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Biomedical subjects

M Bihari-Varga

Publications and source records attributed to M Bihari-Varga.

At least 19 recordsLinked to original sources
PubMed1992

Lp(a) and the risk of coronary heart disease.

A screening study was performed on 106 children with familial risk for coronary heart disease (CHD) and on matched controls. The two groups differed in several parameters. Children of CHD patients exhibited significantly elevated levels of Lp(a) and total cholesterol, reduced HDL apo A1 and apo A2 and increased values of serum hexuronic acid. These results support the concept that genetic and familial factors contribute to the risk of atherosclerosis.

Adolescent↗
PubMed1992

Elastase-type enzymes and their relation to blood lipids in atherosclerotic patients.

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In a further 24 patients with acute myocardial infarction elastase activity, inhibitory capacity and lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower and inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2-cholesterol as well as apo A concentration showed significant negative correlation with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2-concentrations decreased significantly in the first 3 weeks, than gradually approached the initial values. In the patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.

Adult↗
PubMed1991

[Serum elastinolytic activity and blood lipids in various clinical forms of arteriosclerosis and in acute myocardial infarct].

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In further 24 patients with acute myocardial infarction dynamics of elastase activity, inhibitory capacity and of lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower, inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2 cholesterol and apo-A concentrations showed significant negative correlations with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2 concentrations decreased significantly in the first 3 weeks, then gradually approached the initial values. In the subgroup of patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.

Arteriosclerosis↗
PubMed1991

Lipoprotein (a) concentrations as risk indicators for atherosclerosis.

The plasma concentration of different lipoproteins were measured in 102 control children, in 42 children with a parent suffering from coronary heart disease (CHD), and in 50 children with a parent with cerebrovascular disease (CVD). Significant differences between controls and children in the other two groups were found for apolipoprotein A I, apolipoprotein B, and high density lipoprotein-cholesterol. Children of parents with CHD differed from controls in total cholesterol and apolipoprotein A II concentrations. A highly significant difference furthermore was found in lipoprotein (a) concentrations from children of parents with CHD in comparison with controls, but not between children of parents with CVD and controls. The difference in lipoprotein (a) concentrations (children of parents with CHD compared with controls) were only noticed in children above the age of 10 years. This could be explained by the observed rise of lipoprotein (a) between age 2 and 13 years, which was much more pronounced in the group with parents who had CHD. Plasma glycosaminoglycan concentrations were also measured in the three groups. They were significantly higher in children of parents with CHD and CVD compared with controls; they also varied with age.

Adolescent↗
PubMed1991

Serum elastase-type enzymes and their correlation to blood lipids in male patients with atherosclerosis.

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischaemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. Serum elastase-type activity was found to be significantly lower, inhibitory capacity significantly higher, in the groups of patients than in the controls. HDL- and HDL2 cholesterol as well as apo A concentration showed significant negative correlation with elastase inhibitory capacity both in atherosclerotic and in control subjects.

Apolipoproteins A↗
PubMed1990

Extracellular matrix.

A succinct overview of recent results on the biochemistry of extracellular matrix (ECM) is presented. The rapid expansion of this discipline over the best decades renders impossible to give an even approximately complete coverage of matrix biology. Some selected results concerning the four major families of macromolecules composing the ECM, that is, collagens (14 types described), elastin(s), proteoglycans and structural glycoproteins (especially fibronectin) are described. Special attention is directed to a crucial aspect of matrix biology: cell-matrix interactions. A number of cell membrane receptors were recently described mediating the two way information flow from the cells to the matrix via the 'programme' of ECM synthesis coded in the genome and unfolding during differentiation and from the ECM to the cells through the membrane receptors which contact the cytoskeleton. One of them at least, the elastin receptor was shown to be linked through a G-protein-phospholipase C-IP3 mediated relay to the regulation of intracellular calcium. Modifications of the ECM will therefore influence cell behaviour. Derangements of this informational feed back mechanisms appear to be involved in most age-related connective tissue diseases.

Animals↗
PubMed1990

Physicochemical studies of two major subpopulations of low density lipoproteins by differential scanning calorimetry and n.m.r. spectroscopy.

Two subpopulations, layer 2 (density 1.025-1.029 g/ml) and layer 3 (density 1.032-1.043 g/ml) of low density lipoproteins (LDL) were isolated from fresh human plasma of normal lipidaemic subjects by density gradient ultracentrifugation. Chemical analyses demonstrated the ratios of triglyceride/cholesterol ester decreased with increasing densities of subfractions. These subfractions together with triglyceride-rich lipoproteins (layer 1, density less than 1.019 g/ml) were subjected to physicochemical studies by differential scanning calorimetry (d.s.c.) and nuclear magnetic resonance (n.m.r.) spectroscopy. The average transition temperature (Tt) of layer 2 was 34.20 +/- 0.83 degrees C and that of layer 3 was 37.25 +/- 0.35 degrees C. In addition, many of the layer 3, but not layer 2 and layer 1, samples showed structural alteration and gave rise to an average Tt of 39.18 +/- 1.24 degrees C. The structural alteration could be detected with polarizing light microscopy showing birefringent spherulites at body temperature. The peak Tt values obtained by d.s.c. were in good agreement with those by n.m.r. spectroscopy. These results demonstrate the physicochemical heterogeneity within the LDL density region and suggest that layer 3 subpopulation is much more labile than the others.

