Publications by authors named "Varakuta E"

Wound healing of the oral mucosa is an urgent problem in modern dental surgical practice. This research article presents and compares the findings of the investigations of the structural, physicochemical, and biological characteristics of two types of polymeric membranes used for the regeneration of oral mucosa. The membranes were prepared from poly(tetrafluoroethylene) (PTFE) and a copolymer of vinylidene fluoride and tetrafluoroethylene (VDF-TeFE) and analyzed via scanning electron microscopy, atomic force microscopy, X-ray diffraction analysis, and Fourier transform infrared spectroscopy.

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We studied restoration of microvessels in the oral mucosa wound defects under a polymer piezoelectric membrane (group 2) and without it (group 1). The control group included animals with intact mucosa. On day 3, the expression of the vascular endothelial growth factor (VEGF) increased in all experimental groups, while the expression of CD34 increased only in group 2, which attested to intensive neoangiogenesis.

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The numerical density of secretory granules dense-core vesicles (DCV) in the cytoplasm of pinealocytes of the pineal gland was estimated by transmission electron microscopy in male white mice and Wistar rats. The 3-day biorhythm and lunaphase changes in the DCV content in the perikaryon and the processes of pinealocytes, which are manifested significantly in different seasons of the year, are established. The three-day biorhythm in adult male mice in comparison with younger male rats is not expressed uniformly in different phases of the moon.

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Structural changes of eye chorioretinal complex were investigated in 40 adult male outbred albino rats after total transient cerebral ischemia using electron microscopy and morphometric analysis. Furthermore, the influence of a new sterically hindered phenolic antioxidant dibornol on these processes was estimated. Our studies demonstrated that total transient cerebral ischemia in rats resulted in the capillary thrombosis of the choriocapillary lamina of the uvea, structural disturbances of the blood-retinal barrier, degeneration of the retinal neurons and radial glia.

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Along with microangiopathy, one of the main causes of blindness in diabetic retinopathy consists of degeneration of retinal neurons. Electron microscopy and morphometric analysis were used to study structural changes in neurosensory cells, associative, and ganglion neurons in the retina in 30 while mongrel male rats with streptozotocin diabetes for two months and the effects of a new semisynthetic antioxidant 4-methyl-2,6-diisobornylphenol, a screened phenol, were evaluated. Destructive changes were found to affect the outer segments of neurosensory cells and ganglion neurons.

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Changes in contacts between neurons in the internal reticular layer of the retina were studied in white rats 7 and 30 days after exposure to high-intensity light. Osmium preparations on day 7 demonstrated synapse destruction, predominantly of the "light" type of. Contrasting with phosphotungstic acid was used to study juxtamembrane formations of the system of subsynaptic units, i.

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Along with microangiopathy, degeneration of retinal neurons is one of the basic causes of blindness in patients with diabetic retinopathy. Using the electronic microscopy and morphometric analysis, the structural changes of neurosensory cells, associative and ganglionic retinal neurons were studied in 30 albino outbred male rats with long term (2 months) streptozotocin diabetes and the effect of a new semisynthetic antioxidant belonging to a group of strictly hindered phenols (4-methyl-2,6-diisobornylphenol) on these parameters was evaluated. In diabetic rats, the destructive changes of external segments of neurosensory cells and ganglionic retinal neurons were found.

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The changes of interneuronal contacts in the internal reticular layer of albino rat retina were studied 7 and 30 days after the exposure to high intensity light (6000 Lux for 6 h). In osmicated preparations, the "light" type of synapse destruction was predominant 7 days after the light-induced damage. Using the contrasting by phosphotungstic acid, paramembrane structures of the system of subsynaptic units--dense projections and postsynaptic condensations of synapses--were studied.

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The outer part of the blood-retina barrier was most sensitive to light exposure (6000 lx, 6 h) during photodamage. It was manifested in hemodynamic disturbances, endothelial dysfunction, and focal death of the pigment epithelium. The photo effects increased during alloxan diabetes.

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Light exposure (6000 lux, 6 h) caused reactive changes in rat retinal pigmented epithelium and radial glia on day 1. Foci of lesions with virtually complete absence of the layers formed by neurosensory cells appeared on day 7. The number of destructively changed radial gliocytes in these foci was by one order of magnitude higher than in the control.

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Experiments on rats showed that high-intensity light exposure (6000 lux, 6 h) caused focal injuries in the retina. The most sensitive structures were neurosensory cells, pigmented epithelium, radial gliocytes, and choroid capillaries. Injection of ascovertin led to disappearance of foci of injuries, limited blood supply disorders in the retina, and destruction of neurosensory and glial cells.

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The experiments on white mongrel rats showed that the light with the intensity of 6000 1x lasting for 6 hours resulted the destruction of the retinal pigment epithelium, of the internal and the external neurosensory cellular processes with subsequent nuclei piknosis and radial glia replacement. On the 7th day after exposure to light focal effusion of the retina corresponding layers. Under the irradiation in diabetes the amount of cells with karyopyknosis increases in 1.

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The present study was conducted to determine the role of blood mononuclear cells in a morphogenesis of proliferative vitreoretinopathy (PVR) and to detect the peculiarities of PVR development in hyperglycemia. Experiments were performed in 75 mature male Wistar rats. In animals of group 1, the model of PVR was reproduced by injection of mononuclear cells into the corpus vitreum.

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The continuous irradiation of rats with a light (3500 1x) for 48 hours led to destruction of 7.5 +/- 0.43% of neurosensoric cells (the control value was 0.

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Exposure to high-intensity light led to pronounced destructive changes in the retina and focal loss of layers formed by neurosensory cells in rats. Photoinjury led to progressive decrease in the numerical density of nuclei in the outer nuclear layer (by 30% after 2 days, by 75% after 1 week, and more than by 90% after 2 weeks of exposure). After 30 days the photosensory layer completely disappeared, while the outer nuclear layer was presented by solitary nuclei of neurosensory cells.

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