Valeriya I. Nakhod

Cd2+ is a heavy metal cation with some typical for heavy metals as well as unique toxic properties for live components of water ecosystems. The objective of this study was to analyze Cd2+-induced expression of genes of some cellular transportation proteins in several tissues of a fish and its possible correlation with Cd accumulation in tissues. Juvenile Cyprinus carpio were treated with Cd2+ at a preliminarily determinated sublethal concentration for Cyprinidae (6.4 mg/L). The expression of N-methyl-D-aspartate receptor subunit genes (NR2A, NR2B) and ATP-binding cassette subfamily C member 1 gene (ABCC1) was compared between treated and untreated fish. In addition, cadmium accumulation in the fish tissues was assessed. NR2A gene expression was 16.6-fold upregulated by Cd2+ in the eyes (choroid + retina), which accumulated Cd, and was not upregulated in brain, which didn’t accumulate Cd. This may have been caused by the blocking of calcium channels by Cd2+, which has a very similar ionic radius to that of Ca2+. According to the result of the current study, it can be concluded that the similarity of the radius of a heavy metal cation to that of Ca2+ is a major factor contributing to its ability to irreversibly block calcium channels. ABCC1 gene expression was 2.0-fold upregulated in gills and was not upregulated in liver; both tissues accumulated high levels of Cd. This difference may have been caused by the accumulation of predominantly previously inactivated Cd in liver or by some difference in the mechanisms of self-detoxification from Cd2+ in fish gills and liver.

High physical activity often results in complex and ambiguous proteomic changes. This study aimed to analyze possible changes in the composition and content of proteins in plasma samples of elite athletes from sports with various activity levels and intensity. We performed proteomic profiling of blood plasma from 93 elite athletes with over eight years of continuous professional experience. High-resolution tandem mass spectra obtained in the data-independent acquisition mode were analyzed using the PLGS algorithm against a library of known protein sequences, and the PowerNovo algorithm for de novo protein sequencing. Combining the two protein identification strategies improved the completeness of the analysis and expanded the number of identified proteins. We identified changes in levels of circulating proteins that distinguish the high-intensity group from other groups by proteins involved in immune response, lipid transport and metabolism, and oxygen and iron transport. Changes in protein levels in biological samples of professional athletes may be associated with the training load intensity and type of sport.

Understanding the regulatory mechanisms of stress-induced immunosuppression and developing reliable diagnostic methods are important tasks in clinical medicine. This will allow for the development of effective strategies for the prevention and treatment of conditions associated with immune system dysfunction induced by chronic stress. The purpose of this review is to conduct a comprehensive analysis and synthesis of existing data on the regulatory mechanisms of stress-induced immunosuppression. The review is aimed at identifying key neuroendocrine, cytokine, and cellular processes underlying the suppression of the immune response under stress. This study involved a search of scientific literature covering the neuroendocrine, cellular, and molecular mechanisms of stress-induced immunosuppression regulation, as well as modern methods for its diagnosis. Major international bibliographic databases covering publications in biomedicine, psychophysiology, and immunology were selected for the search. The results of the analysis identified key mechanisms regulating stress-induced immunosuppression. The reviewed publications provided detailed descriptions of the neuroendocrine and cytokine processes underlying immune response suppression under stress. A significant portion of the data confirms that the activation of the hypothalamic–pituitary–adrenal (HPA) axis and subsequent elevation of cortisol levels exert substantial immunosuppressive effects on immune cells, particularly macrophages and lymphocytes, leading to the suppression of innate and adaptive immune responses. The data also highlight the crucial role of cortisol and catecholamines (adrenaline and noradrenaline) in initiating immunosuppressive mechanisms under chronic stress.

Background. The article provides the data on the global market volume for implantable medical devices and analyzes the domestic market needs of various branches of medicine. Examples of international and Russian developments of implantable medical devices are given. Promising directions for growing the Russian market are specified.Material and methods. The authors analyzed the information sources considering the state of the implantable medical device market over the last 10 years.Conclusion. Implantable medical devices have been used in practical healthcare for several decades. To date, implantable devices, including new applications, have assisted with treating a wide range of diseases: sleep apnea, panic attacks, Parkinson's disease, epilepsy, urinary incontinence, gastrointestinal diseases, autoimmune diseases, mental disorders, etc.