Adult↗
PubMed1990

Interaction between fibronectin, proteoglycans and lipoproteins.

The effect of purified human plasma fibronectin on LDL-GAG and LDL-PG complex formation was studied. Fibronectin added to LDL or to GAG or even to preformed LDL-GAG-Ca2+ complexes could inhibit complex formation and dissociated preformed complexes. Similar results were obtained with total serum instead of purified LDL: 1.2 mg fibronectin added to 1.0 mg LDL-cholesterol completely inhibited insoluble complex formation in the presence of Ca2+ between LDL and GAGs or LDL and PGs purified from aorta, whatever the order of mixing of the macromolecules. When fibronectin was added to preformed PG-LDL complexes however dissociation was less complete than with preformed LDL-GAG complexes (60% dissociation instead of 100% at similar concentration ratios). It appears therefore that the protein and GAG portions of PGs may not interact at the same sites of LDL and competition by fibronectin would be more efficient at the GAG binding site. Fibronectin could also dissociate LDL-heparin complexes formed on heparin-Sepharose affinity columns. As PG-LDL complexes were isolated from atherosclerotic plaques and fibronectin was also shown to increase in plaque area and exhibit opsonic-like functions, the above findings may well have physiopathological significance.

Binding Sites↗
PubMed1990

Is the atherogenicity of Lp(a) caused by its reactivity with proteoglycans?

Apo B-containing lipoproteins from human plasma were studied for their ability to form complexes with glycosaminoglycans (GAG) and proteoglycans (PG) in the presence of Ca++ and Mg++ ions. We studied low density lipoproteins (LDL), Lp(a) as well as Lpa-, a particle generated from Lp(a) by removing the specific antigen (apo-a). The strongest reactivity with all apo B-containing lipoproteins was found with PG, followed by GAG isolated from human aorta, and by chondroitin-6-sulphate. Lp(a), on the other hand, formed complexes with the highest glycan:lipoprotein ratio using all three complexing agents. Treatment of Lp(a) with neuraminidase did not change the reactivity. The reactivity of Lpa-, on the other hand, was between that of Lp(a) and LDL. Lipoprotein glycan complexes were incubated with mouse peritoneal macrophages. This caused cholesterol ester accumulation and foam cell formation. The amount of cholesterol ester formed correlated highly significantly with the reactivity of a given lipoprotein with different glycans. Sera obtained from patients suffering from myocardial infarction (MI) were incubated with LDL and Lp(a) and the reisolated lipoproteins were also incubated with macrophages. Lipoproteins reisolated from MI plasma caused foam cell formation with MPM to a greater extent than reisolated material incubated with normal plasma. The highest cholesteryl ester accumulation was found when Lp(a) reisolated from MI plasma was incubated with MPM. These results may at least partly explain the higher atherogenicity of Lp(a) in comparison with LDL.

Animals↗
PubMed1989

Effect of glycosaminoglycans and divalent cations on the thermal properties of dipalmitoylphosphatidylcholine.

The effect of glycosaminoglycans (GAG) and divalent cations on the thermal properties of dipalmitoyl-phosphatidylcholine (DPPC)-water systems was examined in order to model some interactions taking place on low density lipoprotein (LDL) surfaces. The thermal properties of these systems were measured by differential scanning calorimetry (DSC). According to the results, all three glycosaminoglycans used (chondroitin-4-sulfate, chondroitin-6-sulfate and heparin) were effective but to a different extent. Calcium ions enhance the interaction more than magnesium ions, probably because divalent cations form bridges between the negatively charged groups of GAGs and the headgroups of lipids. It is conceivable that similar processes might occur in the case of LDL.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1989

Factor, present in plasma, inhibiting the interaction of low density lipoprotein with arterial proteoglycan.

The complex formation of LDL with arterial proteoglycan or glycosaminoglycan was quantitated as precipitation of LDL-cholesterol after incubation in a low ionic strength buffer containing CaCl2 and MgCl2. It was found that human plasma or serum contains a factor which inhibits this complex formation. Upon density gradient centrifugation this factor was found at d greater than 1.24 g/ml. It could be further purified from the d greater than 1.24 g/ml fraction by affinity chromatography on heparin-Sepharose and hydrophobic interaction chromatography on phenyl-Sepharose. The content of inhibitory activity was found to vary over a 4-fold range in sera of apparently healthy persons.

Calcium Chloride↗
PubMed1986

Physicochemical and ultrastructural properties of cholesterol esters bound to elastin.

