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10.1177/1076029620943293 http://scihub22266oqcxt.onion/10.1177/1076029620943293 32735131!7401047!32735131     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Appl+Thromb+Hemost 2020 ; 26 (ä): 1076029620943293 Nephropedia Template TP {{tp|p=32735131|t=2020. COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response |pdf=|usr=}}{{32735131}} gab.com Text COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response JO: Clin Appl Thromb Hemost http://www.kidney.de/pget.php?&tw=1&pmid=32735131 #FOAvip Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC. Twit Text FOAVip COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response ????Clin Appl Thromb Hemost http://www.kidney.de/pget.php?&tw=1&pmid=32735131 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32735131 #FOAvip English Wikipedia <ref>{{Cite pmid|32735131}}</ref> COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response #MMPMID32735131 Jayarangaiah A; Kariyanna PT; Chen X; Jayarangaiah A; Kumar A Clin Appl Thromb Hemost 2020[Jan]; 26 (ä): 1076029620943293 PMID32735131show ga Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC. |*Betacoronavirus[MESH] |Blood Coagulation Disorders/etiology/pathology/*virology[MESH] |COVID-19[MESH] |Coronavirus Infections/*complications/physiopathology/virology[MESH] |Endothelial Cells/pathology/virology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Leukocytes/metabolism/pathology[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications/physiopathology/virology[MESH] |SARS-CoV-2[MESH] |Thrombophilia/immunology/virology[MESH]COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Resp(epmc).pdf DeepDyve Pubget Overpricing