Based on the comparative complex neuromorphological, morphometric and histochemical studies of ganglia of intermuscular plexus multichamber stomach (its departments: the rumen, reticulum, omasum and abomasum) of lambs of edilbaev’s breed located on the induction effect with ewes (control group) and bottle-fed sheep milk substitute (ZOM) Colvo-Start (experience) of adaptive-compensatory changes in the nervous tissue of the organ are set. Adapting to artificial feeding is manifested in the dairy phase (15 days), a decrease in the growth potential of the main population nerve-cell ganglia scar delayed cytodifferentiation in the ganglia of the grid and of rennet, the asynchronous nature of cell differentiation in a medium-sized portion of the stomach, which leads to increased morphological and functional heterogeneity of the nervous tissue of the stomach multicam . Adaptive-compensatory changes are associated with the hypertrophic growth of large neurons, a decrease in their content in the ganglia, change neuro-glial relations, increased ferningdendro-axonal tree and subsequent to the period of transition to the definitive animal feed, reduction of secondary branching dendrites. Changes due to the changing nature of breastfeeding are a reflection of the complex and dynamic processes of compensatory adaptation, which is peculiar to the entire nervous system as a whole, which has a high potency for self-regulation.
Hydronephrosis refers to diseases of the urinary system, which are characterized by high prevalence. Moreover, this pathology of all obstructive uropathies, leading to a decrease in the function of the renal parenchyma, accounts for up to 15% of cases. Therefore, the search for various markers involved in the development and progression of kidney damage is particularly relevant, since in the literature there are very contradictory data. Our article presents the results of a survey of 40 patients with established and confirmed diagnosis of stage I hydronephrosis (according to the classification of N. A. Lopatkin), and 20 completely healthy people (control group). All patients initially and at the end of the study determined the levels of cytokines: IL-1a, IL-1b, IL-1ra and G-CSF. We found that patients with hydronephrosis had higher rates of pro-inflammatory components of the IL-1β system: IL-1β — 104.42 (75% CI [111.8–151.4]) pg/ml, which was significantly higher than in the control group 3.7 times. In patients with hydronephrosis, there is an increase in the levels of IL-1β, IL-1a, and G-CSF against the background of a decrease in IL-1ra. The study of the IL-1 and G-CSF systems in dynamics during hydronephrosis is a very promising direction, opening up enormous opportunities in creating effective diagnostic markers of hydronephrosis in the very early stages of the formation of this pathology. Thus, analysis of the literature indicates that damage to the renal tissue in obstructive uropathies is an extremely complex process, and the initiation of fibrogenesis processes with partial inhibition of resorption leads to remodelling of connective tissue and progression of nephrosclerosis.
Purpose: to study ischemic depolarization in focal cerebral ischemia in rats.Materials and methods. We conducted simulations of focal cerebral ischemia in 30 rats. The animals were divided into three groups: 1) normothermia (n = 10), 2) hypothermia (n = 10), 3) hyperthermia (n = 10). We identified a statistically significant correlation between the animal's body temperature and the number of episodes of depolarization. (r = 0,87, p<0,001). The average number of DC potential deviations in animals with hyperthermia was statistically significantly higher than in animals with normothermia. (p<0,05).Results. Tissue damage as a result of focal cerebral ischemia correlates with body temperature fluctuations. A decrease in body temperature in focal cerebral ischemia leads to a decrease in the size of the ischemia zone, and as a result of a cerebral infarction, and vice versa, a slight increase in body temperature leads to an increase in the area of cerebral infarction.Conclusion. On tissue, temperature fluctuations have physiological and biochemical effects, a statistically significant correlation between episodes of depolarization in cerebral ischemia and the percentage of brain damage after ischemia are not always in a cause-and-effect relationship.
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