Physicochemical and ultrastructural properties of cholesterol ester complexes of fibrous elastin and of K-elastin were studied using differential scanning calorimetry (DSC) and electron-microscopy. The number of molecules of the different fatty acids retained in these elastin complexes varied between large limits according to the nature of the fatty acid of the cholesterol ester, ranging from 0.1 microgram/200 mg of elastin for cholesterol arachidonate to 48 micrograms/200 mg elastin for cholesterol palmitate. The ultrastructural studies confirmed the association of cholesterol esters with fibrous elastin and soluble K-elastin. The DSC-data showed that the temperature of transition between the crystalline and the liquid crystalline state shifts towards higher temperatures (well above body temperature) when cholesterol esters are bound to elastin: no liquid crystalline mesophase was observed in cholesterol oleate or linoleate-elastin complexes at 37 degrees C; melting of the crystalline structures took place at 51 degrees C and at 42 degrees C for the cholester Holeate and linoleate-elastin complexes respectively. These results indicate that in the elastin-bound form the crystalline-liquid crystalline transition is inhibited. The "stabilization" of the crystalline structure of cholesterol esters by fibrous elastin may be of biological significance and account for the crystalline deposits seen in advanced atherosclerotic lesions at sites of elastic fiber breakdown.

Calorimetry, Differential Scanning↗
PubMed1985

The interaction of human plasma low density lipoproteins with glycosamino-glycans: influence of the chemical composition.

Human plasma of 5 normolipemic individuals was incubated for 24 hr at 37 C in the presence or in the absence of lecithin:cholesterol acyltransferase (LCAT)-inhibitors. Plasma stored at 4 C served as a control. The low density lipoprotein (LDL) fractions of the samples were isolated and investigated with respect to changes in chemical composition and complexing activity with glycosamino glycans (GAG). Incubation of plasma in the presence of LCAT inhibitors caused a significant increase of LDL triglycerides at the expense of cholesteryl esters. Incubation with active LCAT not only changed the core but also the surface constituents (decrease in phospholipids and in free cholesterol). The amount of GAG bound per mg of LDL was not uniformly changed in samples incubated after LCAT inhibition. LDL isolated from plasma incubated in the presence of LCAT, on the other hand, showed a significant reduction in GAG binding. The ratio of free cholesterol:GAG in the complex was most significantly reduced in LCAT-modified LDL. There was in addition a highly significant correlation between the LDL:GAG ratio in the complex and the free cholesterol and phospholipid content of the LDL samples. It is concluded that alterations in surface lipid constituents of LDL strongly affect their interaction with sulfated polysaccharides, an effect which may be relevant also in vivo for the interaction of LDL with cell surfaces and intercellular matrices.

Female↗
PubMed1984

Elastase-type activity, elastase inhibitory capacity, lipids and lipoproteins in the sera of patients with ischemic vascular disease.

Elastase-type activity and elastase inhibitory capacity were determined in the sera of 130 atherosclerotic patients, suffering from ischemic vascular disease (IVD) localized at various sites, and of 60 control subjects. The concentrations of serum lipoprotein constituents (triglycerides, total cholesterol, HDL cholesterol, apo-A, apo-B) have also been investigated. HDL cholesterol and apo-A levels were decreased at every site on IVD. Plasma HDL concentration in men was lower than that in women. There was a sex-related difference in the elastase-type activity of the sera: within every atherosclerotic group, elastase-type activity in women was significantly higher than in men. Elastase-type activity did not appear to vary with age and did not show any correlation with the concentration of serum lipoprotein constituents. Pancreatic elastase inhibitory capacity of sera was significantly elevated in the sera of atherosclerotic patients. There was a significant negative correlation between the inhibitory capacity and the HDL cholesterol and apo-A content of sera, respectively. Inhibitory capacity did not show sex-, or age-related variation. There was a significant positive correlation between elastase-type activity and elastase inhibitory capacity measured in control sera. In the sera of atherosclerotic patients this correlation could not be established.

Adult↗
PubMed1984

Changes in the cartilage proteoglycans in relation to age and osteoarthrosis.

Changes in the extracellular components of various connective tissues with time and continuous use, as well as within experimentally-induced and human pathological conditions, were studied by morphological, chemical and biochemical methods. Osteoarthrotic lesions were produced surgically by implantation of polyethylene sheets, by continuous compression of the knee joint, and by intraarticular papain injection. Results of the model experiments showed that, irrespective of the method used for the production of experimental cartilage lesions, the alterations are strikingly similar. Within connective tissues a gradual deterioration takes place, as measured by marked differences in the histological and histochemical patterns. The degradative changes occur primarily in the matrix, resulting in a significant decrease in proteoglycan content. Under conditions of stress, in young animals, chondrocytes seem to revert to the chondroblastic state, showing mitotic figures, and are capable of producing matrix much more rapidly than is normally seen. This increased activity might be regarded as a nonspecific "feed-back" response of cells, leading to a reparative normalization of the various destructive tissue alterations.

Aging↗