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A Ia Gudkova

Publications and source records attributed to A Ia Gudkova.

8 recordsLinked to original sources
PubMed2005

[Phenomena of "micronucleoli" in cardiomyocytes from patients with idiopathic restrictive cardiomyopathy].

Silver staining was used to estimate structural and functional conditions of cardiomyocyte and stromal cell nucleoli in myocardium from 3 patients with idiopathic restrictive cardiomyopathy (RCM). We revealed a prominent increase in the amount of myocardial stromal component cells. The area of nuclei, the area and amount of nucleoli in cells of myocardial stromal component much varied. In some cells of myocardial stromal component we found nuclei, whose area was comparable with that of cardiomyocyte nuclei. In all patients we revealed cardiomyocytes with extranucleolar distribution of argentophilic substance in the nuclei. These data suggest an important pathogenic role of structural rearrangments in the nuclei of cardiomyocytes and stromal component cells in providing specific cell phenotype of myocardium in patients with idiopathic RCM. Extranucleolar (atypical) distribution of argentophilic substance in the nucleus, referred to as "micronucleoli", point out certain disturbances of nucleolar functions in cardiomyocytes in patients with RCM.

Adult↗
PubMed2004

[Apoptosis and heart disorders].

Papers on the significance of cardiomyocyte apoptosis in cardiovascular disorders development are reviewed. Some distinctive features of regulation and morphological manifestations of cardiomyocyte apoptosis are described. Although a great majority of cardiomyocytes are highly differentiated cells, apoptosis-related loss of cellular weight is noted in the number of pathological processes. Data on the role of apoptosis in myocardial ischemia in cardiomyopathies and in heart failure are presented.

Apoptosis↗
PubMed2003

[Elevated expression of argentophilic proteins from the nucleolar organizer regions in myocardium of patients with obstructive hypertrophic cardiomyopathy and mutations in p53 tumor suppressor gene].

Silver staining for nucleolar proteins was used to evaluate the ribosomal genes activity in cardiomyocytes (Cm) and fibroblast-like cells (FBS) of intraventricular septum, and other regions of the left ventricle. Specimens to be analysed were taken from 7 patients with idiopathic obstructive hypertrophic cardiomyopathy (OHCM). In this group the quantity of nucleoli and AgNORs, reflecting the transcriptional and processing level of pre-ribosomal RNA in all type of cells, was at least 2 and 3 times higher than in patients with essential hypertension and in healthy control, respectively. We suggest that nucleolar hypertrophy in patients with hypertrophic cardiomyopathies, inappropriate to hypertrophy in other pathological conditions, may be most probably of compensatory character, and this may be in part explained by nuclear hyperploidy and chromosomal endoreduplication. We have noted a marked heterogeneity in shape, size and quantity of nucleoli, and in AgNORs of FBC. Nuclei with modulated phenotype containing nucleoli of high activity were revealed. This article presents the first data on p53 mutation identification in patients with advanced OHCM.

Adult↗
PubMed1989

[Activity of the nucleolar organizers in cardiomyocytes of patients with arterial hypertension of varying genesis].

A comparative study of the myocyte nucleolar organizer activity (NOA) was performed on silver-stained myocardium from 6 patients who had died from the hypertension disease and 7 others patients with secondary renal hypertension non-complicated by severe coronary atherosclerosis and heart failure. In the first group, positive correlations between NOA of cardiac cells and the level of maximal diastolic pressure (r = 0.8, p less than 0.028), wall thickness of the left ventricle (r = 0.8, p less than 0.028) as well as myocardial weight (r = 1.0, p less than 0.001) were found. In the second group, on the contrary, there was a pronounced negative correlation between NOA of the myocytes and myocardial weight (r = -0.86, p less than 0.005) which may be explained partially by a primary metabolic myocardial deficiency in such patients.

Adult↗