[Mortality from cancer of the population living close to a large nuclear power plant].

There was analyzed cancer mortality of residents of Seversk, located close to the world's largest complex of enterprises of the nuclear industry - the Siberian Chemical Enterprise (the period from 01.01.1970 till 31.

[Glucose, glycotoxins, and protein glycation products: the role in pathogensis].

Arteriosclerosis and atheromatosis are etiologically and pathogenetically different non-physiological processes in atherosclerosis localized in the proximal segments of the arterial bed and elastic-type arteries; both affect the structure and function of the arterial wall. They cause an inflammatory reaction with subsequent compaction (sclerosing) of the walls of large and mid-size arteries, the loss of their elasticity due to structural changes in the loose connective tissue of intima-media, impaired elasticity and enhanced rigidity of the wall, inflammation, fibrosis, and increased pulse wave conduction velocity. Arteriosclerosis is initiated by long-term hyperglycemia, chemical collagen and elastin glycation by glucose and its metabolites (glycotoxins glyoxal and methylglyoxal) forming cross-links between collagen and elastin fibers.

[Low and very low density lipoproteins: pathogenetic and clinical significance].

LDLP and VLDLP have different biological functions: phylogenetically older LDLP transfer FA that serve as substrates for intracellular production of energy and ATP while VLDLP transfer FA--precursors of cell membranes and eicosanoids. The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. VLDLP consist of palmitic and oleic VLDLP and LDLP of linoleic and linolenic LDLP.

[The unity of pathogenesis of insulin resistance syndrome and non-alcoholic fatty disease of liver. The metabolic disorder of fatty acids and triglycerides].

The pathogenesis of non-alcoholic fatty disease of liver (steatosis) is still as unclear as a loss of hepatocytes similar to apoptosis, development of biological reaction of inflammation, its transformation into steatohepatitis with subsequent fibrosis and formation of atrophic cirrhosis. The article suggests that steatosis is developed due to higher concentration of palmitic saturated fatty acid (C 16:0) in food, intensification of its endogenic synthesis from food carbohydrates and glucose and development of insulin resistance. It is displayed in in hormone ability to activate both oxidation in cells of glucose and synthesis of oleic monoene fatty acid from palmitic saturated fatty acid (C 18:1).