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.

10.3389/fimmu.2017.00589 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00589 C5446983!5446983!28611769     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28611769|t=2017. Analysis of Complement C3 Gene Reveals Susceptibility to Severe Preeclampsia |pdf=|usr=}}{{28611769}} gab.com Text Analysis of Complement C3 Gene Reveals Susceptibility to Severe Preeclampsia JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28611769 #FOAvip Preeclampsia (PE) is a common vascular disease of pregnancy with genetic predisposition. Dysregulation of the complement system has been implicated, but molecular mechanisms are incompletely understood. In this study, we determined the potential linkage of severe PE to the most central complement gene, C3. Three cohorts of Finnish patients and controls were recruited for a genetic case-control study. Participants were genotyped using Sequenom genotyping and Sanger sequencing. Initially, we studied 259 Finnish patients with severe PE and 426 controls from the Southern Finland PE and the Finnish population-based PE cohorts. We used a custom-made single nucleotide polymorphism (SNP) genotyping assay consisting of 98 SNPs in 18 genes that encode components of the complement system. Following the primary screening, C3 was selected as the candidate gene and consequently Sanger sequenced. Fourteen SNPs from C3 were also genotyped by a Sequenom panel in 960 patients with severe PE and 705 controls, including already sequenced individuals. Three of the 43 SNPs observed within C3 were associated with severe PE: rs2287845 (p?=?0.038, OR?=?1.158), rs366510 (p?=?0.039, OR?=?1.158), and rs2287848 (p?=?0.041, OR?=?1.155). We also discovered 16 SNP haplotypes with extreme linkage disequilibrium in the middle of the gene with a protective (p?=?0.044, OR?=?0.628) or a predisposing (p?=?0.011, OR?=?2.110) effect to severe PE depending on the allele combination. Genetic variants associated with PE are located in key domains of C3 and could thereby influence the function of C3. This is, as far as we are aware, the first candidate gene in the complement system with an association to a clinically relevant PE subphenotype, severe PE. The result highlights a potential role for the complement system in the pathogenesis of PE and may help in defining prognostic and therapeutic subgroups of preeclamptic women. Twit Text FOAVip Analysis of Complement C3 Gene Reveals Susceptibility to Severe Preeclampsia ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28611769 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28611769 #FOAvip English Wikipedia <ref>{{Cite pmid|28611769}}</ref> Analysis of Complement C3 Gene Reveals Susceptibility to Severe Preeclampsia #MMPMID28611769 Lokki AI; Kaartokallio T; Holmberg V; Onkamo P; Koskinen LL; Saavalainen P; Heinonen S; Kajantie E; Kere J; Kivinen K; Pouta A; Villa PM; Hiltunen L; Laivuori H; Meri S Front Immunol 2017[]; 8 (ä): ä PMID28611769show ga Preeclampsia (PE) is a common vascular disease of pregnancy with genetic predisposition. Dysregulation of the complement system has been implicated, but molecular mechanisms are incompletely understood. In this study, we determined the potential linkage of severe PE to the most central complement gene, C3. Three cohorts of Finnish patients and controls were recruited for a genetic case-control study. Participants were genotyped using Sequenom genotyping and Sanger sequencing. Initially, we studied 259 Finnish patients with severe PE and 426 controls from the Southern Finland PE and the Finnish population-based PE cohorts. We used a custom-made single nucleotide polymorphism (SNP) genotyping assay consisting of 98 SNPs in 18 genes that encode components of the complement system. Following the primary screening, C3 was selected as the candidate gene and consequently Sanger sequenced. Fourteen SNPs from C3 were also genotyped by a Sequenom panel in 960 patients with severe PE and 705 controls, including already sequenced individuals. Three of the 43 SNPs observed within C3 were associated with severe PE: rs2287845 (p?=?0.038, OR?=?1.158), rs366510 (p?=?0.039, OR?=?1.158), and rs2287848 (p?=?0.041, OR?=?1.155). We also discovered 16 SNP haplotypes with extreme linkage disequilibrium in the middle of the gene with a protective (p?=?0.044, OR?=?0.628) or a predisposing (p?=?0.011, OR?=?2.110) effect to severe PE depending on the allele combination. Genetic variants associated with PE are located in key domains of C3 and could thereby influence the function of C3. This is, as far as we are aware, the first candidate gene in the complement system with an association to a clinically relevant PE subphenotype, severe PE. The result highlights a potential role for the complement system in the pathogenesis of PE and may help in defining prognostic and therapeutic subgroups of preeclamptic women. äAnalysis of Complement C3 Gene Reveals Susceptibility to Severe Preecl(epmc).pdf DeepDyve Pubget Overpricing