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Aim. To study the associations of the Tpeak-Tend interval (TpTe) with components of metabolic syndrome (MS) in a sample of Novosibirsk residents.Material and methods. The study included 1042 residents of Novosibirsk (510 (48,9%) men) aged 35-74 years. The examination included the collection of demographic and social data, anthropometry, blood pressure (BP) measurement, and electrocardiography (ECG). MS was determined according to the 2013 criteria. The TpTe interval from the peak, as the maximum positive or negative T wave deviation, to the end of the T wave, was measured manually in lead V5. The corrected TpTe (cTpTe) interval was used in the study.Results. The cTpTe is inversely associated with female sex (B 3,390, 95% confidence interval (CI): (-5,516-2,504), p=0,001). The cTpTe interval is associated with a blood pressure (BP) ≥140/90 mm Hg (B 3,154, 95% CI: (1,614-4,688), p=0,001), low-density lipoprotein cholesterol (LDL-C) >3,0 mmol/l (B 1,818, 95% CI: (0,409-3,544), p=0,030), regardless of other MS components, sex and age. The cTpTe interval was higher in individuals with BP ≥140/90 mm Hg compared with individuals with BP 3,0 mmol/l (68,41 95% CI: 67,11-69,63 vs 66,60 95% CI: 65,02-68,23; p=0,023), compared with individuals with LDL-C

The purpose of this review is to describe the available scientific data on the post-COVID-19 syndrome, formulate the main approaches to classification, determine the potential mechanisms of its pathogenesis, as well as determine the mechanisms of the occurrence of bronchopulmonary system pathology within the framework of the post-COVID-19 syndrome. It is known that long-term persistence of COVID-19 symptoms significantly reduces the quality of life of patients through the direct or indirect effect of the SARS-CoV-2 virus on a number of organs and systems. The review examines in detail the possible pathogenetic mechanisms of the post-COVID-19 syndrome, describes and studies the most common consequences of acute COVID-19, taking into account the severity of the disease, including diseases of the respiratory system, in particular interstitial and broncho-obstructive diseases. Particular attention is paid to the above problems in order to describe and structure the available scientific data on lung diseases within the framework of the post-COVID-19 syndrome. It should be noted, however, that there are very few studies on pathogenesis of changes in the bronchopulmonary system in the post-COVID-19 period. The bulk of them affect only individual manifestations of diseases of the respiratory system, in particular cough and shortness of breath, and are not aimed at determining causeand-effect relationships and the relationship of these symptoms to a specific nosology. Taking into consideration the continued high incidence of COVID-19, there is no doubt that additional studies of bronchopulmonary manifestations of post-COVID-19 syndrome should be conducted. Information from the databases PubMed, eLibrary, Scopus, Jstor was used as literary sources.

The study of DNA methylation status in malignant lymphomas is a new field of research in oncohematology. The aim of this study was to quantify the level of methylation of the MIR-143 gene in the tumor tissue of patients with diffuse large B-cell lymphoma (DLBCL). Material and methods. The study included 81 tumor samples of DLBCL (26 of germinal and 55 of non-germinal origin) and 11 biopsies of reactive lymph nodes. To quantify the methylation of the MIR-143 gene, the method of direct bisulfite sequencing by Sanger was used with the calculation of the average level of methylation of the analyzed CpG-sites. Results. The average level of MIR-143 methylation in tumor samples was significantly lower than the values in reactive lymph nodes (64.43 ± 19.92 и 76.27 ± 4.92 %, respectively, p = 0.049), did not depend on the immunohistochemical subtype of the tumor and showed a greater spread of values. In the lymphoma samples, there was predominant hypomethylation of one of the four analyzed CpG-dinucleotides within the boundaries of the analyzed fragment. Conclusion. The data on a change in the pattern of the MIR-143 gene methylation in the tumor tissue of DLBCL were obtained. To establish the role of microRNA in the pathogenesis of DLBCL further studies aimed at clarifying the mechanisms of epigenetic regulation of MIR-143 expression in lymphoma cells and identification of this microRNA targets are required.

The purpose of the study was to present up-to-date data on the regulation of expression, function in normal tissues and multidirectional activity in the oncogenesis of miR-143/145 microRNAs cluster, as well as to evaluate the possibilities and limitations of the therapeutic use of microRNAs of this cluster in malignant neoplasms. Material and methods. The search for available domestic and foreign literary sources published in PubMed and RSCI databases over the past 10 years has been carried out. 427 articles were found, of which 41 were included in this review. Results. The conservative cluster miR-143/145 is one of the most intensively studied in tumors. Based on the results of the analysis of differential miRNA expression, in vitro experiments in cancer cell lines and in vivo in mouse tumor models, a decrease in miR-143 and miR-145 levels was shown in malignant neoplasms of epithelial origin. Until recently, these miRNAs were considered classical oncosuppressors. The data presented in the review demonstrate that the results of a number of studies taking into account the cellular aspects of microRNA expression contradict this concept. miR-143 microRNA, for example, is known to participate in the metabolic restructuring of the tumor and the activation of neoangiogenesis. It has been shown that the oncosuppressive or pro-oncogenic activity of miR-143 and miR-145 depend on the tissue and cellular context and can be explained by the presence of several regulated targets that have opposite effects on oncogenesis. Taken together, the data obtained suggest the need to exercise caution when choosing the microRNAs of the described cluster for exogenous therapeutic delivery. Conclusion. Further detailed decoding of the mechanisms of miR-143 and miR-145 functioning in various types of tissues and cells, as well as identification of new MRNA targets are necessary for a better understanding of the involvement of these molecules in oncogenesis.

