Nerve growth factor and post-infarction cardiac remodeling

The prevalence of sudden death from chronic heart failure and cardiac arrhythmias caused by myocardial infarction is a complex problem in cardiology. Post-infarction cardiac remodeling occurs after myocardial infarction. This compensatory-adaptive reaction, regulated by mechanical, neurohumoral and genetic factors, includes the structural and functional changes of cardiomyocytes, stromal elements and extracellular matrix, geometry and architectonics of the left ventricular cavity. Adverse left ventricular remodeling is associated with heart failure and increased mortality. The concept of post-infarction cardiac remodeling is an urgent problem, since the mechanisms of development and progression of adverse post-infarction changes in the myocardium are completely unexplored. In recent years, the scientist attention has been focused on neurotrophic factors involved in the sympathetic nervous system and the vascular system remodeling after myocardial infarction. Nerve growth factor (NGF) is a protein from the neurotrophin family that is essential for the survival and development of sympathetic and sensory neurons, which also plays an important role in vasculogenesis. Acute myocardial infarction and heart failure are characterized by changes in the expression and activity of neurotrophic factors and their receptors, affecting the innervation of the heart muscle, as well as having a direct effect on cardiomyocytes, endothelial and smooth muscle vascular cells. The identification of the molecular mechanisms involved in the interactions between cardiomyocytes and neurons, as well as the study of the effects of NGF in the cardiovascular system, will improve understanding of the cardiac remodeling mechanism. This review summarizes the available scientific information (2019–2021) about mechanisms of the link between post-infarction cardiac remodeling and NGF functions

In vitro genotoxic effects of prooxidant therapy

Chronic obstructive pulmonary disease (COPD) is a major problem in industrialized countries. Much evidence suggest that oxidative stress has been associated with chronic diseases, including COPD. There are a number of good experimental and clinical studies clearly showing a strong relationship between oxidative stress and DNA-damage in several diseases. The present study was aimed at establishing whether genome damage is also exists in COPD. Prooxidant therapy mediates its action through the development of oxidative stress that can lead to oxidative modification of DNA. The role of ozone in the genome damage has received little attention. The genotoxicity of ozone is of interest because ozone therapy is used for the treatment of various chronic conditions, including COPD and may impose a possible risk of genotoxic effects for patients. The purpose of this study was to investigate genotoxic effect of different dosing schedules of prooxidant therapy in vitro on the blood of patients with COPD. Peripheral blood was obtained from 20 COPD patients and 15 age- and sex-matched controls. Our present results have shown that ozone induces DNA-damage in human blood cells in vitro. The severity of oxidative DNA-damage in COPD patients directly depends on the concentration of ozone. Clinical results have shown that DNA-damage is an important part of the pathogenesis of the chronic inflammatory process in the bronchopulmonary system

EFFICIENCY OF IMMUNOCORRECTION WITH MEDICAL OZONE IN PROTRACTED PURULENT INFLAMMATORY DISEASES AFFECTING SOFT TISSUES IN THE PATIENTS OF SENIOR AGE GROUP

Abstract. We performed a clinical and immunological study of patients from senior age group suffering with protracted purulent inflammation of soft tissues in maxillo-facial area. The patients underwent either common medication, or combined treatment including ozone therapy. Application of medicinal ozone, along with basic treatment schedule, resulted into more marked and rapid normalization of non-specific resistance markers, Т-cell immunity. This approach allows of reducing the terms of inpatient care and variety of possible complications. (Med. Immunol., 2008, vol. 10, N 2-3, pp 277-282)

Metabolic and Genetic Determinants of Lipid Metabolism Disruption in Non-Alcoholic Fatty Liver Disease

Aim. To present literature data on the metabolic and genetic mechanisms of impaired fatty acid (FA) synthesis in the development and progression of non-alcoholic fatty liver disease (NAFLD).General findings. NAFLD is a widespread disease progressing from steatosis to non-alcoholic steatohepatitis (NASH), increasing the risk of cirrhosis, liver failure and hepatocellular carcinoma. Progression of NAFLD and the development of NASH are closely related to lipid metabolism disorders caused not only by insufficient alimentary intake of fatty acids, but also by a decrease in the efficiency of their endogenous processing. The regulation of fatty acid metabolism involves enzymes desaturase (FADS1, FADS2) and elongase (ELOVL2 and ELOVL5) fatty acids. Desaturases are encoded by the FADS1 and FADS2 genes for fatty acid desaturases. Polymorphisms in the genes of fatty acid desaturases determine the effectiveness of PUFA endogenous processing. Violations in the activity of FADS1 and FADS2 and their genes are accompanied by dysregulation of the metabolic pathway involved in the biosynthesis of fatty acids. This leads to the damage of cell membranes, whose main components are represented by phospholipids. The progression of NAFLD is associated with the powerful toxicity of lipids released in the liver parenchyma upon the loss of the cell biomembrane integrity.Conclusions. Further research into the NAFLD genetic mechanisms regulating the metabolism of fatty acids appears to be promising for a deeper understanding of the pathogenesis of this multifactorial disease

Дисфункция малых дыхательных путей при бронхиальной астме

The small respiratory passages dysfunction (SRPD) is found in the vast majority of patients with bronchial asthma (BA). The SRPD is currently recognized as the important pathogenetic feature of BA. The purpose of this review is to analyze the current scientific knowledge about the poorly studied aspects of the small respiratory passages (SRR) participation in the development of pathological process in BA, as well as the impact of small bronchial dysfunction on the clinical course, the exacerbation frequency and the disease control. The importance of SRPD diagnostics in BA patients for optimal and timely treatment is discussed. The modern methods of RPD pathology diagnostics are described; their informative use in the comparative study aspect is considered.Дисфункция малых дыхательных путей (ДМДП) выявляется у подавляющего большинства пациентов, страдающих бронхиальной астмой (БА). В настоящее время ДМДП признана важной патогенетической чертой БА. Целью настоящего обзора является анализ современных научных знаний о малоизученных аспектах участия малых дыхательных путей (МДП) в развитии патологического процесса при БА, а также влияния дисфункции мелких бронхов на клиническое течение, частоту обострений и контроль над заболеванием. Обсуждается важность диагностики ДМДП у больных БА для назначения оптимального и своевременного лечения. Описываются современные методы диагностики патологии МДП; рассматривается информативность их применения в аспекте сравнительного изучения