Активность каспазы 3 и каспазы 8 в клетках миокарда правого желудочка при экспериментальной артериальной гипертензии

Caspase-3 and caspase-8 activity in right ventricular myocardial cells of rabbits with experimental arterial hypertension (AH) was investigated. Caspase-3 activity significantly increased at 2 and 4 weeks after modeling of AH. Obtained data demonstrated increased apoptosis in right ventricular myocardial cells in experimental arterial hypertension. Absence of significant increasing of caspase-8 activity indicates the predominance of intrinsic apoptogenic signals.Исследована активность каспазы 3 и каспазы 8 в клетках миокарда правого желудочка сердца кроликов с экспериментальной артериальной гипертензией (АГ). Обнаружено достоверное повышение активности каспазы 3 через 2 и 4 недели после моделирования АГ. Полученные результаты свидетельствуют об усилении апоптотической гибели клеток миокарда правого желудочка при экспериментальной артериальной гипертензии. Статистически незначимое повышение активности каспазы 8 указывает на преобладание внутриклеточного апоптогенного сигнала

Особенности генетического полиморфизма HLA-антигенов при приобретенной апластической анемии у детей

This study presents the genetic polymorphism of HLA-antigens in acquired aplastic anemia (AAA) in 147 children (85 boys и 62 girls) aged 1 to 18 with. The control group is consisted of 1700 umbilical cord blood samples of healthy newborns. The genetic polymorphism of HLA was studied in groups of children with AAA, divided by gender and age. Our results revealed distinction in HLA-markers of predisposition and sustainability to AAA. Possible differences in factors of immunogenetic predisposition suggest different mechanisms involved in the development of the disease in different groups of children and reconsider the existing model of the pathogenesis of AAA.В статье представлены результаты исследования генетического полиморфизма HLA-антигенов при приобретенной апластической анемии (ПАА) у 147 детей в возрасте от 1 до 18 лет. Контрольная группа была представлена 1700 образцами пуповинной крови условно здоровых новорожденных детей. Анализ полученных данных позволил выявить отличающиеся у детей разного пола и возраста HLA-маркеры предрасположенности и протекции к ПАА. Вероятное различие в факторах иммуногенетической предрасположенности позволяет предположить участие разных механизмов в развитии заболевания у разных групп детей и по-новому рассматривать уже имеющиеся модели патогенеза ПАА

ВСТРЕЧАЕМОСТЬ ПОЛИМОРФИЗМА Т657С ГЕНА SYCP3 У ЖЕНЩИН РУССКОЙ НАЦИОНАЛЬНОСТИ, ПРОЖИВАЮЩИХ В ЦЕНТРАЛЬНОЙ РОССИИ

SYCP3 (Sinaptonemal complex protein 3) is a DNA binding protein which activity leads to homologous chromosomes pairing and meiotic homologous recombination. In our study we revealed that the genotype frequencies of the SYCP3 T657C polymorphism among the Russian healthy fertile women were TT - 92%, CC - 3%, TC - 5%.SYCP3 представляет собой белок синаптонемального комплекса, способствующий конъюгации гомологичных хромосом во время мейоза и дальнейшей рекомбинации. В настоящем исследовании была изучена встречаемость генотипов по полиморфизму Т657С гена SYCP3 в выборке здоровых фертильных женщин русской национальности, проживающих в Центральной России (TT - 92%, CC - 3%, TC - 5%)

ВСТРЕЧАЕМОСТЬ ПОЛИМОРФИЗМА Т657С ГЕНА SYCP3 У ЖЕНЩИН РУССКОЙ НАЦИОНАЛЬНОСТИ, ПРОЖИВАЮЩИХ В ЦЕНТРАЛЬНОЙ РОССИИ

SYCP3 (Sinaptonemal complex protein 3) is a DNA binding protein which activity leads to homologous chromosomes pairing and meiotic homologous recombination. In our study we revealed that the genotype frequencies of the SYCP3 T657C polymorphism among the Russian healthy fertile women were TT - 92%, CC - 3%, TC - 5%.SYCP3 представляет собой белок синаптонемального комплекса, способствующий конъюгации гомологичных хромосом во время мейоза и дальнейшей рекомбинации. В настоящем исследовании была изучена встречаемость генотипов по полиморфизму Т657С гена SYCP3 в выборке здоровых фертильных женщин русской национальности, проживающих в Центральной России (TT - 92%, CC - 3%, TC - 5%)

Association of VEGFA, factor V and prothrombin gene polymorphisms with early pregnancy loss

