[Changes in serum levels of the key factors of angiogenesis in different outcomes of combined injuries in children]. / Izmeneniia kontsentratsii v syvorotke krovi kliuchevykh faktorov angiogeneza pri razlichnykh iskhodakh sochetannoi travmy u detei.

AIM: To study the changes in the key angiogenic factors VEGF-A and angiogenin (ANG) in children with different outcomes of combined injuries. MATERIAL AND METHODS: Contents of VEGF-A and ANG in blood serum were determined by enzyme immunoassay. The study included 40 patients, 21 boys and 19 girls. Patients were divided into 4 groups according to the outcome of injury: 1 - the recovery or mild residual symptoms; 2 - disabled; 3 - vegetable state; 4 - death. Patients were examined at different times after injury: 1-6 days, 7-11 days, 12-19 and 20-33 days. RESULTS AND CONCLUSION: In the first days after injury, the content of VEGF-A in patients of 1-3 groups was at the level of the reference group, moreover, in patients of the 3rd group it was close to the top edge. In group 4, the content of VEGF-A was maximal in the first days after injury and then gradually decreased to the point of death. In groups 1 and 3, the level of VEGF-A increased significantly starting from the 2nd week while in group 2 this indicator was slightly increased approaching later (up to 33 days of observation) to the upper values in the reference group. In the 3rd group, the content of VEGF-A reached the plateau on the 19th day after injury and was higher than the reference data, but lower than in patients of the 1st group. No correlation between the changes in ANG content at different times after combined injuries and outcome was found. There was a trend towards decreased levels of ANG, especially after 3-4 weeks after injury. The data obtained are important for the control over processes of vascular and tissue reparation after injury and for searching for effective ways of treatment of altered angiogenesis in such patients.

[Lipid peroxidation and antioxidant enzymatic defense in patients with newly detected insulin-dependent diabetes mellitus]. / Perekisnoe okislenie lipidov i antioksidantnaia fermentativnaia zashchita u bol'nykh s vpervye vyiavlennym insulinzavisimym sakharnym diabetom.

Studies of lipid peroxidation and antioxidant enzymic defense in red cell membranes in 23 patients with newly detected insulin-dependent diabetes mellitus have revealed a statistically significant (2-fold) elevation of malonic dialdehyde lipid peroxidation products and a trend to a rise in the levels of lipid peroxides. This is parallelled by a certain overstrain of the cellular antioxidant defense system. The authors discuss the usefulness of administering antioxidant therapy at the onset of the disease in order to prevent the toxic injury of beta-cells and vascular endothelium cells by lipid peroxidation products.

[Effect of ethynyl estradiol and estradiol dipropionate on the esterification of saturated and unsaturated fatty acids in the rat liver]. / Vliianie étiniléstradiola i éstradiola dipropionata na éterifikatsiiu nasyshchennykh i nenasyshchennykh zhirnykh kislot v pecheni krys.

Effect of estradiol ethynyl and estradiol propionate on esterification of saturated and non-saturated fatty acids in liver tissue, as one of possible mechanisms in development of estrogen-induced hypertriglyceridemia, was studied using labelled precursors 3H-palmitic and 14C-linoleic acids. Both these estrogens stimulated the incorporation of exogenous fatty acids into triglycerides. After administration of estradiol dipropionate relative esterification of 14C-linoleic acid into triglycerides was increased as compared with controls. Estradiol ethynyl increased and estradiol dipropionate decreased the incorporation of exogenous fatty acids into liver phospholipids. Both estrogens activated the relative esterification of linoleic acid into phospholipids. A decrease in exogenous fatty acids esterification into fraction of cholesterol esters, caused by both these estrogens, occurred due to an increase in relative incorporation of linoleic acid into these lipids. As shown in experiments of relative esterification of saturated and non-saturated fatty acids, estradiol propionate stimulated synthesis of more non-saturated forms of triglycerides, phospholipids and cholesterol esters in rat liver tissue as compared with the estradiol ethynyl action. The data obtained and the data of literature suggest that activation of exogenous fatty acids esterification into triglycerides and alterations in relative esterification of saturated and non-saturated fatty acids into triglycerides and phospholipids of liver tissue are of importance in pathogenesis of estrogen-induced hypertriglyceridemia.

