Publications by authors named "Gritsenko E"

Comparing pace and standard of living of the world population these days and in the end of the last century, it's quiet true that there has been a significant increase. Therewith, the number of deaths from cardiovascular diseases has increased in recent decades. Scientists around the world attribute this fact to the increase in the number of people with overweight and other metabolic disorders.

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Road traffic injuries are a leading cause of morbidity and mortality in the world. In Russia, a road safety program was implemented in Lipetskaya and Ivanovskaya oblasts (regions) as part of a 10-country effort funded by Bloomberg Philanthropies. The program was focused on increasing seat belt and child restraint use and reducing speeding.

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Reducing vehicle speed is among the most effective road safety strategies. We assess how a new policy in Russia that eliminates fines for driving up to 20 km/h above the speed limit has affected the prevalence of speeding. We measured speeds periodically in 13 districts of two Russian regions during 2011-2013 and analysed the effect of the policy using difference-in-differences to control for seasonality.

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Objective: In Russia, the high Road Traffic Injuries (RTIs) rate has been attributed to two well-known risk factors - the low rates of seatbelt and child restraints use and speeding. Despite the importance of understanding both speeding and seatbelt use patterns for the purpose of direct interventions or monitoring road safety situation, no study has assessed the current status of speeding among all vehicles and seatbelt wearing rates among all vehicle occupants in Russia. We are aware that alcohol is a known risk factor for RTI in the country however the work focused on seat belts and speed.

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Protein fraction able to induce K(+)-selective transport across bilayer lipid membrane was isolated from human blood plasma with the use of the detergent and proteolytic enzyme-free method developed at our laboratory. After addition of the studied sample to the artificial membrane in the presence of 100 mM KCl, a discrete current change was observed. No channel activity was recorded in the presence of calcium and sodium ions.

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Activity of mitochondrial ATP-dependent potassium channel in rats with high genetically determined resistance to hypoxia was higher than in sensitive animals. Adaptation of low resistant rats to hypoxia was accompanied by activation of the channel, facilitation of potassium recycling in mitochondria, and a decrease in the rate of H2O2 formation. Our results indicate that mitochondrial ATP-dependent potassium channel plays an important role in the delayed mechanisms of animal's adaptation to hypoxia.

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Changes in the rate of respiration and functioning of the ATP-dependent potassium channel the liver and heart mitochondria of one-, three-, eight-, and twenty four-month-old Wistar male rats have been investigated. It was shown that the activity of the channel in the mitochondria of both tissues in 24-months-old animals decreases more than three times, and the content of potassium, 1.5-2 times compared with young one-month-old rats.

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The mechanism of tissue protection from ischemic damage by activation of the mitochondrial ATP-dependent K(+) channel (mitoK(ATP)) remains unexplored. In this work, we have measured, using various approaches, the ATP-dependent mitochondrial K(+) transport in rats that differed in their resistance to hypoxia. The transport was found to be faster in the hypoxia-resistant rats as compared to that in the hypoxia-sensitive animals.

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The effect of hypoxenum on bioenergetic processes in heart and liver mitochondria of rats, connected with respiration, the generation of hydrogen peroxide, and the activity of ATP-sensitive K-channel ((mitoK)ATP) has been studied. It was shown that hypoxenum in the concentration range of 0.05-10 microg/ml stimulates respiration, increases the coupling in the respiratory chain, and enhances the formation of H2O2 and energy-dependent swelling associated with potassium transport in mitochondria.

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The localization in the cell of the protein forming the ATP-dependent potassium-selective channels in the bilayer lipid membrane has been studied. The electron microscope investigation of rat liver and heart tissue sections after their incubation with Abs against this protein and the visualization of the protein with secondary Abs conjugated with colloid gold were carried out. Colloid gold particles were observed both in mitochondrial membranes and in membranes of endoplasmic and sarcoplasmic reticulum.

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A low-molecular-weight component (LMC) inducing selective transport of calcium across the bilayer lipid membrane has been isolated from mitochondria of the bovine heart by the method developed in our laboratory, which excludes the use of detergents and proteolytic enzymes. It was shown that, in the presence of 10 mM CaCl2, LMC forms conduction channels in the membrane multiples of 5 pS. The specific inhibitor of mitochondrial calcium uniporter, ruthenium red, closes Ca2(+)-induced channels formed in the membrane by LMC.

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Flavonoid-containing plant preparations (water soluble extracts of Pentaphylloides fruticosa [Extralife], Emblica officinalis Gaerth [Amla], and Bergenia crassifolia [Bergenia]) produced a dose-dependent and tissue-specific effect on activity of mitochondrial ATP-dependent potassium channel. The effect of these preparations was biphasic (activation and inhibition). The activating effect of Extralife was one order of magnitude higher than that of Amla and Bergenia and was observed in a wider concentration range.

