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Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO binds to haemoglobin in erythrocytes, preventing oxygen delivery to tissues, and additionally inhibits mitochondrial respiration. This renders the effect of CO to be closely related to hypoxia reperfusion injury. Oxygen deprivation, as well as CO poisoning and re-oxygenation, are shown to be able to activate the production of reactive oxygen species and to induce oxidative stress. Here, we review the role of reactive oxygen species production and oxidative stress in the mechanism of neuronal cell death induced by carbon monoxide and re-oxygenation. We discuss possible protective mechanisms used by brain cells with a specific focus on the inhibition of CO-induced ROS production and oxidative stress. [ABSTRACT FROM AUTHOR]

Intracellular communication and regulation in brain cells is controlled by the ubiquitous Ca2+ and by redox signalling. Both of these independent signalling systems regulate most of the processes in cells including the cell surviving mechanism or cell death. In physiology Ca2+ can regulate and trigger reactive oxygen species (ROS) production by various enzymes and in mitochondria but ROS could also transmit redox signal to calcium levels via modification of calcium channels or phospholipase activity. Changes in calcium or redox signalling could lead to severe pathology resulting in excitotoxicity or oxidative stress. Interaction of the calcium and ROS is essential to trigger opening of mitochondrial permeability transition pore -- the initial step of apoptosis, Ca2+ and ROS-induced oxidative stress involved in necrosis and ferroptosis. Here we review the role of redox signalling and Ca2+ in cytosol and mitochondria in the physiology of brain cells -- neurons and astrocytes and how this integration can lead to pathology, including ischaemia injury and neurodegeneration. [ABSTRACT FROM AUTHOR]

In order to carry out mathematical modeling of the drug particles or drop movement in the human respiratory system, an approach to reverse prototyping of the studied areas based on the medical data (computed tomography) results is presented. To adapt the computational grid, a mathematical model of airflow in channels of complex geometry (respiratory system) has been developed. Based on the data obtained, the results of computational experiments for a single-phase system are presented. [ABSTRACT FROM AUTHOR]

The paper describes the main methods of ensuring the energy efficiency of rolling stock, and justifies the main generalised functional quality indicators of control systems. There is a description of possible approaches to a comparative assessment of the feasibility of choosing a control method. A proposal to use a generalized target functional for minimizing the cost components of the control processes has been made. The results of the research make it possible to state that economic feasibility and minimisation of labour and material costs for control are the mandatory requirement when choosing methods of controlling the energy efficiency of rolling stock. It is shown that the control of parameters necessary for accounting and planning can be ineffective because of the high cost of acquisition and maintenance of control tools. Expressions for determining the components of the total cost of control are presented. In general terms they consist of the cost of control, the cost of measurement errors and the cost of machine downtime during control. A control system based on an algorithm for measuring fuel consumption by measuring the electrical power of a diesel generator has been developed. The replacement of average normative values of fuel consumption by actual values of total and specific fuel consumption makes it possible to increase the objectivity of rolling stock energy efficiency control.

The article presents the results of studying the effect of the drug flavobetin on the indicators of endogenous intoxication, morbidity and milk production of cows. Flavobetin contains betaine hydrochloride, taurine and agrimony herb, has hepatoprotective, antioxidant and metabolic properties. For the experiment in the dry period two groups of cows were formed, 20 heads each: in the 1st experimental group the drug flavobetin in the dose of 50 g per head was used daily for a month; cows of the 2nd control group were intact. The results of the research indicate that the use of flavobetin in cows during the dry period helps to reduce the blood level of ketone bodies, medium mass molecules and lipid peroxidation products, which positively affects the course of labor and the postpartum period in animals. The preventive efficiency of flavobetin was confirmed by a decrease in the incidence of cows with ketosis – by 15%, retention of the placenta – by 10% and postpartum endometritis – by 15%. The use of the drug had a positive effect on the milk productivity of cows, increasing their milk yield and reducing the number of somatic cells in milk.

The transmembrane receptor for advanced glycation end products (RAGE) is a signaling receptor for many damage‐ and pathogen‐associated molecules. Activation of RAGE is associated with inflammation and an increase in reactive oxygen species (ROS) production. Although several sources of ROS have been previously suggested, how RAGE induces ROS production is still unclear, considering the multiple targets of pathogen‐associated molecules. Here, using acute brain slices and primary co‐culture of cortical neurons and astrocytes, we investigated the effects of a range of synthetic peptides corresponding to the fragments of the RAGE V‐domain on redox signaling. We found that the synthetic fragment (60–76) of the RAGE V‐domain induces activation of ROS production in astrocytes and neurons from the primary co‐culture and acute brain slices. This effect occurred through activation of RAGE and could be blocked by a RAGE inhibitor. Activation of RAGE by the synthetic fragment stimulates ROS production in NADPH oxidase (NOX). This RAGE‐induced NOX activation produced only minor decreases in glutathione levels and increased the rate of lipid peroxidation, although it also reduced basal and β‐amyloid induced cell death in neurons and astrocytes. Thus, specific activation of RAGE induces redox signaling through NOX, which can be a part of a cell protective mechanism. [ABSTRACT FROM AUTHOR]

Neurodegenerative diseases are chronic conditions occurring when neurons die in specific brain regions that lead to loss of movement or cognitive functions. Despite the progress in understanding the mechanisms of this pathology, currently no cure exists to treat these types of diseases: for some of them the only help is alleviating the associated symptoms. Mitochondrial dysfunction has been shown to be involved in the pathogenesis of most the neurodegenerative disorders. The fast and transient permeability of mitochondria (the mitochondrial permeability transition, mPT) has been shown to be an initial step in the mechanism of apoptotic and necrotic cell death, which acts as a regulator of tissue regeneration for postmitotic neurons as it leads to the irreparable loss of cells and cell function. In this study, we review the role of the mitochondrial permeability transition in neuronal death in major neurodegenerative diseases, covering the inductors of mPTP opening in neurons, including the major ones—free radicals and calcium—and we discuss perspectives and difficulties in the development of a neuroprotective strategy based on the inhibition of mPTP in neurodegenerative disorders. [ABSTRACT FROM AUTHOR]