[Effect of adrenocorticotropic hormone on the biosynthesis of glycerolipid components in the rat liver]. / Deistvie adrenokortikotropnogo gormona na biosintez sostavnykh komponentov glitserolipidov v pecheni krys.

Single administration of ACTH led to stimulation of synthesis of saturated and monoenic fatty acids in liver tissue as well as to their esterification with formation of triacyl glycerols. The hormone inhibited elongation and desaturation of fatty acids and decreased the formation of polyenic fatty acids in liver tissue. Cycloheximide alone or simultaneously with ACTH activated synthesis of unsaturated and monoenic fatty acids and stimulated the glycerophosphate shunt of triacyl glycerols synthesis. The tropic hormone activated glyceroneogenesis contributing to an increase in concentration of both alpha-glycerophosphate and long-chain fatty acids in hepatocytes; either ACTH or cycloheximide stimulated the triacyl glycerols synthesis via induction of the key enzymes by excess of the substrates. Consumption of acetyl-CoA, derived from labeled leucine, for biosynthesis of individual lipids was regulated by other mechanisms distinct from those involved in consumption of acetyl-CoA pool, derived from labelled acetate.

[Dynamics of blood fibronectin level in myocardial infarction]. / Dinamika urovnia fibronektina krovi pri infarkte miokarda.

The fibronectin level in the blood of patients with myocardial infarction was measured at varying times from the onset of an angina pectoris attack in order to elucidate the diagnostic importance of blood fibronectin. At the same time these patients were examined over time for the blood content of myoglobin, MB creatine kinase protein and C-reactive protein playing a well-known role in the diagnosis. The blood concentrations of these substances reached the maximal values at different times of myocardial infarction. The mean concentrations of fibronectin in the blood of patients with myocardial infarction ranged within normal starting from the first till the 28th day since the onset of an angina pectoris attack. Moreover, the mean blood fibronectin level in myocardial infarction patients did not differ within the first-third days since the disease onset from that in patients with a clinical picture of unstable angina pectoris which was not accompanied by the development of myocardial infarction. Based on the data obtained it is concluded that measurement of blood fibronectin level does not play any diagnostic role in myocardial infarction. On the other hand, progressive increase in blood fibronectin level throughout 4 weeks starting from the 3d day of the disease and a significantly higher fibronectin content on the 28th day as compared with that on the 3d day is likely to mirror the activity of repair processes occurring in the myocardium.

[Effect of ethinyl-estradiol on the biosynthesis and esterification of fatty acids in the rat liver]. / Vliianie étinil-éstradiola na biosintez i éterifikatsiiu zhirnykh kislot v pecheni krys.

Ethynyl-estradiol was shown to decrease the rate of biosynthesis of saturated, mono-, di-, tri- and tetraenic fatty acids in liver tissue and to increase the esterification of the newly synthesized fatty acids into triglycerides and phospholipids. The most distinct activation of esterification was found, if newly synthesized saturated fatty acids changed to triglycerides and tetraenic acids--into phospholipids. Ethynyl-estradiol stimulated also in liver tissue the esterification of exogenous saturated and unsaturated fatty acids into triglycerides and phospholipids, while relative esterification of unsaturated fatty acids into phospholipids tended to increase. The data obtained suggest that stimulation of endo- and exogenous fatty acids esterification into triglycerides and phospholipids of liver tissue may be important in pathogenesis of estrogen-induced hypertriglyceridemia.

[Cortisol inhibition of cholesterol and phospholipid biosynthesis in the rat liver]. / Tormozhenie kortizolom biosinteza kholesterina i fosfolipidov v pecehni krys.

