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10.1111/jth.15409 http://scihub22266oqcxt.onion/10.1111/jth.15409 34053187!8237059!34053187     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       J+Thromb+Haemost 2021 ; 19 (8): 1914-1921 Nephropedia Template TP {{tp|p=34053187|t=2021. ADAMTS13 regulation of VWF multimer distribution in severe COVID-19 |pdf=|usr=}}{{34053187}} gab.com Text ADAMTS13 regulation of VWF multimer distribution in severe COVID-19 JO: J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=34053187 #FOAvip BACKGROUND: Consistent with fulminant endothelial cell activation, elevated plasma von Willebrand factor (VWF) antigen levels have been reported in patients with COVID-19. The multimeric size and function of VWF are normally regulated through A Disintegrin And Metalloprotease with ThrombSpondin Motif type 1 motif, member 13 (ADAMTS-13)--mediated proteolysis. OBJECTIVES: This study investigated the hypothesis that ADAMTS-13 regulation of VWF multimer distribution may be impaired in severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection contributing to the observed microvascular thrombosis. PATIENTS AND METHODS: Patients with COVID-19 (n = 23) were recruited from the Beaumont Hospital Intensive Care Unit (ICU) in Dublin. Plasma VWF antigen, multimer distribution, ADAMTS-13 activity, and known inhibitors thereof were assessed. RESULTS: We observed markedly increased VWF collagen-binding activity in patients with severe COVID-19 compared to controls (median 509.1 versus 94.3 IU/dl). Conversely, plasma ADAMTS-13 activity was significantly reduced (median 68.2 IU/dl). In keeping with an increase in VWF:ADAMTS-13 ratio, abnormalities in VWF multimer distribution were common in patients with COVID-19, with reductions in high molecular weight VWF multimers. Terminal sialylation regulates VWF susceptibility to proteolysis by ADAMTS-13 and other proteases. We observed that both N- and O-linked sialylation were altered in severe COVID-19. Furthermore, plasma levels of the ADAMTS-13 inhibitors interleukin-6, thrombospondin-1, and platelet factor 4 were significantly elevated. CONCLUSIONS: These findings support the hypothesis that SARS-CoV-2 is associated with profound quantitative and qualitative increases in plasma VWF levels, and a multifactorial down-regulation in ADAMTS-13 function. Further studies will be required to determine whether therapeutic interventions to correct ADAMTS-13-VWF multimer dysfunction may be useful in COVID-microvascular thrombosis and angiopathy. Twit Text FOAVip ADAMTS13 regulation of VWF multimer distribution in severe COVID-19 ????J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=34053187 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34053187 #FOAvip English Wikipedia <ref>{{Cite pmid|34053187}}</ref> ADAMTS13 regulation of VWF multimer distribution in severe COVID-19 #MMPMID34053187 Ward SE; Fogarty H; Karampini E; Lavin M; Schneppenheim S; Dittmer R; Morrin H; Glavey S; Ni Cheallaigh C; Bergin C; Martin-Loeches I; Mallon PW; Curley GF; Baker RI; Budde U; O'Sullivan JM; O'Donnell JS J Thromb Haemost 2021[Aug]; 19 (8): 1914-1921 PMID34053187show ga BACKGROUND: Consistent with fulminant endothelial cell activation, elevated plasma von Willebrand factor (VWF) antigen levels have been reported in patients with COVID-19. The multimeric size and function of VWF are normally regulated through A Disintegrin And Metalloprotease with ThrombSpondin Motif type 1 motif, member 13 (ADAMTS-13)--mediated proteolysis. OBJECTIVES: This study investigated the hypothesis that ADAMTS-13 regulation of VWF multimer distribution may be impaired in severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection contributing to the observed microvascular thrombosis. PATIENTS AND METHODS: Patients with COVID-19 (n = 23) were recruited from the Beaumont Hospital Intensive Care Unit (ICU) in Dublin. Plasma VWF antigen, multimer distribution, ADAMTS-13 activity, and known inhibitors thereof were assessed. RESULTS: We observed markedly increased VWF collagen-binding activity in patients with severe COVID-19 compared to controls (median 509.1 versus 94.3 IU/dl). Conversely, plasma ADAMTS-13 activity was significantly reduced (median 68.2 IU/dl). In keeping with an increase in VWF:ADAMTS-13 ratio, abnormalities in VWF multimer distribution were common in patients with COVID-19, with reductions in high molecular weight VWF multimers. Terminal sialylation regulates VWF susceptibility to proteolysis by ADAMTS-13 and other proteases. We observed that both N- and O-linked sialylation were altered in severe COVID-19. Furthermore, plasma levels of the ADAMTS-13 inhibitors interleukin-6, thrombospondin-1, and platelet factor 4 were significantly elevated. CONCLUSIONS: These findings support the hypothesis that SARS-CoV-2 is associated with profound quantitative and qualitative increases in plasma VWF levels, and a multifactorial down-regulation in ADAMTS-13 function. Further studies will be required to determine whether therapeutic interventions to correct ADAMTS-13-VWF multimer dysfunction may be useful in COVID-microvascular thrombosis and angiopathy. |*COVID-19[MESH] |*von Willebrand Factor[MESH] |ADAMTS13 Protein[MESH] |Humans[MESH] |SARS-CoV-2[MESH]ADAMTS13 regulation of VWF multimer distribution in severe COVID-19 (epmc).pdf DeepDyve Pubget Overpricing