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Buryachkovskaya L.,Institute of Experimental Cardiology | Sumarokov A.,Institute of Clinical Cardiology | Lomakin N.,Marshala Timoshenko Str
Inflammation Research | Year: 2013

Introduction Historical overview of development investigations on inflammation in Russia up to date is presented. Material and methods Analysis of modern Russian language literature (1950-2010) on history of medicine and researchers' activity on inflammation, as well as Russian language content of internet on this theme, was made. Many names of Russian researchers are still little known to the English-speaking Western readers. Results Starting in the eighteenth century, the mystery of the inner workings of the inflammation process attracted the interest of physicians and biologists of the Russian Empire. Accumulated knowledge focused mainly on the etiological factors of inflammation. In the nineteenth century, scientific schools emerged for studying inflammation and established close contacts with leading scientists in other countries. At this time, Ilya Mechnikov formulated his famous biological theory of inflammation, according to which inflammation is a protective adaptation response to an injury. He also developed his teaching on phagocytosis and was awarded the Nobel Prize. In the twentieth century, Russian scientists participated in the discovery of viruses and new bacterial pathogens, and in the investigation of the mechanics of the genesis and development of inflammatory processes. Conclusion Today interest in studies of inflammation in Russia is on the increase; scientists united by the Russian Inflammation Society continue their quest to investigate inflammatory mediators, and study molecular and cellular mechanisms and approaches in the treatment of complications associated with inflammation. © Springer Basel 2013. Source


Tsyplenkova V.G.,Institute of Clinical Cardiology
Kardiologiya | Year: 2013

Endomyocardial biopsies performed in patients with various forms of cardiomyopathies (CMP) and chronic myocarditis in the presence of heart failure identified changes indicative of reduction of functioning cardiomyocytes (CMC) at the account of their destruction, dedifferentiation and inefficient hypertroph". Energy apparatus of CMC was represented by large masses of destructed small mitochondria. Myofibrils were driven to periphery of CMC and appeared atrophic. Products of catabolism (lipofuscin, autophagous vacuoles, protein conglomerates) were accumulated in CMC. This led to impairment of CMC main function - to exert contraction. Reduction of number of capillary vessels per unit of myocardial cross-section area was also found. Discussion of problems of morphogenesis of the observed changes and of pathogenetic treatment is presented in the article. Source


Mentz R.J.,Duke University | Cotter G.,Momentum Research Inc. | Cleland J.G.F.,University of Hull | Stevens S.R.,Duke Clinical Research Institute | And 15 more authors.
European Journal of Heart Failure | Year: 2014

Aims The implications of geographical variation are unknown following adjustment for hospital length of stay (LOS) in heart failure (HF) trials that included patients whether or not they had systolic dysfunction. We investigated regional differences in an international acute HF trial. Methods and results The PROTECT trial investigated 2033 patients with acute HF and renal dysfunction hospitalized at 173 sites in 17 countries with randomization to rolofylline or placebo. We grouped enrolling countries into six regions. Baseline characteristics, in-hospital management, and outcomes were explored by region. The primary study outcome was 60-day mortality or cardiovascular/renal hospitalization. Secondary outcomes included 180-day mortality. Of 2033 patients, 33% were from Eastern Europe, 19% from Western Europe, 16% from Israel, 15% from North America, 14% from Russia, and 3% from Argentina. Marked differences in baseline characteristics, HF phenotype, in-hospital diuretic and vasodilator strategies, and LOS were observed by region. LOS was shortest in North America and Israel (median 5 days) and longest in Russia (median 15 days). Regional event rates varied significantly. Following multivariable adjustment, region was an independent predictor of the risk of mortality/hospitalization at 60 days, with the lowest risk in Russia (hazard ratio 0.39, 95% confidence interval 0.23-0.64 vs. Western Europe) due to lower rehospitalization; mortality differences were attenuated by 180 days. Conclusions In an international HF trial, there were differences in baseline characteristics, treatments, LOS, and rehospitalization amongst regions, but little difference in longer term mortality. Rehospitalization differences exist independent of LOS. This analysis may help inform future trial design and should be externally validated. © 2014 European Society of Cardiology. Source


Sobenin I.A.,Russian Academy of Medical Sciences | Zhelankin A.V.,Russian Academy of Medical Sciences | Sinyov V.V.,Institute of Clinical Cardiology | Bobryshev Y.V.,University of New South Wales | And 2 more authors.
Gerontology | Year: 2015

Atherosclerosis is a complex disease which can be described as an excessive fibrofatty, proliferative, inflammatory response to damage to the artery wall involving several cell types such as smooth muscle cells, monocyte-derived macrophages, lymphocytes, dendritic cells and platelets. On the other hand, atherosclerosis is a typical age-related degenerative pathology, which is characterized by signs of cell senescence in the arterial wall including reduced cell proliferation, irreversible growth arrest and apoptosis, increased DNA damage, the presence of epigenetic modifications, shortening of telomere length and mitochondrial dysfunction. The most prominent characteristics of mitochondrial aging are their structural alterations and mitochondrial DNA damage. The mechanisms of mitochondrial genome damage in the development of chronic age-related diseases such as atherosclerosis are not yet well understood. This review focuses on the latest findings from studies of those mutations of the mitochondrial genome which may play an important role in the development of atherosclerosis and which are, at the same time, also markers of mitochondrial aging and cell senescence. © 2014 S. Karger AG, Basel. Source


Dmitriev L.F.,Institute of Clinical Cardiology
Klinichescheskaya Laboratornaya Diagnostika | Year: 2015

The control of cellular metabolism is present in many organs and tissues and its loss means development of hypo- and hyperglycemia. The high level of glucose results in glycation of proteins and increase of concentration of ketoaldehyde and methyl glyoxal in cells. The increase of level of this ketoaldehyde and D-lactate in organs and tissues also can be a result of formation of methyl glyoxal in particular enzymatic reactions including decomposition of one of substrates of glycolysis and conversion of aminoacetone catalyzed by semicarbazide-sensitive amine oxydase of endothelium cells. The methyl glyoxal attacks arginine residuals of proteins. This aldehyde is related to interruption in transmission of insulin signal, disorder of pro-antioxidant balance, inhibition of enzymes of glycolysis, etc. The model of cellular metabolism is proposed where methyl glyoxal plays a key role in development of resistance to insulin, hyperglycemia, hypokalemia and hypertension. The modes of increase of consumption of glucose in conditions of low activity of protein tyrosine kinase are considered. The possible involvement of tokopherol (its derivatives) in activation of phosphodiesterase in liver and regulation of carbohydrate metabolism is considered too. The role of tokopherol-carrier proteins and effect of tokopherol on functioning of OI-cells is discussed. It is still unclear if there is a direct relationship between low level of tokopherol-carrier proteins and diabetes or hypertension. However, low level of tokopherol-carrier proteins results in "prolonged oxidative stress". Source

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