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Biomedical subjects

A M Aref'eva

Publications and source records attributed to A M Aref'eva.

At least 19 recordsLinked to original sources
PubMed2006

[Markers of inflammation--monocyte chemoattractant protein-1 (MCP-1) and C-reactive protein--in blood of patients with unstable angina pectoris and stable effort angina].

AIM: To estimate concentrations of C-reactive protein (CRP) and MCP-1 in blood plasma of patients with unstable angina (UA) and stable effort angina (SEA). MATERIAL AND METHODS: Multiprojection coronaroangiography was performed in 12 patients with UA and 11 patients with SEA. Hemodynamically significant stenosis (50% and more) at least in one major coronary artery was confirmed in all the patients. CRP and MCP-1 were measured with latex agglutination and enzyme immunoassay (Biosource kits), respectively. RESULTS: UA patients had significantly higher plasma levels of MCP-1 and CRP than those with SEA (107.25 +/- 16.19 vs. 63.0 +/- 16.16 pg/ml and 1.99 +/- 1.64 vs 0.44 +/- 0.28 mcg/ml, respectively). CONCLUSION: Estimation of MCP-1, as a marker of vascular wall inflammation, can be used, in line with other indices, for verification of UA.

Acute Disease↗
PubMed2003

[Effect of matrix composition on chemotaxis response of monocytes stimulated by monocyte chemoattractant protein-1].

MCP-1-stimulated chemotaxic response of monocytic cell line THP-1 and peripheral blood monocytes were investigated through extra cellular matrix proteins fibronectin, fibrinogen and fibrinogen degradation products. Cellular migration was significantly decreased in the presence of fibrinogen as compared with fibronectin. Fibrinogen proteolysis with plasmin generating D and E degradation products, resulted in increase of the chemotaxic response.

Cell Line↗
PubMed2001

[The role of Mac-1 and ICAM-1 molecules in adhesion of cells on fibronogen and its degradation products].

Monocytic cell adhesion to immobilized fibrinogen and fibrinogen degradation products, and involvement of integrins Mac-1 and immunoglobulin-like ICAM-1 adhesion molecules in these processes were investigated. Fibrinogen cleavage with plasmin down-regulated adhesion of cells with predominant Mac-1 expression; in contrast, the attachment of ICAM-1-expressing was up-regulated. By means of function-blocking anti-Mac-1 and anti-ICAM-1 antibodies, and immobilization of known fibrinogen degradation products, it was shown that Mac-1 molecules mediated cell adhesion predominantly to fibrinogen, and its early degradation products, fragments X and Y, while ICAM-1 participated in cell attachment to X- and Y-fragments, rather than to intact fibrinogen or late degradation products, fragments D and E.

Cell Adhesion↗
PubMed1992

[Myocyte polyploidy in human cardiac pathology].

With general atherosclerosis, the ploidy of left ventricle myocytes in the hearts of patients that underwent infarction corresponds to the norm variation irrespective of the ventricle and heart weights. At heart diseases the myocyte nucleus ploidy is often much higher than the norm variability both in hypertrophied ventricles and in those with normal weight. An additional polyploidization is suggested that may occur at some natural ontogenetic periods of human development (in the childhood) during heart diseases both innate or spontaneously appearing at the particular time. Unlike, the myocardial hypertrophy in adults does not stimulate myocyte polyploidy.

Cardiomegaly↗
PubMed1992

[Ploidies of cardiomyocytes in human myocardial hypertrophy].

DNA cytophotometry has been performed in ventricular cardiomyocytes of hypertrophic human hearts. In the cases of hypertrophy in adults (generalized atherosclerosis, postinfarct scars), polyploidy expression did not exceed the limits of normal variability developed during childhood. In the cases of hypertrophy caused by congenital heart defects, high polyploidy has been revealed (the mean level 20c and more, where c is haploid DNA content), which considerably exceeded the upper limit of normal variability (approximately 10c). Our hypothesis has confirmed that heart hypertrophy in adults proceeds in conditions of stable genome rather than due to redundant polyploidization of the ventricular myocytes. The same idea assumes enhanced polyploidization of the myocytes in childhood in humans with congenital heart diseases.

Adult↗
PubMed1989

[The ploidy variability of human cardiomyocytes].

Unlike literature on ploidy of the human myocytes, DNA content and the number of nuclei have been revealed in the same cells. Besides, the cell ploidy were studied separately in the external, central and inner regions in the left ventricule. Considerable binucleation was revealed in normal and hypertrophic ventricles where 4c X2 was the modal cell class and there were 2c X 2, 8c X 2 and single 16c X 2 cells. Two alternative assumptions have been put forward concerning the genome differences: 1) myocytes enter in mitotic cycle under pathologic conditions or 2) the difference causes in genuine variability of the ploidy classes in normal hearts.

Adolescent↗
PubMed1988

[The ratio in the DNA content and protein mass of human cardiomyocytes].

DNA and total protein content were measured in human cardiac myocytes using cytophotometry of Feulgen-naphthol yellow stained cells isolated from the left ventricle. The percentage of DNA classes was 2%, 32%, 53%, 12% and less than 0.5% for diploids, tetraploids (both 4c and 2c X 2), octaploids (8c, 4c X 2 and 2c X 4), hexadecaploids (16c, 8c X 2 and 4c X 4) and 32c cells, respectively. Binuclear cells comprised about 65% of the myocytes; the main class was 4c X 2. A discrepancy between total protein content and gene dose has been pointed out. DNA level ratio in a number of myocytes of different ploidy were 2:4:8:16:32; the same ratio for total protein content was 2:3.5:6:11.4:25.5, respectively.

