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10.1055/s-0040-1718735 http://scihub22266oqcxt.onion/10.1055/s-0040-1718735 33124029!7869061!33124029     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 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       Thromb+Haemost 2020 ; 120 (12): 1629-1641 Nephropedia Template TP {{tp|p=33124029|t=2020. Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19 |pdf=|usr=}}{{33124029}} gab.com Text Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19 JO: Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=33124029 #FOAvip The global coronavirus disease 2019 (COVID-19) pandemic has deranged the recent history of humankind, afflicting more than 27 million individuals to date. While the majority of COVID-19 patients recuperate, a considerable number of patients develop severe complications. Bilateral pneumonia constitutes the hallmark of severe COVID-19 disease but an involvement of other organ systems, namely the cardiovascular system, kidneys, liver, and central nervous system, occurs in at least half of the fatal COVID-19 cases. Besides respiratory failure requiring ventilation, patients with severe COVID-19 often display manifestations of systemic inflammation and thrombosis as well as diffuse microvascular injury observed postmortem. In this review, we survey the mechanisms that may explain how viral entry and activation of endothelial cells by severe acute respiratory syndrome coronavirus 2 can give rise to a series of events including systemic inflammation, thrombosis, and microvascular dysfunction. This pathophysiological scenario may be particularly harmful in patients with overt cardiovascular disease and may drive the fatal aspects of COVID-19. We further shed light on the role of the renin-angiotensin aldosterone system and its inhibitors in the context of COVID-19 and discuss the potential impact of antiviral and anti-inflammatory treatment options. Acknowledging the comorbidities and potential organ injuries throughout the course of severe COVID-19 is crucial in the clinical management of patients affecting treatment approaches and recovery rate. Twit Text FOAVip Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19 ????Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=33124029 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33124029 #FOAvip English Wikipedia <ref>{{Cite pmid|33124029}}</ref> Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19 #MMPMID33124029 Gencer S; Lacy M; Atzler D; van der Vorst EPC; Doring Y; Weber C Thromb Haemost 2020[Dec]; 120 (12): 1629-1641 PMID33124029show ga The global coronavirus disease 2019 (COVID-19) pandemic has deranged the recent history of humankind, afflicting more than 27 million individuals to date. While the majority of COVID-19 patients recuperate, a considerable number of patients develop severe complications. Bilateral pneumonia constitutes the hallmark of severe COVID-19 disease but an involvement of other organ systems, namely the cardiovascular system, kidneys, liver, and central nervous system, occurs in at least half of the fatal COVID-19 cases. Besides respiratory failure requiring ventilation, patients with severe COVID-19 often display manifestations of systemic inflammation and thrombosis as well as diffuse microvascular injury observed postmortem. In this review, we survey the mechanisms that may explain how viral entry and activation of endothelial cells by severe acute respiratory syndrome coronavirus 2 can give rise to a series of events including systemic inflammation, thrombosis, and microvascular dysfunction. This pathophysiological scenario may be particularly harmful in patients with overt cardiovascular disease and may drive the fatal aspects of COVID-19. We further shed light on the role of the renin-angiotensin aldosterone system and its inhibitors in the context of COVID-19 and discuss the potential impact of antiviral and anti-inflammatory treatment options. Acknowledging the comorbidities and potential organ injuries throughout the course of severe COVID-19 is crucial in the clinical management of patients affecting treatment approaches and recovery rate. |*Renin-Angiotensin System[MESH] |COVID-19/epidemiology/*immunology[MESH] |Cardiovascular Diseases/epidemiology/*immunology[MESH] |Hemostasis[MESH] |Humans[MESH] |Immunity[MESH] |Inflammation/*immunology[MESH] |Microcirculation[MESH] |Pandemics[MESH] |SARS-CoV-2/*physiology[MESH]Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms (epmc).pdf DeepDyve Pubget Overpricing