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10.1038/s41467-021-22713-z http://scihub22266oqcxt.onion/10.1038/s41467-021-22713-z 33893295!8065208!33893295     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33893295.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2021 ; 12 (1): 2417 Nephropedia Template TP {{tp|p=33893295|t=2021. COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system |pdf=|usr=}}{{33893295}} gab.com Text COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33893295 #FOAvip SARS-CoV-2 uses ACE2, an inhibitor of the Renin-Angiotensin-Aldosterone System (RAAS), for cellular entry. Studies indicate that RAAS imbalance worsens the prognosis in COVID-19. We present a consecutive retrospective COVID-19 cohort with findings of frequent pulmonary thromboembolism (17%), high pulmonary artery pressure (60%) and lung MRI perfusion disturbances. We demonstrate, in swine, that infusing angiotensin II or blocking ACE2 induces increased pulmonary artery pressure, reduces blood oxygenation, increases coagulation, disturbs lung perfusion, induces diffuse alveolar damage, and acute tubular necrosis compared to control animals. We further demonstrate that this imbalanced state can be ameliorated by infusion of an angiotensin receptor blocker and low-molecular-weight heparin. In this work, we show that a pathophysiological state in swine induced by RAAS imbalance shares several features with the clinical COVID-19 presentation. Therefore, we propose that severe COVID-19 could partially be driven by a RAAS imbalance. Twit Text FOAVip COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33893295 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33893295 #FOAvip English Wikipedia <ref>{{Cite pmid|33893295}}</ref> COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system #MMPMID33893295 Rysz S; Al-Saadi J; Sjostrom A; Farm M; Campoccia Jalde F; Platten M; Eriksson H; Klein M; Vargas-Paris R; Nyren S; Abdula G; Ouellette R; Granberg T; Jonsson Fagerlund M; Lundberg J Nat Commun 2021[Apr]; 12 (1): 2417 PMID33893295show ga SARS-CoV-2 uses ACE2, an inhibitor of the Renin-Angiotensin-Aldosterone System (RAAS), for cellular entry. Studies indicate that RAAS imbalance worsens the prognosis in COVID-19. We present a consecutive retrospective COVID-19 cohort with findings of frequent pulmonary thromboembolism (17%), high pulmonary artery pressure (60%) and lung MRI perfusion disturbances. We demonstrate, in swine, that infusing angiotensin II or blocking ACE2 induces increased pulmonary artery pressure, reduces blood oxygenation, increases coagulation, disturbs lung perfusion, induces diffuse alveolar damage, and acute tubular necrosis compared to control animals. We further demonstrate that this imbalanced state can be ameliorated by infusion of an angiotensin receptor blocker and low-molecular-weight heparin. In this work, we show that a pathophysiological state in swine induced by RAAS imbalance shares several features with the clinical COVID-19 presentation. Therefore, we propose that severe COVID-19 could partially be driven by a RAAS imbalance. |Angiotensin II/administration & dosage/metabolism[MESH] |Angiotensin Receptor Antagonists/administration & dosage[MESH] |Angiotensin-Converting Enzyme 2/antagonists & inhibitors/metabolism[MESH] |Animals[MESH] |COVID-19/metabolism/*physiopathology/virology[MESH] |Female[MESH] |Humans[MESH] |Lung/diagnostic imaging/*physiopathology/virology[MESH] |Magnetic Resonance Imaging/methods[MESH] |Protein Binding/drug effects[MESH] |Renin-Angiotensin System/*physiology[MESH] |Retrospective Studies[MESH] |SARS-CoV-2/*isolation & purification/metabolism/physiology[MESH] |Spike Glycoprotein, Coronavirus/metabolism[MESH] |Swine[MESH]COVID-19 pathophysiology may be driven by an imbalance in the renin-a(epmc).pdf DeepDyve Pubget Overpricing