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Biomedical subjects

M Aviram

Publications and source records attributed to M Aviram.

At least 253 records · Page 14Linked to original sources
PubMed1983

Platelet function and lipoprotein levels after plasma-exchange in patients with familial hypercholesterolaemia.

1. Repeated plasma exchange was carried out on three young patients with severe familial hypercholesterolaemia. There was a 3 week interval between each exchange. After a single exchange, plasma cholesterol, apolipoprotein B and low density lipoprotein-cholesterol levels decreased markedly, but pre-exchange levels were not achieved within 2 weeks. High density lipoprotein-cholesterol and apolipoprotein A-I levels also fell but returned to the original concentration after only 5 days. 2. Platelet aggregation and [14C]serotonin release were increased in all three patients and dropped by 20% and 13% respectively after a single plasma exchange. Platelet function in vitro returned to pre-exchange levels with similar kinetics to that observed with the low density lipoprotein concentration. On removal of 100 g of plasma cholesterol, after repeated exchanges, low density lipoprotein concentration and platelet function were significantly decreased in comparison with values before initiation of plasma exchange. In addition there was a marked regression of xanthoma in all three patients. 3. Since this procedure is instrumental in achieving a negative cholesterol balance as well as inhibiting hypersensitive platelets, it may well result in a downgrading of the atherosclerotic risk.

Adolescent↗
PubMed1983

Increased platelet adhesion and aggregation in hypertensive patients: effect of atenolol.

Fourteen patients with established hypertension followed a double-blind crossover-styled trial to study the effects of 100 mg/day atenolol compared to placebo. Atenolol was found to be an effective antihypertensive agent, reducing both systolic and diastolic blood pressure. Hypertensive patients appear to have increased in vitro platelet adhesion and aggregation. Atenolol significantly reduced platelet adhesion, but had little effect on aggregation. This may be important in contributing towards the now-recognised cardio-protective effect of the beta-adrenoceptor blocking agents. Blood chemistry and haematological parameters were unchanged; but whereas plasma cholesterol and plasma triglyceride levels remained normal, there was a significant fall in plasma high-density lipoprotein cholesterol levels. Side effects were very few.

Adult↗
PubMed1983

Characterization of the effect of plasma lipoproteins on platelet function in vitro.

Thrombin-induced platelet activation is enhanced by very low and low density lipoproteins but decreased by high density lipoprotein. Plasma lipoproteins maximally affect platelet aggregation and 14C-serotonin release in a gel-filtered platelet preparation within 10 min of incubation at 37 degrees C. This effect is saturable and physiologic concentrations of lipoproteins are required in order to attain this saturation. When no aggregating agent is added to the incubation medium, the lipoproteins alone did not alter platelet aggregation. However, 14C-serotonin release is increased by very-low- and low-density lipoproteins alone more than by high density lipoprotein. On removal of the lipoproteins after incubation with the platelets, and subsequent testing of platelet function, minimal influence of these lipoproteins on the platelet function remains. Arachidonic acid causes similar results to thrombin when added to the platelet suspension after incubation with the lipoprotein. Our results further emphasize the 'opposing effects' of very low and low density lipoproteins as compared to high density lipoproteins on platelets and/or platelet-thrombin interaction.

Arachidonic Acid↗
PubMed1983

The effect of blood constituents on platelet function: role of blood cells and plasma lipoproteins.

Platelet aggregation as well as [14C] serotonin release were increased in platelet-rich plasma in comparison to gel-filtered platelet preparation. The addition of red blood cells to platelet-rich plasma enhanced thrombin-induced [14C] serotonin release by 7%, whereas in a gel-filtered platelet preparation free of any plasma constituents a 47% increment was noted. In the presence of white blood cells, no effect could be shown. Purified lipoproteins were incubated (in their normal plasma concentration) with gel-filtered platelets for 30 minutes at 37 degrees C, and the effect on in vitro platelet function was studied. Very low density lipoprotein and low density lipoprotein increased thrombin-induced platelet aggregation and [14C] serotonin release induced by epinephrine, ADP, and thrombin. In contrast, high density lipoprotein inhibited these platelet functions. Lipoprotein-deficient plasma increased platelet aggregation and release reaction. It appears that plasma lipoproteins have a profound effect on in vitro platelet function. Since both platelets and lipoproteins are of importance in atherosclerosis, the platelet-lipoprotein interaction might be of major significance in this process.

Adolescent↗
PubMed1982

The effect of human plasma on platelet function in familial hypercholesterolemia.

