Mouse Anti-Human SELP Hybridoma [XBQT 23.3]

Background: In patients with NAFLD, there is an increased risk of cardiovascular disease (CVD). Selenoprotein P (SelP), a hepatokine, is associated with insulin resistance (IR) and serum SelP was found to be elevated in patients with NAFLD.& para;& para;Aim: This study aimed to determine the risk of CVD in NAFLD patients and the association of serum SelP levels with this NAFLD related CVD risk.& para;& para;Methods: Ninety-three patients with NAFLD and 37 healthy controls were included in the study. Complete blood count, C-reactive protein (CRP), fasting glucose, serum lipid levels, and SelP levels were tested from fasting blood samples. Moreover, body mass index (BMI), HOMA-IR, carotid intima-media thickness (cIMT) and flow-mediated dilatation (FMD) were measured.& para;& para;Results: In patients with NAFLD, the FMD ratio was significantly lower than in controls (P = 0.027) . cIMT measurements were similar in both groups (P = 0.996). Serum SelP levels were significantly higher than controls (P<0.001 ). SelP levels were significantly correlated with BMI, fasting glucose, LDL-cholesterol and HOMA-IR (r = 0.395, P<0.001; r = 0.322, P = 0.002; r = 0.353, P<0.001 ; r = 0.521, P<0.001, respectively). Also, SelP levels were significantly lower andcorrelated with FMD (r= -0.674, P<0.001 ). SelP, ESR and CRP were significantly higher (P<0.05) and FMD ratios were significantly lower (P<0.05) in patients with nonalcoholic steatohepatitis (NASH) when compared to patients with simple steatosis.& para;& para;Conclusion: These results suggest that in young NAFLD patients without additional comorbidi ties, there is an increased risk of CVD. FMD may be a better predictor for assessment of CVD risk when compared with cIMT. We assume that there could also be an important role of SelP in the pathogenesis of NASH. (C) 2017 Elsevier Masson SAS. All rights reserved.

The hypothesis of a causal link between inflammation and atherosclerosis would be strengthened if variants of inflammatory genes were associated with disease. Polymorphisms of 33 genes encoding inflamimatory molecules were tested for association with myocardial infarction (MI). Patients with MI and a parental history of MI (n=312) and controls from the UK (n=317) were genotyped for 162 polymorphisms. Thirteen polymorphisms were associated with MI (P values ranging from 0.003 to 0.041). For three genes, ITGB1, SELP, and TNFRSF1B haplotype frequencies differed between patients and controls (P values<0.01). We further assessed the simultaneous contribution of all polymorphisms and relevant covariates to MI using a two-step strategy of data mining relying on Random Forest and DICE algorithms. In a replication study involving two independent samples from the UK (n-649) and France (n-706), one interaction between the ITGA4/R898Q polymorphism and current smoking status was replicated. This study illustrates a strategy for assessing the joint effect of a large number of polymorphisms on a phenotype that may provide information that single locus or single gene analysis may fail to uncover. Overall, there was weak evidence for an implication of inflammatory polymorphisms on susceptibility to MI.