothesis that genes causing primary HLH regulate pathways linking pulmonary thromboembolism to the presence of SARS-CoV-2 using novel network-informed computational algorithms. This approach led to the identification of Neutrophils Extracellular Traps (NETs) as plausible mediators of vascular thrombosis in severe COVID-19 in children and adults. Taken together, the network-informed analysis led us to propose the following model: the release of NETs in response to inflammatory signals acting in concert with SARS-CoV-2 damage the endothelium and direct platelet-activation promoting abnormal coagulation leading to serious complications of COVID-19. The underlying hypothesis is that genetic and/or environmental conditions that favor the release of NETs may predispose individuals to thrombotic complications of COVID-19 due to an increase risk of abnormal coagulation. This would be a common pathogenic mechanism in conditions including autoimmune/infectious diseases, hematologic and metabolic disorders. Twit Text FOAVip A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19 ????PLoS Comput Biol http://www.kidney.de/pget.php?&tw=1&pmid=33684134 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33684134 #FOAvip English Wikipedia <ref>{{Cite pmid|33684134}}</ref> A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes interactions points to Neutrophil extracellular traps as mediators of thrombosis in COVID-19 #MMPMID33684134 Ding J; Hostallero DE; El Khili MR; Fonseca GJ; Milette S; Noorah N; Guay-Belzile M; Spicer J; Daneshtalab N; Sirois M; Tremblay K; Emad A; Rousseau S PLoS Comput Biol 2021[Mar]; 17 (3): e1008810 PMID33684134show ga Abnormal coagulation and an increased risk of thrombosis are features of severe COVID-19, with parallels proposed with hemophagocytic lymphohistiocytosis (HLH), a life-threating condition associated with hyperinflammation. The presence of HLH was described in severely ill patients during the H1N1 influenza epidemic, presenting with pulmonary vascular thrombosis. We tested the hypothesis that genes causing primary HLH regulate pathways linking pulmonary thromboembolism to the presence of SARS-CoV-2 using novel network-informed computational algorithms. This approach led to the identification of Neutrophils Extracellular Traps (NETs) as plausible mediators of vascular thrombosis in severe COVID-19 in children and adults. Taken together, the network-informed analysis led us to propose the following model: the release of NETs in response to inflammatory signals acting in concert with SARS-CoV-2 damage the endothelium and direct platelet-activation promoting abnormal coagulation leading to serious complications of COVID-19. The underlying hypothesis is that genetic and/or environmental conditions that favor the release of NETs may predispose individuals to thrombotic complications of COVID-19 due to an increase risk of abnormal coagulation. This would be a common pathogenic mechanism in conditions including autoimmune/infectious diseases, hematologic and metabolic disorders. |*Models, Biological[MESH] |Algorithms[MESH] |COVID-19/*complications/*genetics[MESH] |Cell Degranulation/genetics[MESH] |Computational Biology[MESH] |Extracellular Traps/*genetics[MESH] |Gene Expression Regulation[MESH] |Gene Regulatory Networks[MESH] |Genetic Predisposition to Disease[MESH] |Humans[MESH] |Lymphohistiocytosis, Hemophagocytic/*complications/*genetics[MESH] |Pandemics[MESH] |Protein Interaction Maps[MESH] |Pulmonary Embolism/etiology/genetics[MESH] |SARS-CoV-2/*genetics[MESH] |Thrombosis/*etiology/*genetics[MESH]A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohis(epmc).pdf DeepDyve Pubget Overpricing