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10.1371/journal.pone.0253347 http://scihub22266oqcxt.onion/10.1371/journal.pone.0253347 34161337!8221465!34161337     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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2021 ; 16 (6): e0253347 Nephropedia Template TP {{tp|p=34161337|t=2021. SARS-CoV-2 uses major endothelial integrin alphavbeta3 to cause vascular dysregulation in-vitro during COVID-19 |pdf=|usr=}}{{34161337}} gab.com Text SARS-CoV-2 uses major endothelial integrin alphavbeta3 to cause vascular dysregulation in-vitro during COVID-19 JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=34161337 #FOAvip The unprecedented global COVID-19 pandemic has prompted a desperate international effort to accelerate the development of anti-viral candidates. For unknown reasons, COVID-19 infections are associated with adverse cardiovascular complications, implicating that vascular endothelial cells are essential in viral propagation. The etiological pathogen, SARS-CoV-2, has a higher reproductive number and infection rate than its predecessors, indicating it possesses novel characteristics that infers enhanced transmissibility. A unique K403R spike protein substitution encodes an Arg-Gly-Asp (RGD) motif, introducing a potential role for RGD-binding host integrins. Integrin alphaVbeta3 is widely expressed across the host, particularly in the endothelium, which acts as the final barrier before microbial entry into the bloodstream. This mutagenesis creates an additional binding site, which may be sufficient to increase SARS-CoV-2 pathogenicity. Here, we investigate how SARS-CoV-2 passes from the epithelium to endothelium, the effects of alphaVbeta3 antagonist, Cilengitide, on viral adhesion, vasculature permeability and leakage, and also report on a simulated interaction between the viral and host protein in-silico. Twit Text FOAVip SARS-CoV-2 uses major endothelial integrin alphavbeta3 to cause vascular dysregulation in-vitro during COVID-19 ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=34161337 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34161337 #FOAvip English Wikipedia <ref>{{Cite pmid|34161337}}</ref> SARS-CoV-2 uses major endothelial integrin alphavbeta3 to cause vascular dysregulation in-vitro during COVID-19 #MMPMID34161337 Nader D; Fletcher N; Curley GF; Kerrigan SW PLoS One 2021[]; 16 (6): e0253347 PMID34161337show ga The unprecedented global COVID-19 pandemic has prompted a desperate international effort to accelerate the development of anti-viral candidates. For unknown reasons, COVID-19 infections are associated with adverse cardiovascular complications, implicating that vascular endothelial cells are essential in viral propagation. The etiological pathogen, SARS-CoV-2, has a higher reproductive number and infection rate than its predecessors, indicating it possesses novel characteristics that infers enhanced transmissibility. A unique K403R spike protein substitution encodes an Arg-Gly-Asp (RGD) motif, introducing a potential role for RGD-binding host integrins. Integrin alphaVbeta3 is widely expressed across the host, particularly in the endothelium, which acts as the final barrier before microbial entry into the bloodstream. This mutagenesis creates an additional binding site, which may be sufficient to increase SARS-CoV-2 pathogenicity. Here, we investigate how SARS-CoV-2 passes from the epithelium to endothelium, the effects of alphaVbeta3 antagonist, Cilengitide, on viral adhesion, vasculature permeability and leakage, and also report on a simulated interaction between the viral and host protein in-silico. |Antigens, CD/metabolism[MESH] |Binding Sites[MESH] |COVID-19/metabolism/physiopathology[MESH] |Caco-2 Cells[MESH] |Cadherins/metabolism[MESH] |Computer Simulation[MESH] |Endothelium, Vascular/cytology/physiopathology/*virology[MESH] |Host-Pathogen Interactions/drug effects[MESH] |Humans[MESH] |Integrin alphaVbeta3/chemistry/*metabolism[MESH] |Models, Molecular[MESH] |Mutation[MESH] |Permeability[MESH] |SARS-CoV-2/drug effects/genetics/metabolism/*pathogenicity[MESH] |Snake Venoms/*pharmacology[MESH] |Spike Glycoprotein, Coronavirus/chemistry/metabolism[MESH]SARS-CoV-2 uses major endothelial integrin alphavbeta3 to cause vascul(epmc).pdf DeepDyve Pubget Overpricing