Changes in the frequencies of genotypes and mutant alleles of ACE, AGTR1, AGT, and ITGB3 genes were analyzed in patients with arterial hypertension coupled with metabolic syndrome (N=15) and compared with population data and corresponding parameters in patients with isolated hypertension (N=15). Increased frequency of genotype ID of ACE gene (hypertension predictor) was confirmed for both groups. In case of isolated hypertension, M235M genotype (gene AGT) was more frequent, in case of hypertension combined with metabolic syndrome, the frequency of genotypes A1166C and C1166C of the gene AGTR1 was higher in comparison with population data. Comparison of mutant allele frequencies in the two groups showed that at the 90% significance level allele T of the AGT gene was more frequent in hypertension coupled with metabolic syndrome (OR=1.26) and genotype A1166A of the AGTR1 gene was more frequent in the group with isolated hypertension.

This study investigated the renin-angiotensin-aldosterone system (RAAS) gene polymorphisms as possible genetic risk factors for the restenosis development in patients with drug-eluting stents. 113 participants had coronary artery disease and underwent stenting. The control group consisted of 62 individuals with intact coronary arteries. Patients were divided into two groups: with in-stent restenosis (ISR) and without it. The patients with ISR were classified into subgroups by the terms of the restenosis development and age. Real-time PCR and Restriction Fragment Length Polymorphism-PCR were used to genotype the study participants for RAAS gene polymorphisms. We found that the development of restenosis is generally associated with the minor A allele for renin (REN) rs2368564 and the major TT genotype for angiotensinogen (AGT) rs699. The heterozygous genotype for AGT rs4762 acts as a protective marker. A minor A allele for angiotensin II type 2 receptor (AGTR2) rs1403543 is associated with a risk of restenosis in people under 65 years old. Among patients with the early ISR, heterozygotes for angiotensin II type 1 receptor (AGTR1) rs5186 are more frequent, as well as A allele carriers for AGTR2 rs1403543. A minor homozygous genotype for REN rs41317140 and heterozygous genotype for aldosterone synthase (CYP11B2) rs1799998 are predisposed to the late restenosis. Thus, to choose the effective treatment tactics for patients with coronary artery disease, it is necessary to genotype patients for the RAAS polymorphisms, which, along with age and clinical characteristics, will allow a comprehensive assessment of the risk of the restenosis development after stenting.

No abstract

No abstract

Background ― Genetic polymorphisms analysis of metabolic and antioxidant systems pathway genes are associated with male infertility is the most perspective and developed field in andrology. Purpose ― the aim of the research is to reveal the association of the glutathione S-transferase gene GSTP1 polymorphism C/T (rs1138272) with risk of pathospermia in Russian men in Moscow region. Material and Methods ― Case control study was conducted on 68 fertile men and 70 infertile men with various forms of pathospermia. Sperm analysis was performed according to WHO guidelines (WHO, 2010). DNA was extracted from peripheral blood leukocytes. Genotyping of the GSTP1 gene polymorphisms was carried out by generated amplicons from melting curve analysis after real time PCR. Results ― statistically significant association of polymorphism GSTP1 C/T (Ala/Val; rs1138272) with asthenozoospermia (χ2=8.58, p=0.003) and teratospermia (χ2=6.81, p=0.009) risk was found. The frequencies of homozygous and heterozygous carries (CT+TT genotypes) for polymorphic locus GSTP1 gene (rs1138272) are 3 times higher for men with disturbance of motility of spermatozoa and 2.5 times higher for men with abnormalities in morphology of spermatozoa, then for men with normozoospermia. Conclusion ― The GSTP1 C>T polymorphism (rs1138272) associated with risk of teratospermia and asthenozoospermia in male of reproductive age.

No abstract

No abstract

We studied the effect of phosphocreatine and ethylmethylhydroxypyridine succinate on the expression of Bax and Bcl-2 proteins in left-ventricular cardiomyocytes of spontaneously hypertensive rats (SHR). Both drugs have no effect on the expression of Bcl-2, but significantly reduce the level of Bax protein (phosphocreatine produces more pronounced effect). These data attest to an important role of energy deficit and oxidative stress in the induction of cardiomyocyte apoptosis in genetically determined arterial hypertension.