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10.1126/sciimmunol.abd0110 http://scihub22266oqcxt.onion/10.1126/sciimmunol.abd0110 32503877!7274761!32503877     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       Sci+Immunol 2020 ; 5 (48): ä Nephropedia Template TP {{tp|p=32503877|t=2020. Inhibition of Bruton tyrosine kinase in patients with severe COVID-19 |pdf=|usr=}}{{32503877}} gab.com Text Inhibition of Bruton tyrosine kinase in patients with severe COVID-19 JO: Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32503877 #FOAvip Patients with severe COVID-19 have a hyperinflammatory immune response suggestive of macrophage activation. Bruton tyrosine kinase (BTK) regulates macrophage signaling and activation. Acalabrutinib, a selective BTK inhibitor, was administered off-label to 19 patients hospitalized with severe COVID-19 (11 on supplemental oxygen; 8 on mechanical ventilation), 18 of whom had increasing oxygen requirements at baseline. Over a 10-14 day treatment course, acalabrutinib improved oxygenation in a majority of patients, often within 1-3 days, and had no discernable toxicity. Measures of inflammation - C-reactive protein and IL-6 - normalized quickly in most patients, as did lymphopenia, in correlation with improved oxygenation. At the end of acalabrutinib treatment, 8/11 (72.7%) patients in the supplemental oxygen cohort had been discharged on room air, and 4/8 (50%) patients in the mechanical ventilation cohort had been successfully extubated, with 2/8 (25%) discharged on room air. Ex vivo analysis revealed significantly elevated BTK activity, as evidenced by autophosphorylation, and increased IL-6 production in blood monocytes from patients with severe COVID-19 compared with blood monocytes from healthy volunteers. These results suggest that targeting excessive host inflammation with a BTK inhibitor is a therapeutic strategy in severe COVID-19 and has led to a confirmatory international prospective randomized controlled clinical trial. Twit Text FOAVip Inhibition of Bruton tyrosine kinase in patients with severe COVID-19 ????Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32503877 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32503877 #FOAvip English Wikipedia <ref>{{Cite pmid|32503877}}</ref> Inhibition of Bruton tyrosine kinase in patients with severe COVID-19 #MMPMID32503877 Roschewski M; Lionakis MS; Sharman JP; Roswarski J; Goy A; Monticelli MA; Roshon M; Wrzesinski SH; Desai JV; Zarakas MA; Collen J; Rose K; Hamdy A; Izumi R; Wright GW; Chung KK; Baselga J; Staudt LM; Wilson WH Sci Immunol 2020[Jun]; 5 (48): ä PMID32503877show ga Patients with severe COVID-19 have a hyperinflammatory immune response suggestive of macrophage activation. Bruton tyrosine kinase (BTK) regulates macrophage signaling and activation. Acalabrutinib, a selective BTK inhibitor, was administered off-label to 19 patients hospitalized with severe COVID-19 (11 on supplemental oxygen; 8 on mechanical ventilation), 18 of whom had increasing oxygen requirements at baseline. Over a 10-14 day treatment course, acalabrutinib improved oxygenation in a majority of patients, often within 1-3 days, and had no discernable toxicity. Measures of inflammation - C-reactive protein and IL-6 - normalized quickly in most patients, as did lymphopenia, in correlation with improved oxygenation. At the end of acalabrutinib treatment, 8/11 (72.7%) patients in the supplemental oxygen cohort had been discharged on room air, and 4/8 (50%) patients in the mechanical ventilation cohort had been successfully extubated, with 2/8 (25%) discharged on room air. Ex vivo analysis revealed significantly elevated BTK activity, as evidenced by autophosphorylation, and increased IL-6 production in blood monocytes from patients with severe COVID-19 compared with blood monocytes from healthy volunteers. These results suggest that targeting excessive host inflammation with a BTK inhibitor is a therapeutic strategy in severe COVID-19 and has led to a confirmatory international prospective randomized controlled clinical trial. |*Betacoronavirus[MESH] |Agammaglobulinaemia Tyrosine Kinase/*antagonists & inhibitors/metabolism[MESH] |Aged[MESH] |Aged, 80 and over[MESH] |Benzamides/*pharmacology/*therapeutic use[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Coronavirus Infections/*drug therapy/virology[MESH] |Critical Illness[MESH] |Female[MESH] |Follow-Up Studies[MESH] |Humans[MESH] |Inflammation/drug therapy/virology[MESH] |Interleukin-6/metabolism[MESH] |Male[MESH] |Middle Aged[MESH] |Monocytes/metabolism[MESH] |Pandemics[MESH] |Pneumonia, Viral/*drug therapy/virology[MESH] |Prospective Studies[MESH] |Pyrazines/*pharmacology/*therapeutic use[MESH] |Respiration, Artificial[MESH] |SARS-CoV-2[MESH]Inhibition of Bruton tyrosine kinase in patients with severe COVID-19 (epmc).pdf DeepDyve Pubget Overpricing