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Earlier we found that in isolated rat liver mitochondria the reversible opening of the mitochondrial cyclosporin A-insensitive pore induced by low concentrations of palmitic acid (Pal) plus Ca(2+) results in the brief loss of Deltapsi [Mironova et al., J Bioenerg Biomembr (2004), 36:171-178]. Now we report that Pal and Ca(2+), increased to 30 and 70 nmol/mg protein respectively, induce a stable and prolonged (10 min) partial depolarization of the mitochondrial membrane, the release of Ca(2+) and the swelling of mitochondria.

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A Ca(2+)-induced phase separation of palmitic acid (PA) in the membrane of azolectin unilamellar liposomes has been demonstrated with the fluorescent membrane probe nonyl acridine orange (NAO). It has been shown that NAO, whose fluorescence in liposomal membranes is quenched in a concentration-dependent way, can be used to monitor changes in the volume of lipid phase. The incorporation of PA into NAO-labeled liposomes increased fluorescence corresponding to the expansion of membrane.

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A possible role of palmitic acid/Ca2+ (PA/Ca2+) complexes in the cyclosporin-insensitive permeability transition in mitochondria has been studied. It has been shown that in the presence of Ca2+, PA induces a swelling of mitochondria, which is not inhibited by cyclosporin A. The swelling is accompanied by a drop in membrane potential, which cannot be explained only by a work of the Ca2+ uniporter.

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Formation of palmitic acid/Ca(2+) (PA/Ca(2+)) complexes was suggested to play a key role in the non-classical permeability transition in mitochondria (NCPT), which seems to be involved in the PA-induced apoptosis of cardiomyocytes. Our previous studies of complexation of free fatty acids (FFA) with Ca(2+) showed that long-chain (C:16-C:22) saturated FFA had an affinity to Ca(2+), which was much higher than that of other FFA and lipids. The formation of FFA/Ca(2+) complexes in the black-lipid membrane (BLM) was demonstrated to induce a nonspecific ion permeability of the membrane.

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We studied the content of Al, Cd, Co, Cu, Fe, Mg, Mn, P, Pb, S, and Zn in the liver, kidneys, lungs, and spleen of mice with total radiation dose of 7.5 Gy using atomic emission spectral analysis with an inductively coupled argon plasma. The qualitative content of macro- and microelements and coordination between their concentrations statistically determined from coefficients of linear correlation differ between the tissues of the irradiated and control animals.

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A mitochondrial hydrophobic component that forms Ca2+-induced nonspecific ion channels in black-lipid membranes (Mironova et al., 1997) has been purified and its nature elucidated. It consists of long-chain saturated fatty acids--mainly palmitic and stearic.

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The levels of phosphate esters and the activities of thiamine biotransformation enzymes in the blood and tissues of albino rats were studied during oxythiamine-induced B1 deficiency and after metabolic correction with thiamine and taurine. Among thiamine phosphates, the most informative indicators of thiamine deficiency were shown to be triphosphate esters and free thiamine diphosphate. The biosynthetic enzymes thiamine kinase and thiamine diphosphate kinase played a decisive role in maintaining the initial rate and in recovering the physiologically active forms of vitamin B1.

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Biological significance of thiamin in development of experimental allergic encephalomyelitis has been elucidated. It has been shown that at the late preclinical stage of the disease thiamine metabolism is predominantly directed towards the maintaining of cellular metabolic homeostasis, whereas at the stage of clinical symptoms the anabolic process gives way to catabolic decomposition. Among tested thiamine phosphates the triphosphate ester is the most informative parameter in demyelinizing processes.

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Blood of patients with gastric tumor was studied after their admission to the hospital and after the chemotherapeutic course. Formation of the tumor was accompanied by development of hypovitaminoses B1 and PP. The vitamin deficiency was more distinct after treatment of the patients with cyclophosphan: content of thiamine diphosphate (TDP) was decreased by 40%; NAD+NADP, by 30% and NADH+NADPH, by 20%.

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An enzymatic micromethod is proposed for quantification of thiamine biphosphate (TBP) at concentrations from 0.5 ng in 0.1-0.

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Concentrations of phosphate esters in blood of patients with vertebral osteochondrosis and activities of enzymes involved in thiamine metabolism have been investigated. The pathological processes were characterized by a decrease in content of thiamine triphosphate while concentration of coenzyme, thiamine diphosphate, was relatively constant. The enzymes involved in the initial and final steps of biosynthesis and degradation of thiamine phosphorylated derivatives play the main role in maintaining vitamin B1 metabolic homeostasis.

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