Using a platelet-rich plasma (PRP) preparation, platelets from subjects with familial hypercholesterolemia (FH) were found to be more reactive to the aggregating agents epinephrine, ADP and thrombin than platelets obtained from normal individuals. Gel-filtered platelets (GFP) i.e. platelets free of any plasma constituents also showed increased activation as determined by platelet aggregation and 14C-serotonin release. On incubating washed platelets from normal subjects with plasma obtained from FH subjects the platelet response to aggregating agents was significantly increased. Incubation of washed platelets from the FH patients with normal plasma, however, resulted in a significant decrease in platelet activity. Our data suggest that the increased platelet activation in FH patients is the result of a change in the platelets induced by abnormal plasma constituents.

Adenosine Diphosphate↗
PubMed1982

The effect of oestrogen implants on high density lipoproteins and its subfractions in women in their pre-mature menopause.

Oestrogen is recognized as having profound effects on lipid and lipoprotein levels. It is also considered as the agent protecting the pre-menopausal woman from arteriosclerotic cardiovascular disease. High density lipoprotein (HDL) has also been ascribed a protective role against the development of arteriosclerosis. The effect of natural oestrogen (17 beta-oestradiol) administered in the form of a subcutaneous pellet on concentrations of lipids and lipoproteins, particularly high density lipoproteins and its subfractions were determined in three young women with premature menopause. Plasma cholesterol, low density lipoprotein and very low density lipoprotein and very low density lipoprotein levels decreased following oestrogen implantation. High density lipoproteins and in particular subfraction 2 (density cut 1.063-1.125 gm/ml) and subfraction 3 (density cut 1.125-1.21 gm/ml) increased profoundly but there was a slight fall in the HDL 2/HDL 3 cholesterol ratio. The HDL/LDL cholesterol ratio increased from 0.21 to 0.46. A decrease in the urinary FSH levels paralleled these changes in the lipoprotein concentrations. Oestrogen administered in this form, unlike other oestrogen or mixed oestrogen--progestogen compounds is a definite modifier of arteriosclerotic risk, and as such could be given therapeutically in menopausal hypercholesterolemic females.

Adult↗
PubMed1982

Lipid and lipoprotein pattern in thyroid dysfunction and the effect of therapy.

Lipid and lipoprotein concentrations were studied in 12 hypothyroid and 11 hyperthyroid female subjects, both before and after therapy, and in 27 age matched female controls. Recognized clinical and laboratory criteria established the diagnosis. Lipoproteins, including the sub-fractions of the high density lipoproteins (HDL), were isolated by preparative ultracentrifugation, and the cholesterol (c) and protein (p) contents of each were determined. Total cholesterol, and in particular HDL-c, were elevated in the hypothyroid patients. The low density lipoprotein (LDL) -c/HDL-c ratio was 1.9 in this group, compared to 2.2 in the control group and 1.35 in the hyperthyroid patients. The HDL-2/HDL-3 ratio in the hypothyroid group was 3.75, as compared to 1.75 in the controls and 4.2 in the hyperthyroid group. Plasma triglycerides were moderately elevated in the hypothyroid patients and were significantly reduced in the hyperthyroid group. Total cholesterol was significantly lower in the hyperthyroid group as compared to the control group. Very low density (VLDL) cholesterol and protein were significantly increased and LDL and HDL cholesterol were reduced in the hyperthyroid patients. On rendering the patients euthyroid, most of these changes were reversed. Thyroid function profoundly affects lipoprotein concentration and composition. The change in the plasma HDL concentrations of the hypothyroid group questions the relationship of this group to arteriosclerosis. Therapy partially corrects the abnormalities, but complete correction may be related to duration of therapy.

Adolescent↗
PubMed1982

High-density lipoprotein subfractions in normolipidemic patients with coronary atherosclerosis.

High-density lipoprotein (HDL) levels were studied in 10 male patients with severe coronary atherosclerosis and in 10 well-matched controls. All subjects were normolipidemic, and the presence of a disease or other factor influencing HDL levels were excluded. Very low density lipoprotein and low-density lipoprotein levels were similar in both groups, but HDL concentration was significantly lower in the patient group. Analysis of HDL subfractions revealed that both HDL2 and HDL3 concentrations were significantly lower in the patient group. The composition of both HDL subfractions was also altered in the patient group: an increased cholesterol-to-protein ratio was found. These data strengthen the evidence in support of an important and independent role for HDL in the pathogenesis of coronary atherosclerosis. It appears that both HDL2 and HDL3 are implicated and that both the concentration and composition of HDL are important.