Single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene were found by sequencing the clinical exome of a group of men who died of sudden cardiac death (SCD) at the age of 45 years. The aim of the study is to study the association of single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene with SCD in a case-control study using routine molecular genetic analysis. Material and methods. SCD group (n = 400, mean age 53.2 ± 8.7 years, 70.9 % men, 29.1 % women) was formed using the SCD criteria of the European Society of Cardiology from the anonymous DNA bank of the deceased sudden death (1999–2019). The control group (n = 400, mean age 53.1 ± 8.3 years, 68.3 % men, 31.7 % women) was matched by sex and age to the SCD group from DNA banks of international projects MONICA and HAPIEE of living at the time of researches participants. Genotyping was carried out using the polymerase chain reaction followed by analysis of restriction fragment length polymorphism. Results. There were no statistically significant differences in the frequencies of genotypes and alleles of single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene between the SCD group and the control group (p > 0.05). Conclusions. The association of single nucleotide rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene with SCD has not been confirmed.

The study of sudden cardiac death (SCD) and its etiopathogenesis in cardiology practice remains one of the most pressing public health problems. In Western countries, SCD accounts for 20% of the total mortality and 50% of mortality associated with cardiovascular diseases. Considering the electrical instability in the myocardium as one of the main reasons for the development of life-threatening arrhythmias (ventricular tachycardia / ventricular fibrillation) and SCD, one should be aware of such provoking factors as ischemic heart disease, myocarditis, valvular heart disease, pharmacological influences, cardiomyopathy, and channelopathy. An increase or decrease in the duration of the QT interval, which reflects the work of ion channels, as well as ventricular depolarization and repolarization, increases the risk of SCD.The aim of this review was to study and analyze the available literature data on the relationship of molecular genetic markers with the duration of the QT interval.Currently, there is a number of genetic studies that allow to identify a large number of mutations and polymorphisms of known genes that affect the variability of the QT interval, showing their significance in risk stratification of sudden arrhythmic death and choosing the right tactics for managing, preventing, and treating patients, thus reducing the risk of SCD. The predictive value of genetic testing is the highest for long QT syndrome (LQTS), for which a gene-specific risk profile has been established, and lower for other channelopathies. A large amount of genetic data may be a promising approach to quantifying the risk of SCD, especially at a young age, which will be facilitated by further study of this problem.

Introduction. The article discusses the problem of using cognitive visceral cardiobiofeedback as a preventive and non-drug method for correcting disturbed regulation mechanisms associated with an increase in blood pressure in adolescents with essential hypertension (EH) against the background of standard antihypertensive therapy with enalapril. Aim of the study was to investigate the indices of the cardiointervalogram (CIG) during a biofeedback session and to evaluate the effectiveness of cardiobiofeedback in healthy adolescents and adolescents with EH living in Novosibirsk. Material and methods. Each participant underwent a 5-minute CIG recording using the hardware and software complex VedaPulse under physiological rest and during biofeedback session. In the course of biofeedback, the subject was asked to lengthen the expiration phase of the respiratory cycle with parallel relaxation of muscle tone and visual feedback on the dynamics of a multimedia plot reflecting changes in the duration of the cardiac cycle. Results and discussion. We found that the effectiveness of cardiorespiratory synchronization (CRS) is characterized by an increase in SDNN indicators by 8.3% and the total power of spectral influences (TP) by 23.6% due to a significant increase in the parasympathetic spectral index of HF by 29.4%. An increase in the power index of the spectrum of low-frequency oscillations (LF) by 51.3% can be considered as an element of CRS within 0,1 Hz. In healthy adolescents, the reactivity of the suprasegmental levels of regulation (IC) is preserved and their growth is noted by 7.6%. In adolescents with EH, an increase in the duration of the cardiac cycle by 5.2% and TP by 31.2% was recorded in the course of cardiobiofeedback, which is associated with an increase in the power of the spectrum of high-frequency oscillations (HF) by 2.4%. This phenomenon should be considered as a positive pathophysiological response of the autonomic link of the nervous system, which is recorded by a decrease in blood pressure. Conclusion. We assume that the test with cognitive visceral cardiobiofeedback can serve as an effective marker for the analysis of the rigidity of autonomic mechanisms of regulation in adolescents with essential hypertension. Conscious regulation of the heart rate through the mechanism of controlled respiration (biofeedback) can be an effective non-drug method for correcting autonomic regulation disorders in adolescents with arterial hypertension, which is manifested by a significant decrease in blood pressure.