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10.1021/acscentsci.0c01669 http://scihub22266oqcxt.onion/10.1021/acscentsci.0c01669 34056095!8009098!34056095     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       ACS+Cent+Sci 2021 ; 7 (4): 650-657 Nephropedia Template TP {{tp|p=34056095|t=2021. Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19 |pdf=|usr=}}{{34056095}} gab.com Text Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19 JO: ACS Cent Sci http://www.kidney.de/pget.php?&tw=1&pmid=34056095 #FOAvip Severe cases of coronavirus disease 2019 (COVID-19), caused by infection with SARS-CoV-2, are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. Accordingly, therapeutic blockage of neutrophil activation and NETosis, the cell death pathway accompanying NET formation, could limit respiratory damage and death from severe COVID-19. Here, we demonstrate that synthetic glycopolymers that activate signaling of the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral toll-like receptors (TLRs) and plasma from patients with severe COVID-19. Thus, Siglec-9 agonism is a promising therapeutic strategy to curb neutrophilic hyperinflammation in COVID-19. Twit Text FOAVip Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19 ????ACS Cent Sci http://www.kidney.de/pget.php?&tw=1&pmid=34056095 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34056095 #FOAvip English Wikipedia <ref>{{Cite pmid|34056095}}</ref> Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19 #MMPMID34056095 Delaveris CS; Wilk AJ; Riley NM; Stark JC; Yang SS; Rogers AJ; Ranganath T; Nadeau KC; Blish CA; Bertozzi CR ACS Cent Sci 2021[Apr]; 7 (4): 650-657 PMID34056095show ga Severe cases of coronavirus disease 2019 (COVID-19), caused by infection with SARS-CoV-2, are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. Accordingly, therapeutic blockage of neutrophil activation and NETosis, the cell death pathway accompanying NET formation, could limit respiratory damage and death from severe COVID-19. Here, we demonstrate that synthetic glycopolymers that activate signaling of the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral toll-like receptors (TLRs) and plasma from patients with severe COVID-19. Thus, Siglec-9 agonism is a promising therapeutic strategy to curb neutrophilic hyperinflammation in COVID-19. äSynthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated w(epmc).pdf DeepDyve Pubget Overpricing