S. Gerö
Semmelweis University
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Featured researches published by S. Gerö.
Atherosclerosis | 1978
George Füst; Éva Szondy; Judit Székely; Ildikó Nánai; S. Gerö
The presence of circulating immune complexes was studied in 347 samples of serum from 212 patients with various vascular diseases. Two quantitative methods (complement-consumption assay and C1q-solubility test) were used for the measurement of the concentration of the complexes. Immune complexes were detected in each group of patients tested (coronary arteriosclerosis, myocardial infarction, cerebral artery sclerosis, arteriosclerosis obliterans, phlebothrombosis, pulmonary infarction). A high proportion of positivity was recorded in myocardial infarction (in 43 patients out of the 94 tested) and in arteriosclerosis obliterans (7 out of 11 cases). The possible pathogenic role of the circulating immune complexes is discussed.
Atherosclerosis | 1983
Éva Szondy; Mária Horváth; Zsuzsa Mezey; Judit Székely; Éva Lengyel; George Füst; S. Gerö
The cell-mediated immune response against low density lipoproteins (LDL) was demonstrated by the migration inhibition test in patients with various vascular diseases. Anti-high density lipoprotein2 (HDL2) cellular immune response was found only in a few patients. LDL and HDL2 binding factors were detected in about 50% of coronary patients. No significant difference in their occurrence was found between the normolipidemic and hyperlipidemic patients nor between patients with hyperlipidemia type II/b and type IV. On the assumption that lipoproteins may act as auto-antigens by forming immune complexes, the presence of anti-LDL and anti-HDL2 activity was investigated in circulating immune complexes obtained by polyethylene glycol (PEG) precipitation from the sera of coronary patients and controls. Using an ELISA technique, PEG-precipitable anti-LDL activity was detected in 23, 11 and 18% of cases with myocardial infarction, angina pectoris and healthy old subjects, respectively. In the immune complexes obtained from the sera of the healthy young donors no anti-LDL activity was found. Anti-HDL2 activity in the immune complexes was demonstrated only in a few cases from among the patients and elderly persons we investigated.
Mechanisms of Ageing and Development | 1985
Éva Szondy; Éva Lengyel; Zsuzsa Mezey; György Füst; S. Gerö
The incidence of circulating immune complexes, anti-low density lipoprotein (LDL) autoantibodies and the anti-LDL activity of immune complexes was studied in healthy young and aged controls and in patients with vascular diseases. Circulating immune complexes (CIC) frequently occurred both in the young or old patient groups and in the aged healthy control groups, whereas they could not be found in the young controls. Marked differences were found in the incidence of anti-LDL antibodies between the groups tested. In both young and aged control groups such antibodies were very rarely observed (4-5%). In contrast anti-LDL antibodies were present in 35-45% in the aged, or young patients. Similarly, no anti-LDL activity was found in CIC of the controls, whereas in the patients with vascular diseases a significant CIC-associated anti-LDL activity was detected. These results suggest that the presence of anti-LDL antibodies are associated with the arteriosclerotic manifestations, while that of circulating immune complexes is connected by the ageing process itself.
Atherosclerosis | 1973
L. Orosz; G. Erdélyi; László Romics; S. Gerö
Abstract The effect of insulin on postheparin lipoprotein lipase activity was studied in 23 persons with coronary sclerosis and in 18 controls. On the first day the curve of postheparin lipoprotein lipase activity was established, then after infusion of 0.1 IU/kg body weight of insulin, or intravenous administration, respectively, these tests were repeated under the same experimental conditions. The results obtained were as follows: 1. (1) In the plasma of patients with coronary sclerosis the postheparin lipoprotein activity is subnormal. 2. (2) The enzyme activity was normalized by insulin given by infusion. 3. (3) Normal lipoprotein lipase activity was increased by insulin too, but the increase was significantly lower than in the group with coronary sclerosis. 4. (4) Insulin, when injected rapidly, did not cause any significant change. In connection with the potentiating effect that insulin has on the lipoprotein lipase activity the possibility of increased synthesis or mobilization of the enzyme is discussed.
Atherosclerosis | 1978
Éva Szondy; Mária Horváth; G. Fost; Erzsébet link; János Fehér; S. Gerö
Cholesterol-fed rabbits were treated with clofibrate, pyridinol carbamate and with both drugs simultaneously. The quantity of circulating immune complexes in the sera of the animals was measured weekly and the migration inhibition test was carried out in the 12th week of the experiment. The trend of the changes in the concentration of the immune complexes was rather similar to that of the cellular immune response. Compared with the values obtained in the control animals, in the cholesterol-fed group a markedly higher level of immune complexes and a significant migration inhibition could be detected. The administration of clofibrate or pyridinol carbamate alone had no effect on the concentration of immune complexes. Pyridinol carbamate did not influence the migration inhibition; however, it became similar to the healthy controls in the clofibrate-treated group. Simultaneous treatment with both drugs resulted in a decrease in the quantity of immune complexes and a diminution of the migration inhibition.
Archive | 1974
S. Gerö; Judit Székely; Magdolna Bihari-Varga; Éva Szondy
It is generally accepted that arteriosclerosis is a polyaetiologic and presumably polypathogenetic disease caused by a combination of individually different factors. From the considerable amount of information obtained in the last 10 years, it seems likely that allergic and autoimmune processes may also play a role in the chain of events leading to the atheromatous vascular changes (Gero, 1969).
Advances in Experimental Medicine and Biology | 1987
S. Gerö; Éva Szody; Éva Lengyel; Gy. Simon
It was demonstrated by several authors that LDL in vitro and in vivo increase the in vitro platelet aggregation1,2 and other platelet functions.3,4 This hypersensitivity of platelets may contribute in vivo to an accerelated atherogenesis.
The Lancet | 1977
G. Füst; Judit Székely; S. Gerö
Cellular and Molecular Life Sciences | 1973
S. Gerö; Judit Székely; Éva Szondy; A. Jobbágy; A. Orosz; Eva Seregélyi
Atherosclerosis | 1986
George Füst; Éva Szondy; S. Gerö