Background: Many studies conducted to assess the associations between the gene polymorphisms of factor V, prothrombin, and vascular endothelial growth factor gene A and recurrent early pregnancy loss (REPL) have shown conflicting findings. The aim of the study: We designed this study and selected the most common polymorphisms that have been analyzed before, VEGFA −2578C/A (rs699947), VEGFA 936C/T (rs3025039), FVL G1691A (rs6025), and prothrombin FII G20210A (rs1799963) to be the candidate genetic polymorphisms for analysis of their association with idiopathic early pregnancy loss in Russian women. Materials and methods: 100 women with idiopathic early pregnancy loss were enrolled and classified into two subgroups: sporadic early pregnancy loss (SEPL), consisting of 50 women, and recurrent early pregnancy loss (REPL), consisting of 50 women. The control group included 56 women with full-term babies. Genotyping was performed using commercially available kits (Syntol, Russia) for Real time-PCR method. Genotype and allele distributions in studied groups were compared using the chi-square test and Fisher's exact test. The tests and calculation of Odds ratio with 95% confidence intervals (CIs) were conducted employing the statistical software SPSS, version 22. Results: The heterozygous genotype (CA) for VEGFA rs699947 was significantly associated with REPL. Findings have shown that women carrying the heterozygous genotype had a higher REPL risk (OR 9.04, 95% CI 4.33-18.7). No significant associations with SEPL or REPL were found for the other studied polymorphisms. Conclusion: Our findings suggest that heterozygosity for VEGFA rs699947 gene polymorphism may play a role in predisposition to idiopathic early pregnancy loss and can be a genetic risk factor for recurrent early miscarriage in Russian women. © 2020 Research Result. Theoretical and Applied Linguistics. All rights reserved

The effect of ETA receptor blockade on cardiomyocyte apoptosis and myocardial hypertrophy development in genetically hypertensive rats

Cardiomyocyte apoptosis and hypertrophy have been studied in the left and right ventricular myocardium of spontaneously hypertensive rats without treatment and after 10-day administration of the ETA-receptor antagonist BQ-123. It is established that BQ-123 prevents the activation of cardiomyocyte apoptosis and significantly decreases the extent of hypertrophy development in the left ventricular myocardium, but does not influence the same mechanisms in the right ventricular myocardium

Chronobiology of cardiac ventricular fibrillation development in experimental acute coronary failure

Numerous experiments on simulation of acute coronary failure in initially intact rabbits showed that under the same experimental conditions irreversible ventricular fi brillation developed in some animals and did not develop anothers. We hypothesize that the probability of fi brillation development was determined by the time of the day, during which acute coronary failure developed. The study was carried out on 2 groups of rabbits in winter in Moscow. In group 1, the failure was induced by ligation of the left descending coronary artery at the interface between its middle and lower thirds at 11.00-18.00 with 30-min intervals. In group 2, the microcirculatory status of the left-ventricular myocardium was studied by light microscopy and morphometry at 12.00 and 18.00. Induction of coronary failure during the period from 15.30 to 18.00 led to irreversible ventricular fi brillation and death in 100% cases. Modeling of the condition from 11.00 to 15.00 caused no ventricular fi brillation in 89% cases, and the animals survived. The area of left-ventricular myocardial capillaries at 12.00 virtually 2-fold surpassed that at 18.00. Presumably, the electrolyte balance and metabolic characteristics of the myocardium switch over to the nocturnal mode of functioning at 15.30 due to changes in blood fi lling of the myocardium. The appearance of an ischemic focus in the myocardium during this period inevitably leads to the development of irreversible ventricular fi brillation. © 2010 Springer Science+Business Media, Inc

Apoptosis of myocardial cells in spontaneously hypertensive rats

Myocardial cell apoptosis in genetically determined arterial hypertension was investigated. Male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats of different ages (8, 15, 52 weeks) were used in the experiment. Caspase-3 and caspase-8 activity in ventricular myocardial cell lysates was assessed by colometric assays based on hydrolysis of the peptide substrate. A significant increase in caspase-3 and caspase-8 activity was revealed in left ventricular myocardium of SHR at the age of 15 weeks. These results show the enhancement of receptor-induced caspase-dependent apoptotic death of left ventricular myocardial cells in genetically determined arterial hypertension. No significant changes of caspase activity were detected in right ventricular myocardium

Chronobiology of cardiac ventricular fibrillation development in experimental acute coronary failure

Numerous experiments on simulation of acute coronary failure in initially intact rabbits showed that under the same experimental conditions irreversible ventricular fi brillation developed in some animals and did not develop anothers. We hypothesize that the probability of fi brillation development was determined by the time of the day, during which acute coronary failure developed. The study was carried out on 2 groups of rabbits in winter in Moscow. In group 1, the failure was induced by ligation of the left descending coronary artery at the interface between its middle and lower thirds at 11.00-18.00 with 30-min intervals. In group 2, the microcirculatory status of the left-ventricular myocardium was studied by light microscopy and morphometry at 12.00 and 18.00. Induction of coronary failure during the period from 15.30 to 18.00 led to irreversible ventricular fi brillation and death in 100% cases. Modeling of the condition from 11.00 to 15.00 caused no ventricular fi brillation in 89% cases, and the animals survived. The area of left-ventricular myocardial capillaries at 12.00 virtually 2-fold surpassed that at 18.00. Presumably, the electrolyte balance and metabolic characteristics of the myocardium switch over to the nocturnal mode of functioning at 15.30 due to changes in blood fi lling of the myocardium. The appearance of an ischemic focus in the myocardium during this period inevitably leads to the development of irreversible ventricular fi brillation. © 2010 Springer Science+Business Media, Inc

Effect of Phosphocreatine and Ethylmethylhydroxypyridine Succinate on the Expression of Bax and Bcl-2 Proteins in Left-Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats

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. © 2015, Springer Science+Business Media New York