Adult↗
PubMed1981

High density lipoprotein and arteriosclerosis. Different patterns in primary hypothyroidism and type IIa hyperlipoproteinemia.

Concentrations of high density lipoprotein (HDL) and its subfractions were contrasted in two groups of patients with hypercholesterolemia and a control group of normocholesterolemic subjects. HDL-cholesterol and HDL-protein were low in patients with Type IIa hyperlipoproteinemia, but elevated in patients with primary hypothyroidism. HDL-3 levels were low whereas those of HDL-2 remained unchanged in patients with Type IIa hyperlipoproteinemia. In contrast, in the hypothyroid patients, HDL-3 remained unchanged, while HDL-2 levels were high. The role of HDL in the development of arteriosclerosis in patients with primary hypothyroidism is therefore questioned. Our findings also suggest that measurement of HDL-cholesterol alone cannot be regarded as an accurate indicator of changes in total HDL concentration in different clinical situations.

Arteriosclerosis↗
PubMed1980

The concentration of high density lipoprotein in patients with type IV hyperlipoproteinemia and the effect of clofibrate.

Lipid and lipoprotein concentrations, including high density lipoproteins (HDL) and its subfractions, were contrasted in subjects with Type IV hyperlipoproteinemia, before and after therapy with clofibrate. Very low density lipoprotein (VLDL) levels were raised, whereas both low density lipoprotein (LDL) and HDL values were reduced in the patient group. Clofibrate reversed this trend and VLDL cholesterol and protein levels fell to approximate control values. LDL and HDL cholesterol increased but remained significantly lower than in normal controls. However, LDL and HDL protein did approach control values. Of the HDL subfractions, HDL-3 was significantly reduced in the group with Type IV hyperlipoproteinemia. Clofibrate resulted in a significant increase in the HDL-2: HDL-3 cholesterol ratio, but had only a modest effect on HDL-3 concentrations. HDL-3 may be the critical HDL subfraction responsible for the inverse correlation between levels of HDL and the development of ischemic heart disease.

Adult↗
PubMed1978

Defective high-density lipoprotein composition in patients on chronic hemodialysis. A possible mechanism for accelerated atherosclerosis.

We determined serum high-density lipoprotein cholesterol content and analyzed the approtein structure of the various lipoprotein fractions in 21 patients on chronic hemodialysis. High-density lipoprotein cholesterol was significantly reduced in all patients as compared with 11 normal persons (mean +/-1 standard deviation: 26 +/- 13 vs. 52 +/- 9 mg per 100 ml; P less than 0.001) whether or not triglyceride levels were raised. In seven of those with Type IV hyperlipoproteinemia, protein content of high-density lipoprotein and its subfractions 1, 2 and 3 were also reduced (P less than 0.001) in parallel with reductions in cholesterol in these fractions. Apoprotein electrophoresis showed an increase in "arginine-rich" peptide in very-low-density lipoprotein and high-density lipoprotein fraction 1, and a reduction in apoprotein Cll in very-low-density and high-density lipoprotein. In addition to their reduced high-density lipoprotein cholesterol levels, a major factor in the atherosclerosis of these patients may be their abnormal high-density lipoprotein composition. Their raised triglyceride levels could be due to defective lipoprotein lipase activation by the reduced very-low-density lipoprotein apoprotein.

Adolescent↗
PubMed1977

Interconversion of multiple forms of tyrosine aminotransferase in vitro and in vivo in cultured hepatoma cells.

Corticosteroid-induced tyrosine aminotransferase (EC 2.6.1.5) from cultured hepatoma cells was separated by carboxymethyl-Sephadex chromatography into three molecular forms resembling those described previously in the rat liver. Enzyme forms were isolated and used as purified substrates to examine their in vitro interconversion by various subcellular fractions. Isolated form III was converted to forms II and I, and isolated form II was converted to form I by the coarse particulate fraction sedimenting at 1000 X g. This activity was inhibited by the serine enzyme inhibitor phenylmethane sulfonyl fluoride or by raising the pH to 8.7. Conversion of enzyme forms in vitro in the opposite direction (I leads to II leads to III) could not be detected. The distribution of enzyme forms in vivo was examined by the use of experimental conditions that prevent their in vitro interconversion during cell extraction. Tyrosine aminotransferase extracted from cell subjected to various treatments that affect the rates of enzyme synthesis or degradation existed always predominantly as form III. It appears, therefore, that multiple forms of tyrosine aminotransferase are not related to the turnover of this enzyme in vivo.

Carcinoma, Hepatocellular↗