I. Yu. Malyshev

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Adaptation of rats to repcated short-term stress exposure prevents, to a considerable extent, contractural and arrhythmogenic effects of high concentrations of extracellular Ca2+ on isolated heart. Increased efficiency of SR Ca2+-pump functioning and a significant increase in Ca2+ pump resistance to autolysis are proved to play the main role in this effect.
  • Prof. F. Z. Meerson, I. Yu. Malyshev, A. V. Zamotrinsky
  • 1991
Adaptation of animals to short-term stress exposure (ASE) protected the heart against arrhythmias in acute ischemia and reperfusion and eliminated the decrease in threshold of fibrillation and arrhythmias in acute myocardial infarction and postinfarction cardiosclerosis. Cardioprotective effect of ASE was provided not only by the activation of GABAergic,(More)
  • I. P. Khomenko, L. Yu. Bakhtina, +4 authors I. Yu. Malyshev
  • 2007
Preadaptation of cultured HT22 mouse hippocampal neurons to oxidative stress prevented cell damage induced by severe oxidative stress. This protection manifested in a decrease in metabolic disturbances in neurons. Adaptation of neurons to oxidative stress was accompanied by accumulation of HSP32 and HSP70. HSP synthesis inhibitor quercetin abolished the(More)
An important role in the development of the immune response is played by macrophages that acquire either anti-inflammatory M1 or anti-inflammatory M2 phenotype depending on their microenvironment. The possibility of targeted reprogramming of the initial M2 macrophage phenotype towards M1 phenotype and vice versa using macrophage reprogramming factors IFN-γ(More)
This study has shown that the maximal activation of the IP3-DAG regulatory circuit is observed on the 14th day of adaptation to repeated stresses. This activation is characterized by increased activity of phospholipase C and of the positive inotropic response of isolated heart to an alpha-agonist. Simultaneously, this activation is accompanied by the(More)
  • E. B. Manukhina, M. G. Pshennikova, +4 authors I. Yu. Malyshev
  • 2008
NO synthesis disturbances play an important role in the development of neurodegenerative damage in Alzheimer disease. We previously showed that adaptation to intermittent hypobaric hypoxia prevents cognitive disturbances in rats with experimental Alzheimer disease [6]. Here we evaluated the role of NO in cognitive disorders and development of adaptive(More)
  • E. N. Atochina-Vasserman, E. V. Abramova, +6 authors I. Yu. Malyshev
  • 2009
This work was designed to study the role of surfactant protein D in the regulation of NO synthesis by “non-alveolar” microphages. We evaluated whether the effects of surfactant protein D depend on the phenotype of macrophages. In the absence of surfactant protein D, the LPS-induced iNOS response was shown to decrease in macrophages of native and(More)
  • I. Yu. Malyshev, F. Z. Meerson
  • 2004
Adaptation to stress has been shown to increase the resistance of the isolated heart to reperfusion injury and heat shock [4], to high Ca z+ concentrations and toxic doses of catecholamines [1, 8], and cellular structures (elements of the sarcoplasmic reticulum of the mitochondrion and nucleus), isolated from the myocardium of adapted animals, have been(More)
  • M. G. Pshennikova, L. Yu. Golubeva, B. A. Kuznetsova, M. V. Shimkovich, E. V. Malysheva, I. Yu. Malyshev
  • 2006
Control and acutely stressed August rats have corticosterone levels 62% and 15% higher, respectively, than their Wistar counterparts, indicating that the activity of stress-mediating hypothalamic-pituitary-adrenal system in August rats is higher. On the other hand, the intensity of stress reactions and, consequently, the degree of activation of this system(More)
  • I. Yu. Malyshev, F. Z. Meerson
  • 2004
During adaptation to short periods of stress a sufficiently effective mechanism of limitation of arrhythmia arising during ischemic and, in particular, reperfusion injury is formed at the level of the heart itself [2]. When this mechanism is studied it must be recalled that reperfusion regularly increases the Ca 2+ inflow into the cardiomyocyte sarcoplasm(More)