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10.1016/j.immuni.2021.10.004 http://scihub22266oqcxt.onion/10.1016/j.immuni.2021.10.004 34715018!9338439!34715018     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunity 2021 ; 54 (11): 2632-2649.e6 Nephropedia Template TP {{tp|p=34715018|t=2021. APOL1 risk variants in individuals of African genetic ancestry drive endothelial cell defects that exacerbate sepsis |pdf=|usr=}}{{34715018}} gab.com Text APOL1 risk variants in individuals of African genetic ancestry drive endothelial cell defects that exacerbate sepsis JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=34715018 #FOAvip The incidence and severity of sepsis is higher among individuals of African versus European ancestry. We found that genetic risk variants (RVs) in the trypanolytic factor apolipoprotein L1 (APOL1), present only in individuals of African ancestry, were associated with increased sepsis incidence and severity. Serum APOL1 levels correlated with sepsis and COVID-19 severity, and single-cell sequencing in human kidneys revealed high expression of APOL1 in endothelial cells. Analysis of mice with endothelial-specific expression of RV APOL1 and in vitro studies demonstrated that RV APOL1 interfered with mitophagy, leading to cytosolic release of mitochondrial DNA and activation of the inflammasome (NLRP3) and the cytosolic nucleotide sensing pathways (STING). Genetic deletion or pharmacological inhibition of NLRP3 and STING protected mice from RV APOL1-induced permeability defects and proinflammatory endothelial changes in sepsis. Our studies identify the inflammasome and STING pathways as potential targets to reduce APOL1-associated health disparities in sepsis and COVID-19. Twit Text FOAVip APOL1 risk variants in individuals of African genetic ancestry drive endothelial cell defects that exacerbate sepsis ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=34715018 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34715018 #FOAvip English Wikipedia <ref>{{Cite pmid|34715018}}</ref> APOL1 risk variants in individuals of African genetic ancestry drive endothelial cell defects that exacerbate sepsis #MMPMID34715018 Wu J; Ma Z; Raman A; Beckerman P; Dhillon P; Mukhi D; Palmer M; Chen HC; Cohen CR; Dunn T; Reilly J; Meyer N; Shashaty M; Arany Z; Hasko G; Laudanski K; Hung A; Susztak K Immunity 2021[Nov]; 54 (11): 2632-2649.e6 PMID34715018show ga The incidence and severity of sepsis is higher among individuals of African versus European ancestry. We found that genetic risk variants (RVs) in the trypanolytic factor apolipoprotein L1 (APOL1), present only in individuals of African ancestry, were associated with increased sepsis incidence and severity. Serum APOL1 levels correlated with sepsis and COVID-19 severity, and single-cell sequencing in human kidneys revealed high expression of APOL1 in endothelial cells. Analysis of mice with endothelial-specific expression of RV APOL1 and in vitro studies demonstrated that RV APOL1 interfered with mitophagy, leading to cytosolic release of mitochondrial DNA and activation of the inflammasome (NLRP3) and the cytosolic nucleotide sensing pathways (STING). Genetic deletion or pharmacological inhibition of NLRP3 and STING protected mice from RV APOL1-induced permeability defects and proinflammatory endothelial changes in sepsis. Our studies identify the inflammasome and STING pathways as potential targets to reduce APOL1-associated health disparities in sepsis and COVID-19. |Animals[MESH] |Apolipoprotein L1/blood/*genetics[MESH] |Black People/*genetics/statistics & numerical data[MESH] |COVID-19/*genetics/pathology[MESH] |DNA, Mitochondrial/metabolism[MESH] |Endothelial Cells/metabolism[MESH] |Genetic Predisposition to Disease/*genetics[MESH] |Humans[MESH] |Inflammation/genetics/pathology[MESH] |Membrane Proteins/antagonists & inhibitors/genetics/metabolism[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Mitophagy/genetics[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors/genetics/metabolism[MESH] |Risk Factors[MESH] |Sepsis/*genetics/pathology[MESH] |Severity of Illness Index[MESH]APOL1 risk variants in individuals of African genetic ancestry drive e(epmc).pdf DeepDyve Pubget Overpricing