All of them remained significant in a subset of individuals without manifest cardiovascular disease. Matrix metalloproteinase-12 (MMP-12), growth/differentiation factor 15 (GDF-15), urokinase plasminogen activator surface receptor (uPAR), TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2), lectin-like oxidized LDL receptor 1 (LOX-1), hepatocyte growth factor (HGF), matrix metalloproteinase-10 (MMP-10) and matrix metalloproteinase-1 (MMP-1) were positively associated, while endothelial cell-specific molecule 1 (ESM-1) and interleukin-27 subunit alpha (IL27-A) showed inverse associations. Results: We found 30 proteins to be significantly associated with current cigarette smoking in PIVUS (FDR<5%) and ten were replicated in ULSAM (p<0.05). Levels of the 80 proteins were measured using the proximity extension assay, a novel PCR-based proteomics technique. Methods: Smoking status was self-reported and defined as current smoker, former smoker or never-smoker. We investigated the associations between cigarette smoking and 80 protein markers known to be related to cardiovascular diseases in two community-based cohorts, the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS, n = 969, 50% women, all aged 70 years) and the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 717, all men aged 77 years). Studies of smoking in relation to cardiovascular-related protein markers can provide novel insights into the biological effects of smoking. Conclusions: Our work provides preliminary information for a standardized method potentially useful for genotyping rs153109, and suggests its utility as a candidate approach to evaluate IL-27 p28 polymorphisms as additional clinical predictors of response to therapies in HCV infected patients.īackground and aims: Cardiovascular diseases account for the largest fraction of smoking-induced deaths. Moreover, the analysis of allelic distribution of rs153109 highlighted a predominance of allele A in all genotypes in spite of allele G. By contrast, the genotype G/G was absent in non-responder and relapser patients. The genotype distribution of the c.-964 A>G polymorphism was more present in patients who did not achieve a SVR. Results: This method has been applied in a preliminary study on patients with chronic hepatitis C to provide information for a standardized assay useful to genotyping of rs153109 SNPs of IL-27p28. Amplification products were studied by direct sequencing. Methods: rs153109, corresponding to position c.-964A>G of the IL-27 locus, was amplified from genomic DNA extracted from 15 patients with chronic hepatitis C stratified by sustained viral response (SVR), relapser and nonresponder, after treatment with peginterferon-alpha (PegIFN-alpha) combined with ribavirin (RBV). In this study we have investigated the potential role of SNPs in the promoter region of IL27 p28 gene (alleles rs153109) on the outcome of HCV infected patients. Little is known about the relationship between IL-27 single nucleotide polymorphisms and therapy response in patients infected by hepatitis C virus (HCV). Recent studies revealed that single nucleotide polymorphisms (SNPs) of the IL-27 promoter region modulate the development of infectious diseases and individual's susceptibility to therapeutic response. Anti-Mouse IgG2a polyclonal antibody Īnti-Mouse IgG2a monoclonal antibody Īnti-Mouse IgG2a monoclonal antibody, clone LO-MG2a-9 īackground: Interleukin 27 (IL-27) has pleiotropic properties that can either limit or enhance immune responses.
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