Search PubMed⌕ Search

Biomedical subjects

Z A Gabbasov

Publications and source records attributed to Z A Gabbasov.

At least 19 recordsLinked to original sources
PubMed2005

Detection of circulating stromal stem cells with osteogenic potential in the blood of coronary patients by laser flow cytometry.

The number of cells expressing antigen to osteonectin was appreciably increased in the blood of coronary patients, but no cells of this kind were detected in donors. The number of CD34+ stem cells in these patients virtually did not differ from that in normal subjects. A close relationship between atherosclerosis development and presence of stromal stem cells with osteogenic potential in the blood is hypothesized.

Antigens, CD34↗
PubMed2000

[Platelet aggregation in patients with hypertrophic cardiomyopathy].

AIM: To examine correlation between platelet aggregation and the degree of left ventricular hypertrophy (LVH) in patients with hypertrophic cardiomyopathy (HC). MATERIAL AND METHODS: Routine clinical examination, ECG, echo-CG, measurement of platelet aggregation, routine biochemical blood tests were made in 45 HC males and 15 healthy controls. RESULTS: HC patients were characterized with high induced and spontaneous platelet aggregation which increased with left ventricular myocardial mass. In LVH, platelets were especially sensitive to the aggregation inductor U-46619, thromboxane A2 analogue. CONCLUSION: It is demonstrated that there is a positive correlation between platelet aggregation and the degree of LVH in HC patients.

Cardiomyopathy, Hypertrophic↗
PubMed2000

[Platelet aggregation in patients with various forms of left ventricular hypertrophy and its changes at long-term follow-up and treatment].

AIM: To study platelet aggregation (PA) in patients with left ventricular hypertrophy (LVH) in essential hypertension (EH) and hypertrophic cardiomyopathy (HTCM), and to assess aspirin treatment effects. MATERIAL AND METHODS: A general clinical examination, echocardiography, 24-h monitoring of ECG and arterial pressure, bicycle exercise, test for platelet aggregation, routine blood biochemical tests were performed in 30 males with EH and LVH, 30 males with HTCM and 10 healthy controls. RESULTS: It was found that the patients had high platelet sensitivity to aggregation inductors as well as high spontaneous aggregation. LVH severity correlated positively with activation of spontaneous and induced platelet aggregation. This dependence is unrelated to arterial pressure or the disease duration. Patients with episodes of silent myocardial ischemia had a more pronounced rise in spontaneous and induced platelet aggregation than those without silent ischemia. A long-term administration of aspirin significantly lowered spontaneous and induced platelet aggregation, depression of ST segment. The above changes occurred both in HTCM and in hypertensive patients with LVH. CONCLUSION: Platelet aggregation correlates with severity of LVH and episodes of silent myocardial ischemia both in patients with hypertension, LVH and HTCM.

Aspirin↗
PubMed1998

[Determination of the activity of Willebrand's factor by laser analyzer of platelet aggregation].

A modification of von Willebrand' factor/ristocetin cofactor activity test is proposed. Agglutination of formalin-treated platelets is monitored in the aggregation analyzer from changes in the light transmission in the specimen. The test is sensitive and reproducible. It is intended for clinical laboratories to be used in patients with hematological diseases and the endotheliopathy syndrome of different etiology.

Hemagglutination↗
PubMed1994

[The functional characteristics of the thrombocytes in patients with hypertension and "silent" myocardial ischemia].

Functional platelet characteristics were studied in hypertensive subjects having episodes of silent myocardial ischemia. A total of 36 patients with essential hypertension (EH) stage II (WHO criteria, 1979) underwent echocardiography and 24-h ECG monitoring. Platelet aggregation induced by adenosine diphosphate was assessed by laser aggregation analyzer. It is demonstrated that platelet aggregation in EH patients with silent ischemia was increased 5-fold as compared to healthy subjects and 2-fold versus EH patients without ischemia. No significant differences existed between the two groups by such parameters as systolic or diastolic pressure and left ventricular myocardial mass. An involvement of elevated platelet aggregation can be suggested in the genesis of coronary insufficiency in EH associated with episodes of silent myocardial ischemia.

Analysis of Variance↗
PubMed1992

Three types of naturally occurring modified lipoproteins induce intracellular lipid accumulation due to lipoprotein aggregation.

