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10.3390/cells10102785 http://scihub22266oqcxt.onion/10.3390/cells10102785 34685765!8535032!34685765     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cells 2021 ; 10 (10): ä Nephropedia Template TP {{tp|p=34685765|t=2021. Shedding Light on the Possible Link between ADAMTS13 and Vaccine-Induced Thrombotic Thrombocytopenia |pdf=|usr=}}{{34685765}} gab.com Text Shedding Light on the Possible Link between ADAMTS13 and Vaccine-Induced Thrombotic Thrombocytopenia JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=34685765 #FOAvip Several recent reports have highlighted the onset of vaccine-induced thrombotic thrombocytopaenia (VITT) in some recipients (approximately 1 case out of 100k exposures) of the ChAdOx1 nCoV-19 vaccine (AstraZeneca). Although the underlying events leading to this blood-clotting phenomenon has yet to be elucidated, several critical observations present a compelling potential mechanism. Thrombus formation requires the von Willebrand (VWF) protein to be in ultra-large multimeric state. The conservation of this state is controlled by the ADAMTS13 enzyme, whose proteolytic activity reduces the size of VWF multimers, keeping blood clotting at bay. However, ADAMTS13 cannot act on VWF that is bound to platelet factor 4 (PF4). As such, it is of particular interest to note that a common feature between subjects presenting with VITT is high titres of antibodies against PF4. This raises the possibility that these antibodies preserve the stability of ultra-large VWF complexes, leading to the formation of endothelium-anchored VWF strings, which are capable of recruiting circulating platelets and causing uncontrolled thrombosis in terminal capillaries. Here, we share our viewpoint about the current understanding of the VITT pathogenesis involving the prevention of ADAMTS13's activity on VWF by PF4 antibody-mediated stabilisation/ protection of the PF4-VWF complex. Twit Text FOAVip Shedding Light on the Possible Link between ADAMTS13 and Vaccine-Induced Thrombotic Thrombocytopenia ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=34685765 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34685765 #FOAvip English Wikipedia <ref>{{Cite pmid|34685765}}</ref> Shedding Light on the Possible Link between ADAMTS13 and Vaccine-Induced Thrombotic Thrombocytopenia #MMPMID34685765 Szostek-Mioduchowska A; Kordowitzki P Cells 2021[Oct]; 10 (10): ä PMID34685765show ga Several recent reports have highlighted the onset of vaccine-induced thrombotic thrombocytopaenia (VITT) in some recipients (approximately 1 case out of 100k exposures) of the ChAdOx1 nCoV-19 vaccine (AstraZeneca). Although the underlying events leading to this blood-clotting phenomenon has yet to be elucidated, several critical observations present a compelling potential mechanism. Thrombus formation requires the von Willebrand (VWF) protein to be in ultra-large multimeric state. The conservation of this state is controlled by the ADAMTS13 enzyme, whose proteolytic activity reduces the size of VWF multimers, keeping blood clotting at bay. However, ADAMTS13 cannot act on VWF that is bound to platelet factor 4 (PF4). As such, it is of particular interest to note that a common feature between subjects presenting with VITT is high titres of antibodies against PF4. This raises the possibility that these antibodies preserve the stability of ultra-large VWF complexes, leading to the formation of endothelium-anchored VWF strings, which are capable of recruiting circulating platelets and causing uncontrolled thrombosis in terminal capillaries. Here, we share our viewpoint about the current understanding of the VITT pathogenesis involving the prevention of ADAMTS13's activity on VWF by PF4 antibody-mediated stabilisation/ protection of the PF4-VWF complex. |ADAMTS13 Protein/*metabolism[MESH] |Antibodies[MESH] |Autoantibodies/immunology[MESH] |Blood Platelets/metabolism[MESH] |COVID-19 Vaccines/*adverse effects[MESH] |COVID-19/*prevention & control[MESH] |ChAdOx1 nCoV-19[MESH] |Crystallography, X-Ray[MESH] |Endothelial Cells/immunology[MESH] |Humans[MESH] |Platelet Factor 4/metabolism[MESH] |Polymorphism, Genetic[MESH] |Protein Domains[MESH] |Thrombocytopenia/etiology/*immunology[MESH] |Thrombosis/etiology[MESH]Shedding Light on the Possible Link between ADAMTS13 and Vaccine-Induc(epmc).pdf DeepDyve Pubget Overpricing