Влияние микроструктуры сплавов на основе магния на катодное выделение водорода

Solubility of several transition metal chlorides (NiCl2, CrCl2, MoCl3, FeCl2) was measured in KCl-AlCl3 based melts. It was found that the solubility of studied metal chlorides depends on K : Al mole ratio. MoCl3 solubility decreases with increasing AlCl3 content. Solubility of CrCl2 and FeCl2 reaches maximum at K : Al ratio of 1 and decreases when this ratio either de-creases or increases. The dependence of NiCl2 solubility on K : Al mole ratio is V-shaped with the maximum near 0.9–0.95. The effect of temperature on solubility of transition metal chlorides in KCl-AlCl3 melts was also investigated. Increasing temperature does not  alter the character of «solubility – K : Al mole ratio» dependences.Исследована эволюция зеренной структуры магниевых сплавов в процессе равноканального углового прессования (РКУП) при 200 ºС. Показано, что РКУП приводит к формированию сильно неоднородной структуры. Установлено, что деформация не оказывает влияния на кинетику реакции выделения водорода (РВВ), но оказывает воздействие на скорость катодного процесса. Сплав AZ31 является более эффективным катодным материалам в щелочных средах по сравнению с магнием и сплавом ZK60

Computing for Ongoing Experiments on High Energy Physics in LPP, JINR

The computer infrastructure made at the Laboratory of Particle Physics, JINR, purposed for active participation of JINR experts in ongoing experiments on particle and nuclear physics is presented. The principles of design and construction of the personal computer farm have been given and the used computer and informational services for effective application of distributed computer resources have been described

S-15176 Difumarate Salt Can Impair Mitochondrial Function through Inhibition of the Respiratory Complex III and Permeabilization of the Inner Mitochondrial Membrane

S-15176 difumarate salt, a derivative of the anti-ischemic metabolic drug trimetazidine, has been intensively studied for its impact on cellular metabolism in animal models of ischemia-reperfusion injury of the liver, heart, spinal cord, and other organs. Despite evidence of some reduction in oxidative damage to cells, the results of therapy with S-15176 have been mostly disappointing, possibly because of the lack of data on its underlying mechanisms. Here, we aimed to investigate in more detail the role of complexes I-IV of the electron transport chain and membrane permeability transition in mitochondrial toxicity associated with S-15176. Using rat thymocyte and liver mitochondria, we demonstrated that: (1) acute exposure to S-15176 (10 to 50 μM) dose-dependently decreased the mitochondrial membrane potential; (2) S-15176 suppressed the ADP-stimulated (State 3) and uncoupled (State 3UDNP) respiration of mitochondria energized with succinate or malate/glutamate, but not ascorbate/TMPD, and increased the resting respiration (State 4) when using all the substrate combinations; (3) S-15176 directly inhibited the activity of the respiratory complex III; (4) low doses of S-15176 diminished the rate of H2O2 production by mitochondria; (5) at concentrations of above 30 μM, S-15176 reduced calcium retention capacity and contributed to mitochondrial membrane permeabilization. Taken together, these findings suggest that S-15176 at tissue concentrations reached in animals can impair mitochondrial function through suppression of the cytochrome bc1 complex and an increase in the nonspecific membrane permeability

Mitochondrial Transplantation Therapy Ameliorates Muscular Dystrophy in <i>mdx</i> Mouse Model

Duchenne muscular dystrophy is caused by loss of the dystrophin protein. This pathology is accompanied by mitochondrial dysfunction contributing to muscle fiber instability. It is known that mitochondria-targeted in vivo therapy mitigates pathology and improves the quality of life of model animals. In the present work, we applied mitochondrial transplantation therapy (MTT) to correct the pathology in dystrophin-deficient mdx mice. Intramuscular injections of allogeneic mitochondria obtained from healthy animals into the hind limbs of mdx mice alleviated skeletal muscle injury, reduced calcium deposits in muscles and serum creatine kinase levels, and improved the grip strength of the hind limbs and motor activity of recipient mdx mice. We noted normalization of the mitochondrial ultrastructure and sarcoplasmic reticulum/mitochondria interactions in mdx muscles. At the same time, we revealed a decrease in the efficiency of oxidative phosphorylation in the skeletal muscle mitochondria of recipient mdx mice accompanied by a reduction in lipid peroxidation products (MDA products) and reduced calcium overloading. We found no effect of MTT on the expression of mitochondrial signature genes (Drp1, Mfn2, Ppargc1a, Pink1, Parkin) and on the level of mtDNA. Our results show that systemic MTT mitigates the development of destructive processes in the quadriceps muscle of mdx mice