Adult↗
PubMed1985

[Change n the ploidy classes of left ventricular myocytes in rats after ligation of the left coronary artery].

Heterogeneous response of cardiomyocytes in left atria of rats to ligation of the left coronary artery was observed. Ploidy may greatly increase reaching 32 c per cell. More than 90% of myocytes are normally mononuclear diploid cells, while after the ligation the number of such cells diminishes to 10%. The majority of cells become polyploid: above 50% of cells are 2 X 2 c ploid, about 30% of cells are 4 X 2 c ploid and a great number of cells are highly ploid.

Animals↗
PubMed1983

[Measurement of the absolute cell count in the heart and liver. The quantitative preservation of proteins and DNA in isolated cells].

Some improvement has been made of the Belov et al. (1975) method of alkaline dissociation of tissues. No cell loss occurs during cell suspension preparation or other procedures. The improved method was shown to be suited for determination of absolute numbers of cardiomyocytes and hepatocytes. Comparison of the living and dissociated hepatocytes revealed preservation of the total cell dry weight and DNA content (classes of ploidy) in the cells treated with formol and concentrated alkali. The method is recommended for studying the cell number, weight, ploidy and mitoses, and for DNA autoradiography.

Animals↗
PubMed1983

[Number and mass of the myocytes of the mouse heart].

The mean number of cardiomyocytes is constant in the heart ventricles of 1, 1.5-2, 3-4, 5-6 and 12-month old mice. However, differences in the myocyte number among mice of the same age and with similar heart weight may reach 30%. There are only small differences in the mean ploidy among these mice. The mean protein content in the myocytes correlates to the ventricle weight. In some mice, however, no correlation was observed between the myocyte and ventricle weights, or between the calculated dry and wet weights of myocytes.

Aging↗
PubMed1983

[DNA and protein in the postnatal growth of mouse cardiomyocytes].

DNA and protein were measured in the cell on bicolour smears stained with the Feulgen reagent and with Naphtol yellow S. The mean protein quantity and histograms are the same for mononuclear and binuclear myocytes with the same ploidy. The growth rate of these cells is also the same. A discrepancy is revealed between the protein content and the gene dosage in growing myocytes: doubling of ploidy was not followed by a corresponding increase in the amount of protein.

Animals↗
PubMed1982

[Growth of cardiac muscle cells during rat adaptation to altitude hypoxia].

The weight of the right heart ventricle in 1.5-month-old rats kept after birth in the mountains of 3400 m altitude is higher and its muscle cell cytoplasm mass is much larger compared to those in 1.5-month-old animals raised at 800 m altitude. The hypertrophy of cells is not due to their polyploidization. Only a small increase in the relative number of polyploid cells takes place under high altitude hypoxia. The weight of the right ventricle and myocyte mass in 3-month-old rats kept 1.5-3 months after the birth at 3400 m altitude also increases, although this augmentation is significantly less than in the animals grown in the mountains for 1.5 months immediately after the birth. The myocyte ploidy of adult animals adapted to hypoxia does not essentially differ from that of 1.5- and 3-month-old control rats: about 80 per cent of these cells are polyploid. Thus, the growth of cardiac myocytes under the heart hyperfunction in the case of high altitude hypoxia proceeds mainly on the ground of the stable polyploid genome, as well as normal ontogenetic growth of these cells.

Adaptation, Physiological↗
PubMed1978

[Cytophotometry of DNA in isolated mouse heart myocytes].

Submicroscopic structure of parenchymatous cells was investigated in the liver of rats given CCL4 (0.12 ml/100 g body wt) for 25 days. After cessation of this treatment the animals were subjected to the action of extreme stimulants (immobilization or overheating under sunlight or both). CCL4 poisoning led to the appearance of many lipid incorporations in the cytoplasm of hepatocytes serving as the basis for fat infiltration in the liver. The action of extreme factors was followed by accumulation of lipids in the lumina of the granular cytoplasmic reticulum never found in any other pathological conditions, and apparently reflecting profound disturbances of intracellular metabolism.

Animals↗
PubMed1976

[DNA content in the Purkinje cells of the rat cerebellum spontaneously infected with Kilham virus].

The DNA content in the cerebellum Purkinje cells of rats naturally contaminated with the Kilham virus and in the animals, in which no infection was observed, was determined cytospectrophotometrically on the Feulgen-stained preparations. The incidence of the cells with hyperdiploid nuclei was shown to be equal in the groups compared. It was concluded that the nonmultiple increase of the DNA content in the Purkinje cells of rat cerebellum was apparently unrelated to the virus infection.

Animals↗
PubMed1975

[Fluctuations in amino acid-H3 incorporation into the proteins of the isolated retina].

The rate of amino acid incorporation into the mouse retina proteins was measured in dynamics of dark adaptation and at different terms of their stimulation by light. It was found that variations in dry weight of the ganglion retinal cells and in the incorporation of amino acids into their proteins occurred rhythmically, with the period of about one hour.

Amino Acids↗