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10.21203/rs.3.rs-33390/v1 http://scihub22266oqcxt.onion/10.21203/rs.3.rs-33390/v1 32702726!7336704!32702726     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       Res+Sq 2020 ; ä (ä): ä Nephropedia Template TP {{tp|p=32702726|t=2020. SARS-CoV2 drives JAK1/2-dependent local and systemic complement hyper-activation |pdf=|usr=}}{{32702726}} gab.com Text SARS-CoV2 drives JAK1/2-dependent local and systemic complement hyper-activation JO: Res Sq http://www.kidney.de/pget.php?&tw=1&pmid=32702726 #FOAvip Patients with coronavirus disease 2019 (COVID-19) present with a range of devastating acute clinical manifestations affecting the lungs, liver, kidneys and gut. The best-characterized entry receptor for the disease-causing virus SARS-CoV2, angiotensin converting enzyme (ACE) 2, is highly expressed in these tissues. However, the pathways that underlie the disease are still poorly understood. Here we show that the complement system is unexpectedly one of the intracellular pathways most highly induced by SARS-CoV2 infection in lung epithelial and liver cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Modelling the regulome of host genes induced by COVID-19 and the drugs that could normalize these genes both implicated the JAK1/2-STAT1 signaling system downstream of type I interferon receptors, and NF-kB. Ruxolitinib, a JAK1/2 inhibitor and the top predicted pharmaceutical candidate, normalized interferon signature genes, IL-6 (the best characterized severity marker in COVID-19) and all complement genes induced by SARS-CoV2, but did not affect NF-kB-regulated genes. We predict that combination therapy with JAK inhibitors and other agents with the potential to normalize NF-kB-signaling, such as anti-viral agents, may serve as an effective clinical strategy. Twit Text FOAVip SARS-CoV2 drives JAK1/2-dependent local and systemic complement hyper-activation ????Res Sq http://www.kidney.de/pget.php?&tw=1&pmid=32702726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32702726 #FOAvip English Wikipedia <ref>{{Cite pmid|32702726}}</ref> SARS-CoV2 drives JAK1/2-dependent local and systemic complement hyper-activation #MMPMID32702726 Yan B; Freiwald T; Chauss D; Wang L; West E; Bibby J; Olson M; Kordasti S; Portilla D; Laurence A; Lionakis MS; Kemper C; Afzali B; Kazemian M Res Sq 2020[Jun]; ä (ä): ä PMID32702726show ga Patients with coronavirus disease 2019 (COVID-19) present with a range of devastating acute clinical manifestations affecting the lungs, liver, kidneys and gut. The best-characterized entry receptor for the disease-causing virus SARS-CoV2, angiotensin converting enzyme (ACE) 2, is highly expressed in these tissues. However, the pathways that underlie the disease are still poorly understood. Here we show that the complement system is unexpectedly one of the intracellular pathways most highly induced by SARS-CoV2 infection in lung epithelial and liver cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Modelling the regulome of host genes induced by COVID-19 and the drugs that could normalize these genes both implicated the JAK1/2-STAT1 signaling system downstream of type I interferon receptors, and NF-kB. Ruxolitinib, a JAK1/2 inhibitor and the top predicted pharmaceutical candidate, normalized interferon signature genes, IL-6 (the best characterized severity marker in COVID-19) and all complement genes induced by SARS-CoV2, but did not affect NF-kB-regulated genes. We predict that combination therapy with JAK inhibitors and other agents with the potential to normalize NF-kB-signaling, such as anti-viral agents, may serve as an effective clinical strategy. äSARS-CoV2 drives JAK1/2-dependent local and systemic complement hyper-(epmc).pdf DeepDyve Pubget Overpricing