Background. The article provides the data on the global market volume for implantable medical devices and analyzes the domestic market needs of various branches of medicine. Examples of international and Russian developments of implantable medical devices are given. Promising directions for growing the Russian market are specified.Material and methods. The authors analyzed the information sources considering the state of the implantable medical device market over the last 10 years.Conclusion. Implantable medical devices have been used in practical healthcare for several decades. To date, implantable devices, including new applications, have assisted with treating a wide range of diseases: sleep apnea, panic attacks, Parkinson's disease, epilepsy, urinary incontinence, gastrointestinal diseases, autoimmune diseases, mental disorders, etc.

Metabolomics investigates final and intermediate metabolic products in cells. Assessment of the human metabolome relies principally on the analysis of blood, urine, saliva, sweat, and feces. Tissue biopsy is employed less frequently. Understanding the metabolite composition of biosamples from athletes can significantly improve our knowledge of molecular processes associated with the efficiency of training and recovery. Such knowledge may also lead to new management opportunities. Successful execution of metabolomic studies requires simultaneous qualitative and quantitative analyses of numerous small biomolecules in samples under test. Unlike genomics and proteomics, which do not allow for direct assessment of enzymatic activity, metabolomics focuses on biochemical phenotypes, providing unique information about health and physiological features. Crucial factors in ensuring the efficacy of metabolomic analysis are the meticulous selection and pre-treatment of samples.

Biobanks are involved in a broad range of studies, including both basic and clinical research, so their functions and roles are evolving. Digital biobanks have emerged due to digitalization in this field; however, it also entails an increasing number of ethical and legal issues, in particular those related to the protection of donor data and potential commercial applications. The development of biobanks and the size of stored datasets lay the groundwork for proceeding to digital biobanks that intensely employ artificial intelligence tools. Digital biobanks can simplify the search for and access to biological specimens, thus contributing to the conduction of research and creating new collaborations. They are becoming an increasingly important tool for personalized medicine and an individualized approach to disease treatment, contributing to the elaboration of more accurate diagnostic methods and the development of innovative therapeutic strategies.

Physical overexertion surpassing the functional capacity of the nervous system causes the hyperactivation of the neural structures of the cerebellum. In turn, it causes the depletion of intracellular resources and progressive structural changes in cerebellar cells and fibers. These degenerative changes may lead to cerebellar dysfunction, including the worsening of coordination, balance, and motor functions. In order to maintain the health and functioning of the cerebellum and the nervous system in general, one needs to avoid physical overexertion and have enough time to recover. Three major types of Purkinje cells were identified in control group animals. After the forced swimming test, animals had significant morphological changes in pyriform cells, granule cells, internuncial neurons, and neuroglial cells. In particular, the extreme degeneration of granule cells was manifested via their fusion into conglomerates. These changes demonstrate that neurodegeneration in the cerebellum takes place in response to physical overexertion.

Traumatic brain injury (TBI) is one of the leading causes of mortality and disability among young and middle-aged individuals. Adequate and timely diagnosis of primary brain injuries, as well as the prompt prevention and treatment of secondary injury mechanisms, significantly determine the potential for reducing mortality and severe disabling consequences. Therefore, it is crucial to have objective markers that indicate the severity of the injury. A number of molecular factors—proteins and metabolites—detected in the blood immediately after trauma and associated with the development and severity of TBI can serve in this role. TBI is a heterogeneous condition with respect to its etiology, clinical form, and genesis, being accompanied by brain cell damage and disruption of blood–brain barrier permeability. Two oppositely directed flows of substances and signals are observed: one is the flow of metabolites, proteins, and nucleic acids from damaged brain cells into the bloodstream through the damaged blood–brain barrier; the other is the infiltration of immune cells (neutrophils and macrophages) and serological proteins. Both flows aggravate brain tissue damage after TBI. Therefore, it is extremely important to study the key signaling events that regulate these flows and repair the damaged tissues, as well as to enhance the effectiveness of treatments for patients after TBI.

According to the Centers for Disease Control and Prevention (CDC), the national public health agency of the United States, traumatic brain injury is among the leading causes of mortality and disability worldwide. The consequences of TBI include diffuse brain atrophy, local post-traumatic atrophy, arachnoiditis, pachymeningitis, meningocerebral cicatrices, cranial nerve lesions, and cranial defects. In 2019, the economic cost of injuries in the USA alone was USD 4.2 trillion, which included USD 327 billion for medical care, USD 69 billion for work loss, and USD 3.8 trillion for the value of statistical life and quality of life losses. More than half of this cost (USD 2.4 trillion) was among working-age adults (25–64 years old). Currently, the development of new diagnostic approaches and the improvement of treatment techniques require further experimental studies focused on modeling TBI of varying severity.