Association of three polymorphisms (1082G/A, 819C/T, and 592C/A) of the promotor region of the anti-inflammatory IL-10 gene with malignancy of female reproductive organs was revealed by SNP (single nucleotide polymorphism) method in ethnic groups of Adygei Republic. Breast cancer, cervical cancer, and cancer of the uterine corpus are associated with allele 592A (р=0.042) in Circassians and with polymorphism 819T in Russians (р=0.046). Irrespective of the ethnicity, allele 819T was signifi cantly more often (р<0.05) detected in prevalent forms of breast cancer involving regional lymph nodes. 1082G polymorphism is associated with low-differentiated adenocarcinoma. In women of Adygei Republic, ATA/GCA gaplotypes are associated with high risk factors for breast cancer.

Despite the success in the tactics of treating COVID-19, there are many unexplored issues related to the development and progression of the process in the lungs, brain, and other organs, as well as the role of individual elements, in particular, nitric oxide (NO), and in the pathogenesis of organ damage. Based on the analyzed literature data, we considered a possible pathophysiological mechanism of action of NO and its derivatives in COVID-19. It can be noted that hyperimmune systemic inflammation and “cytokine storm” are enhanced by the production of NO, products of its oxidation (“nitrosative stress”). It is noted in the work that as a result of the oxidation of NO, a large amount of the toxic compound peroxynitrite is formed, which is a powerful proinflammatory agent. Its presence significantly damages the endothelium of the vascular walls and also oxidizes lipids, hemoglobin, myoglobin, and cytochrome, binds SH-groups of proteins, and damages DNA in the target cells. This is confirmed by the picture of the vessels of the lungs on computed tomography and the data of biochemical studies. In case of peroxynitrite overproduction, inhibition of the synthesis of NO and its metabolic products seems to be justified. Another aspect considered in this work is the mechanism of damage by the virus to the central and peripheral nervous system, which remains poorly understood but may be important in understanding the consequences, as well as predicting brain functions in persons who have undergone COVID-19. According to the analyzed literature, it can be concluded that brain damage is possible due to the direct effect of the virus on the peripheral nerves and central structures, and indirectly through the effect on the endothelium of cerebral vessels. Disturbances in the central nervous regulation of immune responses may be associated with the insufficient function of the acetylcholine anti-inflammatory system. It is proposed to further study several approaches to influence various links of NO exchange, which are of interest for theoretical and practical medicine.

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Цель. Исследование ассоциации A1166/166C полиморфизмов гена сосудис-того рецептора 1 типа ангиотензина II (AGT2R1) с развитием коронарного и периферического атеросклероза в этнических группах населения Респу-блики Адыгея. Материал и методы. Распределение A1166/166C полиморфных вариантов гена AGT2R1 исследовано "single nucleotide polymorphism" (SNP) -методом с аллель-специфическими праймерами и электрофоретической детекцией результатов (НПФ "Литех"). Полиморфизмы гена AGT2R1 (rs5186) с нуклео-тидной заменой аденина на цитозин (А>C) в 1166 позиции гена AGT2R1 типи-рованы в образцах геномной ДНК доноров (n=143) и больных с сердечно-сосу-дистыми заболеваниями (n=39) в возрасте 23-65 лет из двух этнических групп -адыгов и русских. Экспериментальные данные проанализированы адекватными статистическими методами SPSS Statistics 17.0. Результаты. В группе больных с осложнениями коронарного и перифериче-ского атеросклероза выявлено статистически значимое повышение частоты мутантной 1166С аллели и патологического гомозиготного генотипа С1166С. Риск развития сердечно-сосудистых заболеваний у носителей 1166С аллеля возрастает в 3,77 раз (c 2 =26,07; р=0,00003), а в случае с гомозиготным "мутантным" СС генотипом -в 10,36 раз (c 2 =31,20; р=0,00002), что позволяет использовать 1166C аллель и С1166С генотип AGT2R1 в качестве генетических предикторов коронарного атеросклероза и маркеров донозологической диа-гностики ишемической болезни сердца (c 2 =42,96; р=0,0000005; OR (95%)=17,37). Заключение. Полученные экспериментальные данные в сочетании с допол-нительными инструментальными исследованиями функционального состоя-ния сердечно-сосудистой системы, будут способствовать улучшению точно-сти диагностики атеросклероза и возможных осложнений последнего на ран-них этапах, что позволит снизить инвалидизацию и смертность среди лиц трудоспособного возраста. Aim. The investigation of A1166/166C polymorphisms of the vascular receptor 1 type of angiotensine II gene (AGT2R1) association with the development of coronary and peripheral atherosclerosis in ethnic groups of Adyghea Republic inhabitants. Material and methods. The spread of A1166/166C polymorphic variants of the gene AGT2R1 was studied via the "single nucleotide polymorphism" (SNP) -method with allele-specific primers and electrophoretic results detection (by SPF "Litech"). Gene polymorphisms AGT2R1 (rs5186) with nucleotide replacement of adenine by cytosine (А>C) in the 1166th position of gene AGT2R1 were typified in the samples of donors genomic DNA (n=143) and of those with cardiovascular diseases (n=39) at the age 23-65 y. o. from two ethnic subgroups -Adyghes and Russians. The data was processed via software SPSS Statistics 17.0. Results. In the group of those with complicated coronary and peripheral atherosclerosis there was statistically significant increase of the prevalence of mutant 1166C allele and of pathological monozygous genotype C1166C. The risk of cardiovascular diseases in the carriers of 1166C allele increases 3,77 times (c 2 =26,07; р=0,00003), and in the case ...

The 14 kDa protein was purified from human platelets. It displays high cytotoxic activity to the human ACL cells at 10 M concentration (21.8 ±7.1%). Its N-terminal sequence is YAPQXQFGP-, being highly homologous to region 241-249 residues of the human Cls complement component.