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10.1126/sciadv.abh2434 http://scihub22266oqcxt.onion/10.1126/sciadv.abh2434 34516880!8442885!34516880     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34516880.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Adv 2021 ; 7 (37): eabh2434 Nephropedia Template TP {{tp|p=34516880|t=2021. Platelets amplify endotheliopathy in COVID-19 |pdf=|usr=}}{{34516880}} gab.com Text Platelets amplify endotheliopathy in COVID-19 JO: Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=34516880 #FOAvip Given the evidence for a hyperactive platelet phenotype in COVID-19, we investigated effector cell properties of COVID-19 platelets on endothelial cells (ECs). Integration of EC and platelet RNA sequencing revealed that platelet-released factors in COVID-19 promote an inflammatory hypercoagulable endotheliopathy. We identified S100A8 and S100A9 as transcripts enriched in COVID-19 platelets and were induced by megakaryocyte infection with SARS-CoV-2. Consistent with increased gene expression, the heterodimer protein product of S100A8/A9, myeloid-related protein (MRP) 8/14, was released to a greater extent by platelets from COVID-19 patients relative to controls. We demonstrate that platelet-derived MRP8/14 activates ECs, promotes an inflammatory hypercoagulable phenotype, and is a significant contributor to poor clinical outcomes in COVID-19 patients. Last, we present evidence that targeting platelet P2Y(12) represents a promising candidate to reduce proinflammatory platelet-endothelial interactions. Together, these findings demonstrate a previously unappreciated role for platelets and their activation-induced endotheliopathy in COVID-19. Twit Text FOAVip Platelets amplify endotheliopathy in COVID-19 ????Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=34516880 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34516880 #FOAvip English Wikipedia <ref>{{Cite pmid|34516880}}</ref> Platelets amplify endotheliopathy in COVID-19 #MMPMID34516880 Barrett TJ; Cornwell M; Myndzar K; Rolling CC; Xia Y; Drenkova K; Biebuyck A; Fields AT; Tawil M; Luttrell-Williams E; Yuriditsky E; Smith G; Cotzia P; Neal MD; Kornblith LZ; Pittaluga S; Rapkiewicz AV; Burgess HM; Mohr I; Stapleford KA; Voora D; Ruggles K; Hochman J; Berger JS Sci Adv 2021[Sep]; 7 (37): eabh2434 PMID34516880show ga Given the evidence for a hyperactive platelet phenotype in COVID-19, we investigated effector cell properties of COVID-19 platelets on endothelial cells (ECs). Integration of EC and platelet RNA sequencing revealed that platelet-released factors in COVID-19 promote an inflammatory hypercoagulable endotheliopathy. We identified S100A8 and S100A9 as transcripts enriched in COVID-19 platelets and were induced by megakaryocyte infection with SARS-CoV-2. Consistent with increased gene expression, the heterodimer protein product of S100A8/A9, myeloid-related protein (MRP) 8/14, was released to a greater extent by platelets from COVID-19 patients relative to controls. We demonstrate that platelet-derived MRP8/14 activates ECs, promotes an inflammatory hypercoagulable phenotype, and is a significant contributor to poor clinical outcomes in COVID-19 patients. Last, we present evidence that targeting platelet P2Y(12) represents a promising candidate to reduce proinflammatory platelet-endothelial interactions. Together, these findings demonstrate a previously unappreciated role for platelets and their activation-induced endotheliopathy in COVID-19. äPlatelets amplify endotheliopathy in COVID-19 (epmc).pdf DeepDyve Pubget Overpricing