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Based on studies of certain gene-candidate polymorphism, the authors studied markers of early development and unfavorable course of pneumoconiosis in post-contact period. Analysis covered occurrence of genotypes and allels of I/D polymorphism of gene CCRS, 4a/b polymorphism of gene NOS3, VNTR polymorphism of gene ILRN, I/D polymorphism of CASP8 and mutation GLU342LYS (rs28929474) and GLU264VAL (rsl7S80) in gene SERPINAl in patients with various terms of pneumoconiosis formation. Findings are individual criteria of early formation and progress of pneumoconiosis in post-contact period..

Objectives. Authors studied the levels of pro- (IL-1Β, TNF-α, IL-6, IL-8, IFN-γ) and anti-inflammatory cytokines (IL-1Ra, IL-10, IL-4) in the blood serum at 1st and 2nd day of acute period of ischemic stroke with hemorrhagic transformation (IS HT). Material and methods. We compared cytokines levels in the blood serum of patients with IS HT and in patients with ischemic (IS) and hemorrhagic stroke (HT). Results. In patients with IS HT, significantly lower levels of IL-1Β, TNO-α and higher levels of IL-6 were noted at 1st and 2nd day compared to patients with IS and HS. Significantly lower levels of IFN-γ and IL-10 with increased levels of IL-4 were noted at 1st and 2nd day of IS HT compared to IS. There were no differences in concentrations of IFN-γ, IL-10 and IL-4 between IS HT and HS groups. Conclusion. Cytokines are not only involved in the development of HT in IS but can be predictors of HT.

Obtained results of molecular genetics testing of workers' groups exposed to dust show the elimination of carriers of defective variants in the CFTR gene among workers exposed to dust. We can establish a fact that in spite of law frequency of detected major mutations of the CFTR gene in explored selections they have big importance as individual factors in the stage of preliminary medical examinations in terms of prediction of possible occupational development risk and progression of productionally mediated visceropathies and diseases, as well as a conscious choice of occupation by an individual.

Systemic leucocyte-induced oxidative stress in prolonged occupational exposure to dust modifies oxidative metabolism of neutrophils and RBC, causes inflammatory and destructive, autoimmune processes in gastric lining and possible subsequent occupational gastropathies. To verify gastropathies caused by technogenic dust aerosols, search of preclinical biologic markers of gastric lining damage is essential. The article presents main steps in occupational gastropathies formation, trigger mechanisms, leading pathogenetic factors of gastric lining damage and of atrophic fundus gastritis. Using the mentioned complex of biomarkers in gastric lining state monitoring among workers at periodic and thorough medical examination is main item in forecasting individual risk of occupational gastropathies and in possible approach to their prevention and treatment.

The article covers basic mechanisms and major pathogenetic factors of pneumoconiosis formation and course in after contact period. The authors provide results of metabolic disorders analysis in the patients vairable in tolerance to industrial aerosol, to forecast pneumoconiosis course after discontinued contact with the hazard.

The authors present main mechanisms and leading pathogenetic factors underlying occupationally mediated dust nephropathies. The article covers results of analysis concerning biochemical and hemocoagulation criteria to evaluate the risk of nephropathy in workers exposed to high concentrations of industrial dust aerosols.

The authors present results of evaluating molecular genetic markers to estimate individual risk and forecast visceropathies development in workers exposed to high concentrations of industrial dust aerosols.

Forty-three patients with metabolic syndrome (MS) were examined. The urinary (uroporphyrin--UP and coproporphyrin--CP) and fecal (CP and protoporphyrin) fractions of porphyrin, as well as the urinary excretion of porphyrin precursors (S-aminolevulinic acid and porphobilinogen) were measured. Porphyrin metabolic disturbances were registered in 33 (76.7%) patients. Nine of these patients displayed such qualitative changes as fraction mismatch (CP/UP < 1; the normal value is 2.1 +/- 0.4), and an increase in the level of porphyrin precursors, while their total urinary porphyrin level was normal. In 24 patients pathological changes in porphyrin exchange were characterized by such quantitative changes as a many-fold increase in urinary and/or fecal porphyrin fraction as well as the development of secondary biochemical coproporphyrinuria syndromes, symptomatic elevation of fecal porphyrin level, and latent late cutaneous porphyria. Changes in porphyrin exchange in patients with metabolic syndrome broaden the scope of disturbances occurring in this syndrome, and allow considering these changes as additional criteria.