Low density lipoprotein (LDL) from patients with coronary atherosclerosis and diabetes mellitus as well as in vitro desialylated LDL, glycosylated LDL, and lipoprotein (a) caused a twofold to fourfold rise in cholesteryl ester in cultured human blood monocytes and intimal smooth muscle cells isolated from normal aorta. Native LDL from healthy subjects failed to induce intracellular lipid accumulation. We have demonstrated by laser correlative photometry and gel filtration chromatography that in vivo and in vitro modified lipoproteins form aggregates under cell culture conditions. The degree of modified lipoprotein aggregation directly correlated with the ability of these lipoproteins to elevate the cholesteryl ester content of cultured cells. Modified lipoprotein aggregates isolated by gel filtration induced a threefold to fivefold elevation in cellular cholesteryl ester content. Aggregates of 125I-modified LDL were taken up and degraded fivefold to sevenfold more effectively as compared with nonaggregated lipoproteins. The uptake and degradation of 125I-labeled aggregates were strongly inhibited by unlabeled aggregates, latex beads, and cytochalasin B but not by native or acetylated LDL. These data indicate that uptake of lipoprotein aggregates occurred by phagocytosis. Obtained results suggest that modified lipoprotein aggregation may be the key condition for lipid accumulation.

Cells, Cultured↗
PubMed1992

Three types of naturally occurring modified lipoproteins induce intracellular lipid accumulation in human aortic intimal cells--the role of lipoprotein aggregation.

Blood monocytes or intimal smooth muscle cells from normal aorta were incubated with low density lipoprotein (LDL) from patients with coronary atherosclerosis, or with LDL from diabetic patients, or with lipoprotein(a) (Lp(a)). In each case there was a 2- to 4-fold rise in the intracellular cholesteryl ester content. LDL from healthy subjects failed to induce intracellular lipid accumulation in these cells. LDL from patients with coronary atherosclerosis, LDL from diabetic patients, and Lp(a) form aggregates under cell culture conditions. The ability of these lipoproteins to increase the cholesteryl ester content of cultured cells is directly correlated to the degree of lipoprotein aggregation. When aggregates were removed from the lipoprotein preparations by filtration, the latter became less effective in promoting intracellular lipid accumulation. Incubation of cells with lipoprotein aggregates, isolated by gel filtration, induced a 3- to 5-fold elevation of the cellular cholesteryl ester content. These results suggest that LDL from atherosclerotic patients, or LDL from diabetic patients, or Lp(a) have a tendency to form aggregates and that these aggregates are avidly taken up by intimal smooth muscle cells followed by lipid accumulation. This aggregation tendency may play a role in atherogenesis.

Aorta↗
PubMed1992

Multiple-modified desialylated low density lipoproteins that cause intracellular lipid accumulation. Isolation, fractionation and characterization.

BACKGROUND: The basic differences between sialylated (sialic acid rich) and desialylated (sialic acid poor) human low density lipoproteins (LDL) are not fully defined. It is not known whether there are any differences in the LDL composition of coronary atherosclerosis patients and healthy individuals. EXPERIMENTAL DESIGN: Sialylated (45 to 94% of total LDL) and desialylated (6 to 55%) LDL were separated by affinity chromatography on Ricinus communis agglutinin-agarose, and their chemical composition and physical properties were examined. RESULTS: Sialic acid contents in sialylated LDL fractions of healthy subjects and patients were the same and 1.5 to 3-fold higher than in desialylated LDL. Desialylated LDL had smaller sizes and greater electrophoretic mobility than sialylated ones. Desialylated, but not sialylated LDL, induced 1.5- to 4-fold accumulation of neutral lipids in human aortic smooth muscle cells and human blood monocytes. Subfractions of desialylated LDL containing lower amount of sialic acid revealed higher ability to accumulate lipids in cultured cells. Desialylated LDL contained lower amounts of cholesteryl esters, free cholesterol and triglycerides as compared with sialylated LDL. On the other hand, concentration of di-, monoglycerides and free fatty acids in desialylated LDL was 2 to 3-fold higher than in sialylated lipoproteins. Desialylated LDL fraction was characterized by lower levels of phosphatidylcholine, sphingomyelin, phosphatidylethanolamine, but higher content of lysophosphatidylcholine. Freshly isolated sialylated and desialylated LDL contained equal amounts of thiobarbituric acid reactive substances, but oxidation of desialylated LDL was more pronounced in presence of Cu(2+)-ions. Desialylated LDL had higher level of oxysterols and lower amounts of vitamin A and E. Content of free amino groups of lysine in desialylated LDL of patients was 2-fold lower than in sialylated LDL. This difference was partially due to masking of amino groups caused by conformational change in the tertiary structure of apolipoprotein, partially to chemical modification of amino groups. When subfractionated by density gradient ultracentrifugation, desialylated LDL was represented by higher density particles than sialylated LDL. Sialic acid content in desialylated LDL subfractions decreased with rise of lipoprotein density. Higher density desialylated LDL and in less extent sialylated LDL contained smaller amounts of free and esterified cholesterol and phospholipids. Only the densest subfractions of desialylated LDL from healthy subjects caused intracellular lipid accumulation. Ability of patients' desialylated LDL to accumulate cholesterol in cells increased with particle density. CONCLUSIONS: Extensive biochemical and biophysical analysis performed in this study shows that desialylated LDL differ from these sialylated LDL in many respects. The LDL of coronary atherosclerosis patients differ from those in healthy individuals in several parameters.

