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10.1016/j.biochi.2020.04.008 http://scihub22266oqcxt.onion/10.1016/j.biochi.2020.04.008 32305506!7161528!32305506     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       Biochimie 2020 ; 174 (ä): 30-33 Nephropedia Template TP {{tp|p=32305506|t=2020. Renin-angiotensin system at the heart of COVID-19 pandemic |pdf=|usr=}}{{32305506}} gab.com Text Renin-angiotensin system at the heart of COVID-19 pandemic JO: Biochimie http://www.kidney.de/pget.php?&tw=1&pmid=32305506 #FOAvip Significant aspects of COVID-19 pandemic remain obscure. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19. Twit Text FOAVip Renin-angiotensin system at the heart of COVID-19 pandemic ????Biochimie http://www.kidney.de/pget.php?&tw=1&pmid=32305506 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32305506 #FOAvip English Wikipedia <ref>{{Cite pmid|32305506}}</ref> Renin-angiotensin system at the heart of COVID-19 pandemic #MMPMID32305506 Alifano M; Alifano P; Forgez P; Iannelli A Biochimie 2020[Jul]; 174 (ä): 30-33 PMID32305506show ga Significant aspects of COVID-19 pandemic remain obscure. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19. |Aged[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Betacoronavirus[MESH] |COVID-19[MESH] |Cardiovascular Diseases/complications[MESH] |Coronavirus Infections/complications/metabolism/*physiopathology[MESH] |Female[MESH] |Humans[MESH] |Hypertension/complications[MESH] |Male[MESH] |Middle Aged[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/genetics/metabolism[MESH] |Pneumonia, Viral/complications/metabolism/*physiopathology[MESH] |Renin-Angiotensin System/*physiology[MESH] |Risk Factors[MESH]Renin-angiotensin system at the heart of COVID-19 pandemic (epmc).pdf DeepDyve Pubget Overpricing