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Development stages of anaplastic liver cancer were investigated in the experiment at rats. Carcinogen (DMBA) diluted in the solution of medical bile, used as cocancirogen, injected intrahepatically. Histologic discomplexation signs of stringer structures in the liver lobules were revealed after 30 days from the beginning of experiment, mostly, subcapsular zones, hyperplasia of hepatocytes with enlargement nuclear‐cytoplazmatic correlation. Formation trabecular and tubular structures from large hepatocytes with large hyperchomic nuclears and signs of hepatocytes' dysplasia of different expressed degree was marked on 60 day of the experiment. Singular massy hepatocytes proliferation with signs of cells' atipism was revealed after 90 days from the beginning of experiment. Trabecular and tubular structures from hepatic cells in the condition of severe dysplasia are remained among massy foci. Morphologic picture of anaplastic cancer is observed after 120 days in the liver of rats.Research results confirm hepatocellular origin of anaplastic liver cancer.Development stages of anaplastic liver cancer of rats are following: progressing dysplasia of hepatocytes; formation of atypical trabecular and tubular structures from large hepatocytes, discomplexation of tubular and trabecular structures with hepatocytes' anaplasia.

Periprosthetic fractures in the area of the femoral component after hip replacement are one of the reasons for performing revision surgery. The treatment is always associated with many complications and therefore does not lose its relevance. The aim of our research was a pathomorphological study of bone tissue repair and reactive changes in the soft tissues around the periprosthetic fracture after arthroplasty. The research results will predict the long-term outcome and stability of the revision endoprosthesis. Materials and methods. The materials for pathomorphological studies were biopsy, (11 periprosthetic fractures in the zone of the femoral component, 5 from the hip joint), fragments of bone tissue from the zone of the periprosthetic fracture, femoral canal, altered connective tissue obtained by repeated interventions in the area of periprosthetic fracture, and revision endoprosthetics. Pathomorphological studies of biopsy specimens of bone fragments and soft tissues were carried out after conventional histological processing with the production of histological sections, 57 m thick, followed by staining with hematoxylin and eosin and according to Van Gieson. Results. Morphological signs of structural disorganization of bone tissue in the fracture zone were revealed after fragments of bone and soft tissues were removed from the fracture zone; various options for repair of bone tissue were investigated, as well as reactive changes up to ischemia from the surrounding soft tissues were observed. Signs of damage to the tubules, lacunae and trabeculae, and with them the intraosseous branches of the supplying artery were noticed. Bone tissue repair in the area of periprosthetic fractures was carried out in various ways: due to activation of osteoblasts, through endesmal osteogenesis (from preexisting fibrous structures), endochondral osteogenesis (from provisional corns), as well as mixed osteogenesis from complexes of bonecartilaginous tissue. Slowing of osteogenesis was the reason for the formation of appositional gluing lines in bone trabeculae, which are considered as a morphological sign of delayed osteogenesis. The absence of multinucleated osteoclasts in the bone tissues we studied is apparently due to the fact that pathological osteolysis with signs of ischemia does not develop in the fracture zone. Conclusion. The results of our histopathological studies indicate that by the time of revision endoprosthetics in the area of femoral fractures, morphological signs of a slowdown in reparative osteogenesis develop with the pathological functional remodeling of bone tissue and microischemia in the bone and, of course, in the surrounding soft tissues.

Rats subjected to coal dust combined with radiation dose of 6 Gy in long-term period demonstrated cytogenetic disorders and changes in bronchial mucosa, arterial and arterioli walls in lung stroma, destructive changes in liver parenchyma with colliquation necrosis foci in liver lobules, on oxidative stress background. Findings are that combined experimental exposure to dust and radiation on oxidative stress background increases carcinogenic and genotoxic risks in animals.