Adult↗
PubMed1991

[ADP-induced thrombocyte aggregation in hypertension patients with different degrees of left ventricular hypertrophy].

Adenosine diphosphate (ADP)-induced platelet aggregation was studied in 59 patients suffering from essential hypertension, stages I and II (WHO, 1979) with different degree of left ventricular hypertrophy (LVH) by a new optical method. Using a laser aggregation analyzer the mean aggregate radius was measured in relative units. The left ventricular myocardial mass was estimated by echocardiography. Using laser aggregatograms the significant differences in aggregation responses were revealed with 0.5 microM ADP. In a group of patients without LVH, the aggregation response to 0.5 microM ADP did not differ from that in a group of healthy volunteers. With the growth of LVH from moderate to severe the response increased in succession. The same differences which were not, however, significant were observed with higher ADP concentrations. It was also found that the new method of laser aggregometry is more sensitive than the classic Born method.

Adenosine Diphosphate↗
PubMed1990

[Aggregates of modified low density lipoproteins indicate accumulation of lipids in human aortic intima cells in vitro].

Spontaneous aggregation of glycosylated, desialated, oxidized and malondialdehyde modified low density lipoprotein (LDL) as well as LDL of coronary heart disease patients has been discovered using methods for determination of light transmission fluctuations in suspensions and gel filtration. At the same time; LDL of healthy donors failed to aggregate under conditions of cellular culture. On the other hand, human aortic cells from unaffected intima incubated with modified LDL, but not native LDL of healthy donors, showed a rise in esterified cholesterol levels. There was a strong correlation between the degree of LDL aggregation and intracellular cholesterol ester accumulation (r-0.86, p 0.001, n-21). Removal of aggregates by passing preparations through and 0.1 um filter significantly inhibited the accumulation of cholesterol esters. The obtained data point to the essential, if not decisive, role of LDL aggregation in the processes of lipid accumulation by intimal cells in vitro.

Aorta↗
PubMed1989

Lipoprotein aggregation as an essential condition of intracellular lipid accumulation caused by modified low density lipoproteins.

We have tested a hypothesis that aggregates of modified low density lipoproteins (LDL) play the key role in the accumulation of lipids by cells of unaffected aortic intima. It was demonstrated using analysis of relative dispersion of light transmission fluctuations as well as gel filtration on Sepharose CL-2B that LDL modified by oxidation, glycosylation, desialylation and malondialdehyde treatment form aggregates under the conditions of culture. Native LDL failed to aggregate under the same conditions. It was demonstrated that modified LDL, unlike native LDL, bring about a 2- to 3-fold rise in cholesteryl ester levels of cultured cells. Moreover, direct and strong correlation (r = 0.86) was observed between the degree of lipoprotein aggregation and the amount of cholesteryl esters accumulated. Removal of modified LDL aggregates by filtration through a 0.1 micron filter or gel filtration completely prevented the intracellular accumulation of cholesteryl esters. These findings indicate that LDL aggregates play an essential, if not the decisive, role in the intracellular accumulation of lipids in vitro.

Aorta↗
PubMed1989

Platelet aggregation: the use of optical density fluctuations to study microaggregate formation in platelet suspension.

A new approach to the investigation of microaggregate formation kinetics in platelet suspension is described. The method is based on the analysis of light transmission fluctuations produced by the changes in the number of platelets in optical channel. The relative dispersion of such fluctuations (D) was used as a parameter to estimate the degree of platelet aggregation and to analyze the aggregation kinetics. It was found that a continuous recording of this parameter allows to detect microaggregate formation during spontaneous aggregation and aggregation induced by very low concentrations of ADP (0.05-0.15 uM) in platelet-rich citrate plasma. When 3-10 uM ADP was added to acid citrate-dextrose anticoagulated plasma at pH 6.5, microaggregate formation was detected by increase in D, whereas light transmission decreased by 15-20%. Analysis by scanning electron microscopy and the use of standard inhibitors of aggregation confirmed that in all these cases the microaggregate formation did take place.

Adenosine Diphosphate↗
PubMed1989

[A new highly sensitive method of analysis of thrombocyte aggregation].

The new method for studies of the platelet aggregation kinetics is based on the creation of a platelet stream through the optic canal and on an analysis of fluctuations in the intensity of the luminous flux that has passed through the sample. The relative dispersion of fluctuations in the intensity of the light passed through the sample is suggested as a parameter for the estimation of the platelet aggregation and for analysis of their aggregation kinetics. The method permits recording the platelet aggregation in citrate plasma, enriched for platelets, after exposure to the inductor in very low concentrations (0.05-0.15 microM ADP). Scanning electron microscopy has shown that aggregates are indeed formed in such cases, and they can be recorded from the increase of the relative dispersion in the fluctuations in the passed light intensity but cannot be recorded by Born's optic method.

Adenosine Diphosphate↗