We examined hematological changes influenced by the experimental hypervitaminosis A. The 3D confocal optical profilometer was applied for assessment of the erythrocytes' membrane structural changes influenced by an overdose of vitamin A. The blood smears were evaluated in terms of alterations of geometrical and optical parameters of erythrocytes for two groups of animals: oil base and retinol palmitate (n = 9 animals for each group). The results demonstrate that an overdose of retinol palmitate causes changes in the torus curvature and pallor of discocytes, their surface area and volume. The observed structural malformations of the shape of red blood cells become visible at the earlier preclinical stage of changes in animal state and behavior. With this in mind, the results of the study open a new area of research in the certain dysfunction diagnosis of red blood cells and have a great potential in the further development of new curative protocols. Tatiana A. Lomanovskaya and Gennadii A. Piavchenko are same impact authors.

Resume. Acute cerebral circulatory disorders are characterised by various changes in brain cells, often leading to mass death. This review presents a list of markers associated with different types of cell death occurring in acute cerebral circulation disorders and identifies the importance of these markers in the diagnosis of haemorrhagic and ischaemic stroke. Acute cerebral circulation disorder is one of the most debated issues in modern resuscitation and medicine, as it is a severe condition leading to stroke and subsequent patient death, if not treated promptly. However, rapid treatment and diagnosis of stroke is difficult due to the lack of study of morphological signs and biomarkers to reliably determine the nature of the injury. An in-depth analysis and systematization of the available information on this topic is needed. Purpose of the review: to reveal the correspondence between the molecular mechanisms of cell death in acute disorders of cerebral circulation and their morphological manifestations. Material and Methods. A total of 50 most relevant sources of information were selected. The sources were selected from the databases of medical and biological publications PubMed, Scopus, Web of Science, RSCI, and fundamental works of scientific literature on the considered topic were involved. Results. The main mechanisms of cell death in stroke were identified and analyzed, the morphological and histological features of the observed processes and their structural manifestations were reviewed. Besides, the most frequently detected molecular markers specific for each type of cell death were listed. Conclusion. The study of molecular pathways and cellular reorganization processes characteristic of different types of cell death as well as their corresponding biological markers is of important diagnostic value in the detection of cerebral circulatory disorders. Determination of morphological and molecular markers typical for this condition will allow a prompt diagnosis of stroke and minimization of its negative consequences.

Acute cerebral circulation disorder is one of the most discussed issues in modern intensive care and neurology, as it is a severe condition, leading to disability or death of the patient, in the absence of immediate medical care. This review discusses general and specific biological markers of stroke, genetic markers of stroke, and current data on their diagnostic significance. The main mechanisms of brain tissue cell death in stroke, such as apoptosis, necrosis, ferroptosis, parthanatosis, sarmoptosis, autolysis, autophagy, oncosis, excitotoxic death are analyzed; the morphological features of the observed processes and their structural manifestations are reviewed. For each type of cell death in nervous tissue, the most frequently detected molecular markers are discussed: specific kinases, Toll-like receptors in the case of apoptosis; serine-threonine protein kinases, components of the polyubiquitin system detected in necrosis; transferrin 1 receptors, typical for ferroptosis; poly(ADP-ribose)-polymerase, whose activity increases in parthanatosis; slow Wallerian degeneration protein that accumulates during sarmoptosis; and other biomarkers characteristic of both individual types of nerve cell death and general pathological processes affecting the brain.

The aim of the work was to analyze the available therapeutic options for the conventional therapy of hereditary myopathies.Materials and methods. When searching for the material for writing a review article, such abstract databases as PubMed and Google Scholar were used. The search was carried out on the publications during the period from 1980 to September 2022. The following words and their combinations were selected as parameters for the literature selection: “myopathy”, “Duchenne”, “myodystrophy”, “metabolic”, “mitochondrial”, “congenital”, “symptoms”, “replacement”, “recombinant”, “corticosteroids”, “vitamins”, “tirasemtiv”, “therapy”, “treatment”, “evidence”, “clinical trials”, “patients”, “dichloracetate”.Results. Congenital myopathies are a heterogeneous group of pathologies that are caused by atrophy and degeneration of muscle fibers due to mutations in genes. Based on a number of clinical and pathogenetic features, hereditary myopathies are divided into: 1) congenital myopathies; 2) muscular dystrophy; 3) mitochondrial and 4) metabolic myopathies. At the same time, treatment approaches vary significantly depending on the type of myopathy and can be based on 1) substitution of the mutant protein; 2) an increase in its expression; 3) stimulation of the internal compensatory pathways expression; 4) restoration of the compounds balance associated with the mutant protein function (for enzymes); 5) impact on the mitochondrial function (with metabolic and mitochondrial myopathies); 6) reduction of inflammation and fibrosis (with muscular dystrophies); as well as 7) an increase in muscle mass and strength. The current review presents current data on each of the listed approaches, as well as specific pharmacological agents with a description of their action mechanisms.Conclusion. Currently, the following pharmacological groups are used or undergoing clinical trials for the treatment of various myopathies types: inotropic, anti-inflammatory and antifibrotic drugs, antimyostatin therapy and the drugs that promote translation through stop codons (applicable for nonsense mutations). In addition, metabolic drugs, metabolic enzyme cofactors, mitochondrial biogenesis stimulators, and antioxidants can be used to treat myopathies. Finally, the recombinant drugs alglucosidase and avalglucosidase have been clinically approved for the replacement therapy of metabolic myopathies (Pompe’s disease).