Effect of hydrocortisone on biosynthesis of cholesterol and phospholipids in liver tissue was studied using intact rats, in adrenalectomy, under conditions of stimulation of lipid biosynthesis by cholestyramine and Triton WR-1339. Hydrocortisone was shown to inhibit biosynthesis of cholesterol and phospholipids in rat liver tissue if 2-14C-acetate was used as a precursor. The hormone inhibited biosynthesis of lipid components in membranes of adrenalectomized rats. Under conditions of preactivation of the lipid biosynthesis, using simulation with cholestyramine and Trition WR-1339, hydrocortisone decreased the synthesis of cholesterol and phospholipids.

[Effect of cholestyramine on lipoprotein metabolism in rat blood]. / Vliianie kholestiramina na metabolizm lipoproteidov v krovi krys.

The effect of cholestyramine on lipoprotein metabolism in the rat blood has been explored. Administration of cholestyramine changed both the concentration and the ratio of lipid components in all the classes of lipoproteins. Despite the fact that the activity of postheparin lipoprotein lipase was unchanged upon cholestyramine action, almost double rise in the activity of LChAT and an increase in the specific radioactivity of LDL attests to the intensification of VLDL metabolism. Therefore, the increased biosynthesis of VLDL by the liver is the main reason for the development of hypertriglyceridemia upon the action of cholestyramine.

[Characteristics of lipoprotein metabolic disorders during treatment with oral contraceptives]. / Kharakteristika narushenii obmena lipoproteidov pod vliianiem oral'nykh kontratseptivov.

It has been shown in rat experiments that ethinyl estradiol and estradiol dipropionate increase hepatic biosynthesis of phospholipids, free fatty acids and their esterification to form mono-, di- and triglycerides. Cholesterol biosynthesis is enhanced only by ethinyl estradiol. The specific radioactivity of VLDL- and HLD-apoproteins increases in plasma. This is the result of enhanced lipoprotein formation and secretion. Injections of ethinyl estradiol to rats lead to less pronounced metabolic disturbances compared to those induced by the action of estradiol dipropionate. The activating effect of ethinyl estradiol on hepatic lipoprotein biosynthesis is one of the pathogenetic events of hyperlipoproteinemia development.

[Cholestyramine activating effect on lipoprotein biosynthesis in the rat liver]. / Aktiviziruiushchee vliianie kholestiramina na biosintez lipoproteidov v pecheni krys.

The cholestyramine effect on the biosynthesis of lipids and lipoproteins in the rat liver was investigated in order to elucidate the mechanisms of serum triglyceride concentration increase. Cholestyramine feeding produces an increase in the biosynthesis of neutral lipids by the liver and a considerable rise in specific radioactivity of serum free cholesterol and triglycerides. Cholestyramine intensifies the biosynthesis of apoproteins of very low density lipoproteins (VLDL), formation of lipoproteins and their secretion into the blood. Increased secretion of newly synthesized VLDL, the major component of which are triglycerides, leads to hypertriglyceridemia.

[Prostaglandins, cyclic nucleotides and heart adaptation to acute and chronic pressure overload]. / Prostaglandiny, tsiklicheskie nukleotidy i adaptatsiia serdtsa k octroi i khronicheskoi peregruzke davleniem.

The content of prostaglandins (PGs) and cyclic nucleotides was determined in the rat heart at different time following coarctation of the abdominal aorta. The animals were divided into three groups according to the rate and degree of hypertrophy. The rats with the best adaptability (the highest level of hypertrophy) showed the highest myocardial PG content. An increase in myocardial weight in response to the overload correlated with an enhancement in PGE/PGF2 ratio. The relationship between the myocardial levels of PGs and cyclic nucleotides during the period of adaptation was also observed. Prostaglandins are suggested to play an important role in the heart adaptation to pressure overloads.