Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1002/kjm2.12237 http://scihub22266oqcxt.onion/10.1002/kjm2.12237 32492292!7300771!32492292     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kaohsiung+J+Med+Sci 2020 ; 36 (6): 389-392 Nephropedia Template TP {{tp|p=32492292|t=2020. Two hits to the renin-angiotensin system may play a key role in severe COVID-19 |pdf=|usr=}}{{32492292}} gab.com Text Two hits to the renin-angiotensin system may play a key role in severe COVID-19 JO: Kaohsiung J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=32492292 #FOAvip The spike glycoprotein on the virion surface docking onto the angiotensin-converting enzyme (ACE) 2 dimer is an essential step in the process of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in human cells-involves downregulation of ACE2 expression with systemic renin-angiotensin system (RAS) imbalance and promotion of multi-organ damage. In general, the RAS induces vasoconstriction, hypertension, inflammation, fibrosis, and proliferation via the ACE/Ang II/Ang II type 1 receptor (AT1R) axis and induces the opposite effects via the ACE2/Ang (1-7)/Mas axis. The RAS may be activated by chronic inflammation in hypertension, diabetes, obesity, and cancer. SARS-CoV-2 induces the ACE2 internalization and shedding, leading to the inactivation of the ACE2/Ang (1-7)/Mas axis. Therefore, we hypothesize that two hits to the RAS drives COVID-19 progression. In brief, the first hit originates from chronic inflammation activating the ACE/Ang II/AT1R axis, and the second originates from the COVID-19 infection inactivating the ACE2/Ang (1-7)/Mas axis. Moreover, the two hits to the RAS may be the primary reason for increased mortality in patients with COVID-19 who have comorbidities and may serve as a therapeutic target for COVID-19 treatment. Twit Text FOAVip Two hits to the renin-angiotensin system may play a key role in severe COVID-19 ????Kaohsiung J Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=32492292 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32492292 #FOAvip English Wikipedia <ref>{{Cite pmid|32492292}}</ref> Two hits to the renin-angiotensin system may play a key role in severe COVID-19 #MMPMID32492292 Tseng YH; Yang RC; Lu TS Kaohsiung J Med Sci 2020[Jun]; 36 (6): 389-392 PMID32492292show ga The spike glycoprotein on the virion surface docking onto the angiotensin-converting enzyme (ACE) 2 dimer is an essential step in the process of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in human cells-involves downregulation of ACE2 expression with systemic renin-angiotensin system (RAS) imbalance and promotion of multi-organ damage. In general, the RAS induces vasoconstriction, hypertension, inflammation, fibrosis, and proliferation via the ACE/Ang II/Ang II type 1 receptor (AT1R) axis and induces the opposite effects via the ACE2/Ang (1-7)/Mas axis. The RAS may be activated by chronic inflammation in hypertension, diabetes, obesity, and cancer. SARS-CoV-2 induces the ACE2 internalization and shedding, leading to the inactivation of the ACE2/Ang (1-7)/Mas axis. Therefore, we hypothesize that two hits to the RAS drives COVID-19 progression. In brief, the first hit originates from chronic inflammation activating the ACE/Ang II/AT1R axis, and the second originates from the COVID-19 infection inactivating the ACE2/Ang (1-7)/Mas axis. Moreover, the two hits to the RAS may be the primary reason for increased mortality in patients with COVID-19 who have comorbidities and may serve as a therapeutic target for COVID-19 treatment. |*Betacoronavirus/pathogenicity/physiology[MESH] |Angiotensin II/physiology[MESH] |Angiotensin Receptor Antagonists/therapeutic use[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH] |COVID-19[MESH] |Comorbidity[MESH] |Coronavirus Infections/drug therapy/epidemiology/*physiopathology[MESH] |Humans[MESH] |Models, Biological[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/physiology[MESH] |Pneumonia, Viral/drug therapy/epidemiology/*physiopathology[MESH] |Receptor, Angiotensin, Type 1/physiology[MESH] |Renin-Angiotensin System/drug effects/*physiology[MESH] |SARS-CoV-2[MESH]Two hits to the renin-angiotensin system may play a key role in severe(epmc).pdf DeepDyve Pubget Overpricing