No abstract

The need to intensify milk production urgently dictates the need to continue research on the physiology of cattle of any age. It is customary to attach great importance to blood, consisting of uniform elements and plasma, constantly circulating through the vessels. It provides gas exchange, metabolism and the delivery of hormones and bioregulators in their tissues. The success of hemocirculation strongly determines the completeness of the realization of the genetic growth potential and productivity of the animal and is closely related to the activity of aggregation of blood cells. Purpose: to find out the activity of aggregation of the main formed elements of the blood in newborn calves. The work was carried out on 32 newborn calves of black-motley breed, born of healthy cows after 2-3 pregnancies. The calves were examined on 1-2, 3-4, 5-6, 7-8 and 9-10 days of life. In the work, hematological and statistical research methods are applied. For newborns in calves, a tendency towards increased aggregation activity of red blood cells was revealed. This was combined with a low platelet aggregation, which tended to increase. The low aggregation of neutrophils in these calves also gradually increased. In newborn calves of optimal physiological status, there is a tendency to increase the aggregation of the main formed elements of the blood, which is a response to environmental influences.

We studied population polymorphism of active nucleolar organizing regions in residents of the Kursk region and the association of activity of chromosomal nucleolar organizing regions with intensity of the synthesis of erythrocyte membrane protein. We revealed a tendency towards increasing of the amount of the major erythrocyte membrane proteins (primarily, spectrins and band 5 protein) with increasing total transcriptional activity of nucleolar organizing regions of chromosomes. The intensity of protein synthesis affects cell proliferation, determines the rate of tissue growth and its function, which determines its participation in the development of various diseases.

No abstract

Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.