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Introduction: Chronic hyperglycemia as the main link in DM pathogenesis leads to systemic vessels and nerves lesion with chronic bone complications development consequently. The aim: To evaluate influence of hyperglycemia on reparative osteogenesis after perforated tibial fracture in rats. Materials and methods: A total of 30 white adult rats were subdivided into two groups: 15 healthy rats in Group 1 (control) and 15 rats with alloxan induced hyperglycemia in Group 2 (investigated) and were carried out of experiment on the 10th, 20th and 30th day after the fracture. Hyperglycemia in rats was verificated as the postprandial glycemic rate ≥ 8,0 mmol/l. Tibia diaphysis fracture was modeled by a cylindrical defect with a diameter of 2 mm with portable frezer. Morphological evaluation. A complex morphological studies included histological, morphometric and immunohistochemical examination. Results: This is confirmed by an increase in MMP-9 expression in connective tissue, a decrease in TGF-β expression in all phases, an increase in the expression of CD3 and CD20 and a marked decrease in the expression of all vascular markers. During hyperglycemia, incomplete blood supply to the tissues occurs, necrosis of bone and soft tissues develop in the area of the fracture, the reparative reaction slows down considerably and manifests itself in the development of fibrous and, less commonly, cartilage tissue. Conclusions: In hyperglycemia rats, there was a delay in the callus formation, a decrease in proliferation and ossification, and a slowdown in the processes of angiogenesis.

Introduction: Vascular endothelium function interruption has the main role among mechanisms of development and progression of chronic kidney disease. In numerous experimental and clinical studies, it was proved that activated vascular endothelium is a structural and functional unit that matches processes of inflammation with intravascular coagulation, fibrinolysis and haemorheological disorders. The aim: To identify special features of endothelium morphological structure in kidney vessels, coronary arteries and aorta during chronic kidney disease. Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used. Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwent profound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.

Ф ормирование опухолевых тромбов в просвете почечной и нижней полой вены (НПВ) представляет собой одну из особенностей почечно-клеточного рака. Данный феномен обнаруживают у 4-10% пациентов. Он до сих пор является предметом множества дискуссий как в клинической, так и в морфологической среде [1-3]. Фактически не изученными остаются иммуногистохимические характеристики этих опухолей и не сформулирована общая теория формирования внутривенозных неопластических тромбов. Считается, что способность почечно-клеточного рака к инвазии во многом определяется разрушением опухолью экстрацеллюлярного матрикса путем местной продукции желатиназных энзимов, в частности матриксных металлопротеиназ (ММР) [4,5]. Биологический потенциал этих ферментов-способность разрушать протеины экстрацеллюлярного матрикса, прежде всего коллаген IV типа, что обусловливает повышенную миграцию клеток, принимающих участие в ангиогенезе новообразований. Вместе с тем, усиление миграционной способности клеток связано не только с деструкцией базальных мембран и межклеточного матрикса, но и с изменением состояния гликопротеинов эндотелия, обладающих адгезивными свойствами, такого как маркер эндотелиальных клеток

On the model of the combined effects of passive smoking and reducing of energy intake diet of pregnant female rats was shown that their offspring of both sexes in the postnatal life have disrupted age ensuring body’s thyroid hormone. At the same time a significant number of offspring at an early age have expressed hyperthyroidism at the background of lower body weight. It was expected that this impact is the cause of a high percentage the death of pups of mothers during the first months of life, as had been shown by the authors earlier. It was found that the stress functioning of thyroid system in female offspring of experimental mothers has changing influence on hypothyroid status and leads to obesity at young age.