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10.1038/ng.3379 http://scihub22266oqcxt.onion/10.1038/ng.3379 C4552599!4552599!26258845     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 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       Nat+Genet 2015 ; 47 (9): 1085-90 Nephropedia Template TP {{tp|p=26258845|t=2015. Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases |pdf=|usr=}}{{26258845}} gab.com Text Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases JO: Nat Genet http://www.kidney.de/pget.php?&tw=1&pmid=26258845 #FOAvip Human leukocyte antigen (HLA) genes confer strong risk for autoimmune diseases on a log-additive scale. Here we speculated that differences in autoantigen binding repertoires between a heterozygote?s two expressed HLA variants may result in additional non-additive risk effects. We tested non-additive disease contributions of classical HLA alleles in patients and matched controls for five common autoimmune diseases: rheumatoid arthritis (RA, Ncases=5,337), type 1 diabetes (T1D, Ncases=5,567), psoriasis vulgaris (Ncases=3,089), idiopathic achalasia (Ncases=727), and celiac disease (Ncases=11,115). In four out of five diseases, we observed highly significant non-additive dominance effects (RA: P=2.5×1012; T1D: P=2.4×10?10; psoriasis: P=5.9×10?6; celiac disease: P=1.2×10?87). In three of these diseases, the dominance effects were explained by interactions between specific classical HLA alleles (RA: P=1.8×10?3; T1D: P=8.6×1027; celiac disease: P=6.0×10?100). These interactions generally increased disease risk and explained moderate but significant fractions of phenotypic variance (RA: 1.4%, T1D: 4.0%, and celiac disease: 4.1%, beyond a simple additive model). Twit Text FOAVip Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases ????Nat Genet http://www.kidney.de/pget.php?&tw=1&pmid=26258845 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26258845 #FOAvip English Wikipedia <ref>{{Cite pmid|26258845}}</ref> Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases #MMPMID26258845 Lenz TL; Deutsch AJ; Han B; Hu X; Okada Y; Eyre S; Knapp M; Zhernakova A; Huizinga TW; Abecasis G; Becker J; Boeckxstaens GE; Chen WM; Franke A; Gladman DD; Gockel I; Gutierrez-Achury J; Martin J; Nair RP; Nöthen MM; Onengut-Gumuscu S; Rahman P; Rantapää-Dahlqvist S; Stuart PE; Tsoi LC; Van Heel DA; Worthington J; Wouters MM; Klareskog L; Elder JT; Gregersen PK; Schumacher J; Rich SS; Wijmenga C; Sunyaev SR; de Bakker PI; Raychaudhuri S Nat Genet 2015[Sep]; 47 (9): 1085-90 PMID26258845show ga Human leukocyte antigen (HLA) genes confer strong risk for autoimmune diseases on a log-additive scale. Here we speculated that differences in autoantigen binding repertoires between a heterozygote?s two expressed HLA variants may result in additional non-additive risk effects. We tested non-additive disease contributions of classical HLA alleles in patients and matched controls for five common autoimmune diseases: rheumatoid arthritis (RA, Ncases=5,337), type 1 diabetes (T1D, Ncases=5,567), psoriasis vulgaris (Ncases=3,089), idiopathic achalasia (Ncases=727), and celiac disease (Ncases=11,115). In four out of five diseases, we observed highly significant non-additive dominance effects (RA: P=2.5×1012; T1D: P=2.4×10?10; psoriasis: P=5.9×10?6; celiac disease: P=1.2×10?87). In three of these diseases, the dominance effects were explained by interactions between specific classical HLA alleles (RA: P=1.8×10?3; T1D: P=8.6×1027; celiac disease: P=6.0×10?100). These interactions generally increased disease risk and explained moderate but significant fractions of phenotypic variance (RA: 1.4%, T1D: 4.0%, and celiac disease: 4.1%, beyond a simple additive model). äWidespread non-additive and interaction effects within HLA loci modula(epmc).pdf DeepDyve Pubget Overpricing