The influence of the magnesium alloys microstructure on the cathodic hydrogen evolution

Исследована эволюция зеренной структуры магниевых сплавов в процессе равноканального углового прессования (РКУП) при 200 ºС. Объектом исследования служили образцы чистого магния и сплавы на его основе – AZ31 (96 % Mg, 3 % Al, 1 % Zn, вес. %) и ZK60 (94 % Mg, 5.5 % Zn, 0.5 % Zr, вес. %). Показано, что РКУП приводит к формированию сильно неоднородной структуры. Установлено, что деформация не оказывает влияния на кинетику реакции выделения водорода (РВВ), но оказывает воздействие на скорость катодного процесса. Сплав AZ31является более эффективным катодным материалам в щелочных средах по сравнению с магнием и сплавом ZK60. Показано,что каталитическую активность материалов можно увеличить введением бóльшего количества алюминия или деформацией, реализуемой, например, при помощи равноканального углового прессования.Evolution of grain structure of magnesium AZ31 and ZK60 alloys during equal channel angular pressing (ECAP) at the 200 ºC temperatures is researched. It is shown that ECAP leads to forming of very inhomogeneous structure. It has been found that deformation affects the rate of the cathodic process. AZ31 alloy is more effective cathode material in alkaline solution environment in comparison with Mg and ZK60 alloys. The object of study were samples of pure magnesium and alloys on its basis – AZ31 (96 % Mg, 3% Al, 1 % Zn weight%) and ZK60 (94 % Mg, 5.5 % Zn, 0.5 % Zr, wt.%). It is shown that pressing leads to the formation of strongly inhomogeneous structure. It is established that the deformation does not affect the kinetics of the reaction extract the water-kind (RVV), but affects the speed cathodic process. Alloy AZ31является more effective cathode materials in alkaline environments compared with magnesium and alloy ZK60. It is shown that the catalytic activity of the materials can be enhanced by the introduction of larger amounts of aluminum or deformed, implemented, for example, by equal-channel angular pressing.Работа выполнена при финансовой поддержке Министерства образования Пермского края (соглашение № С-26/2011)

BK_Ca Activator NS1619 Improves the Structure and Function of Skeletal Muscle Mitochondria in Duchenne Dystrophy

Duchenne muscular dystrophy (DMD) is a progressive hereditary disease caused by the absence of the dystrophin protein. This is secondarily accompanied by a dysregulation of ion homeostasis, in which mitochondria play an important role. In the present work, we show that mitochondrial dysfunction in the skeletal muscles of dystrophin-deficient mdx mice is accompanied by a reduction in K+ transport and a decrease in its content in the matrix. This is associated with a decrease in the expression of the mitochondrial large-conductance calcium-activated potassium channel (mitoBKCa) in the muscles of mdx mice, which play an important role in cytoprotection. We observed that the BKCa activator NS1619 caused a normalization of mitoBKCa expression and potassium homeostasis in the muscle mitochondria of these animals, which was accompanied by an increase in the calcium retention capacity, mitigation of oxidative stress, and improvement in mitochondrial ultrastructure. This effect of NS1619 contributed to the reduction of degeneration/regeneration cycles and fibrosis in the skeletal muscles of mdx mice as well as a normalization of sarcomere size, but had no effect on the leakage of muscle enzymes and muscle strength loss. In the case of wild-type mice, we noted the negative effect of NS1619 manifested in the inhibition of the functional activity of mitochondria and disruption of their structure, which, however, did not significantly affect the state of the skeletal muscles of the animals. This article discusses the role of mitoBKCa in the development of DMD and the prospects of the approach associated with the correction of its function in treatments of this secondary channelopathy