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Mukhamadiyarov R.A.,Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases | Radionov I.A.,Kemerovo State Medical Academy | Razumov A.S.,Kemerovo State Medical Academy | Kudryavtseva Y.A.,Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases
Russian Journal of Biopharmaceuticals | Year: 2016

It is shown that when perftoran, empty liposomes and liposomal form are administered to animals with the modelled chronic pancreatitis a decrease in oxidative stress manifestations were observed. Various medications differed in the degree of inhibition and accumulation of primary and secondary products of lipid peroxidation and in the impact on antioxidant defense enzymes’ activity. Empty liposomes and liposomal perftoran had the best protective effect. Liposomal form of perftoran as opposed to empty liposomes not only increased the total antioxidant activity, but also activated genuine antioxidant enzymes of blood and tissues. High efficacy of liposomal compositions in decreasing of oxidative stress manifestations shows the perspective of the studies aimed at the creation of highly-efficient pharmaceuticals for pancreatitis treatment on their basis. © 2016, Folium Ltd. All Rights Reserved.


Mukhamadiarov R.A.,Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases | Khaliulun I.G.,University of Bristol | Veremeev A.V.,Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases
Russian Journal of Biopharmaceuticals | Year: 2015

The work is focused on the effect of liposome preparations of different compositions on the contractile function of the isolated rat heart. The results show that liposomes containing antioxidants, but not high-energy phosphates, exhibit marked protective effect during ischemia and reperfusion. © 2015, Folium Ltd. All rights reserved.


PubMed | Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases
Type: | Journal: Patient preference and adherence | Year: 2015

To analyze the influence of recipient-related metabolic factors on the rate of structural dysfunction caused by the calcification of xenoaortic bioprostheses.We retrospectively analyzed clinical status, calcium-phosphorus metabolism, and nonspecific markers of inflammatory response in bioprosthetic mitral valve recipients with calcific degeneration confirmed by histological and electron microscopic studies (group 1, n=22), and in those without degeneration (group 2, n=48).Patients with confirmed calcification of bioprostheses were more likely to have a severe clinical state (functional class IV in 36% in group 1 versus 15% in group 2, P=0.03) and a longer cardiopulmonary bypass period (112.818.8 minutes in group 1 versus 97.223.6 minutes in group 2, P=0.02) during primary surgery. Patients in group 1 demonstrated moderate hypovitaminosis D (median 34.0, interquartile range [21.0; 49.4] vs 40 [27.2; 54.0] pmol/L, P>0.05), osteoprotegerin deficiency (82.5 [44.2; 115.4] vs 113.5 [65.7; 191.3] pg/mL, P>0.05) and osteopontin deficiency (4.5 [3.3; 7.7] vs 5.2 [4.1; 7.2] ng/mL, P>0.05), and significantly reduced bone-specific alkaline phosphatase isoenzyme (17.1 [12.2; 21.4] vs 22.3 [15.5; 30.5] U/L, P=0.01) and interleukin-8 levels (9.74 [9.19; 10.09] pg/mL vs 13.17 [9.72; 23.1] pg/mL, P=0.045) compared with group 2, with an overall increase in serum levels of proinflammatory markers.Possible predictors of the rate of calcific degeneration of bioprostheses include the degree of decompensated heart failure, the duration and invasiveness of surgery, and the characteristics of calcium-phosphorus homeostasis in the recipient, defined by bone resorption and local and systemic inflammation. The results confirm the hypothesis that cell-mediated regulation of pathological calcification is caused by dysregulation of metabolic processes, which are in turn controlled by proinflammatory signals.

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