The expression of Ki-67 proliferation marker was studied in vaginal biopsy specimens from women with stress urinary incontinence treated using a Fotona nonablative erbium laser. Cells expressing Ki-67 were located in all cases in the parabasal and basal levels of stratified squamous epithelium, the index of labeled nuclei before Er:YAG laser exposure was 19.05±2.86%. After 1-2 months of laser therapy, the index of labeled nuclei in the epithelium increased significantly and reached 31.79±2.25%. These changes were interpreted as a result of epithelial-stromal interactions. Presumably, the increase in proliferative activity of the vaginal epithelium after exposure to Er:YAG laser was due to the presence of an appreciable level of synthetically active fibroblasts in the subepithelial stroma.

No abstract

When administered intravenously, extracellular vesicles derived from multipotent stromal cells (MSC EVs) immediately pass through the lungs along with the blood and regularly spread to all organs. When administered intraperitoneally, they are absorbed either into the blood or into the lymph and are quickly disseminated throughout the body. The possibility of generalized spread of MSC EVs to distant organs in case of local intratissular administration remains unexplored. However, it is impossible to exclude MSC EV influence on tissues distant from the injection site due to the active or passive migration of these injected nanoparticles through the vessels. The research is based on findings obtained when studying the samples of lungs, heart, spleen, and liver of outbred rabbits of both sexes weighing 3–4 kg at various times after the injection of EVs derived from MSCs of bone marrow origin and labeled by PKH26 into an artificially created defect of the proximal condyle of the tibia. MSC EVs were isolated by serial ultracentrifugation and characterized by transmission electron microscopy and flow cytometry. After the introduction of MSC EVs into the damaged proximal condyle of the tibia of rabbits, these MSC EVs can be found most frequently in the lungs, myocardium, liver, and spleen. MSC EVs enter all of these organs with the blood flow. The lungs contained the maximum number of labeled MSC EVs; moreover, they were often associated with detritus and were located in the lumen of the alveoli. In the capillary network of various organs except the myocardium, MSC EVs are adsorbed by paravasal phagocytes; in some cases, specifically labeled small dust-like objects can be detected throughout the entire experiment—up to ten days of observation. Therefore, we can conclude that the entire body, including distant organs, is effected both by antigenic detritus, which appeared in the bloodstream after extensive surgery, and MSC EVs introduced from the outside.

Morphofunctional activity of mast cells in renal cancer is studied on specimens from the center of the tumor, peritumorous zone (with an obligatory fragment of the pseudocapsule), and from renal tissues maximally distant from the tumor. The counts and areas of tumor cells were maximum in the peritumorous zone in comparison with intact kidney tissue and central zone of the tumor. Analysis of correlations revealed a direct correlation between the tumor cell count in the peritumorous zone and some clinical morphological parameters of the tumor (anaplasia degree, size, presence of invasion and metastases, and angiogenesis). The count of mast cells in the renal peritumorous zone inversely correlated with 5-year survival: 100% cumulative 5-year survival in patients with mast cell count <6.7±1.6 per field of view.

Intracellular reorganization of mouse adrenocorticocytes after single whole body hyperthermia is determined by the two main events: development of the general adaptation syndrome and inhibition of the regeneratory plastic reactions in cells resultant from endotoxication and redistribution of plastic resources between organs and tissues. Stress-induced changes manifest in significant exhaustion of lipid droplets in the adrenocorticocytes of all adrenocortical zones, particularly in the zona fasciculata. Intracellular changes in adrenocorticocytes reflecting the development of regeneratory plastic insufficiency manifest in annular transformation of the nucleoli, segregation of the nucleolonema into granular and fibrillar components, intensification of autophagocytosis, and destructive changes in mitochondria and Golgi complex elements. The most pronounced changes were observed in adrenocorticocytes of the zona reticularis.

The morphogenesis of anthracycline-induced dilated cardiomyopathy was studied after single sublethal dose of doxorubicin. Cardiomyocyte depopulation (up to 27%) and decrease in their regeneratory plastic reactions were the main mechanisms of cardiac failure development after anthracycline (doxorubicin) treatment, determining the type of heart remodeling by the dilatation variant. Cardiomyocyte elimination and atrophy during the development of anthracycline-induced regeneratory plastic cardiac insufficiency were paralleled by hypertrophy of remaining cardiomyocytes and diffuse and small focal sclerosis of the myocardium, which could be regarded as a correlated compensatory reaction of the connective tissue to the decrease in the number of muscle fibers.

Effect of alkoxyamines on normal and tumor cells was studied in vitro and in vivo. In vitro experiments showed that alkoxyamines produce a dose-dependent toxic effect on cells of human breast tumor MCF7 line. Transplantation of Krebs-2 ascites carcinoma cells preincubated with alkoxyamines to mice did not induce tumor growth. An opposite effect was observed in normal mouse cells: functional activity of peritoneal macrophages increased. The possibility of using alkoxyamines as theranostic agents is discussed.

Ultrastructural changes in rat cardiomyocytes were studied after single administration of cyclophosphamide in the therapeutic dose. The major signs of cyclophosphamide-induced damage to cardiomyocytes included moderate lysis of myofibrils, dilation of vesicles in the granular and agranular sarcoplasmic reticulum, and destruction of mitochondria with the formation of myelin-like residual bodies. Ultrastructural changes in cardiomyocyte nuclei primarily manifested in variations of the shape, deep invaginations of the nuclear membrane, and translocation into the subsarcolemmal region.