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Biomedical subjects

M Aviram

Publications and source records attributed to M Aviram.

At least 235 records · Page 13Linked to original sources
PubMed1984

Residual small airways lesions after kerosene pneumonitis in early childhood.

To assess residual lung damage after a single insult early in life, we studied 14 asymptomatic children, 10 years after an episode of kerosene pneumonitis. Immediately after kerosene ingestion all patients developed pulmonary symptoms. Eight had abnormal chest radiographs (group 1) whereas in six there were no radiographical changes (group 2). The average age at follow-up was 11.4 (range: 9.4-13.2). Lung volumes, expiratory flow-rates and their density dependence were measured and compared to an age, sex, and a height-matched control group. The volume of isoflow (Viso V) was significantly higher in patients in group 1 (27.75% +/- 6.7) when compared to group 2 (5.48% +/- 3.56) or controls (5.63% +/- 2.31) (P less than 0.02). The mean delta V max 50 was 13.5% +/- 3 for group 1, and 27.9% +/- 4.11 for group 2 (P less than 0.005). Airway reactivity assessed by an exercise test was normal in all children. Four of the eight patients from group 1 still had abnormal chest radiographs 10 years after kerosene pneumonitis. Thus, subclinical, prolonged small airway abnormalities after kerosene pneumonitis seem to be related to the severity of the acute insult.

Adolescent↗
PubMed1984

Platelet adhesion determination in whole blood using a simple stagnation flow method.

A simple stagnation flow method for the determination of platelet adhesivity has been developed. The sensitivity of the method to its main operational parameters was tested, resulting in recommended standard flow conditions. The method was shown to be dependent on the surface properties of the test slide, on which platelets are deposited, thus proving its suitability to elucidate variations in the surface interaction of the platelets. Normal values were established for males and females.

Adult↗
PubMed1984

Increased concentration of high density lipoprotein in plasma and decreased platelet aggregation in primary biliary cirrhosis.

Plasma lipoprotein concentration and composition were studied in 7 female patients with primary biliary cirrhosis and compared with 6 normal, age-matched controls. The effect of the lipoproteins derived from these patients on the function of normal platelets was also tested. High levels of plasma cholesterol and phospholipids and a raised free/esterified cholesterol ratio were found. In 4 of the patients, both HDL cholesterol and HDL protein were increased, and high levels of plasma apoprotein A-I and A-II were evident. This abnormal HDL did not contain excess apolipoprotein E. The VLDL and LDL fractions were also abnormal, as evidenced by a high cholesterol/protein ratio. Little correlation between lipoprotein disorders and clinical condition was found. Platelet function was reduced in all patients. LDL from the patients reduced aggregation of normal platelets, whereas HDL had a minimal effect. The abnormal lipoproteins in these patients may contribute to their abnormal in vitro platelet aggregation.

Adult↗
PubMed1984

Abnormal plasma lipoprotein composition in hypercholesterolaemic patients induces platelet activation.

Increased platelet activation has been shown to be a feature of patients with familial hypercholesterolaemia. Plasma lipoprotein concentration and composition were studied in eleven male patients with familial hypercholesterolaemia and in ten age-matched healthy controls. Increased levels of cholesterol were found in very-low- and low-density lipoproteins (53 and 275%, respectively), whereas in high-density lipoprotein, both cholesterol and apolipoprotein A-I were decreased by 21 and 26%, respectively. On incubation of gel-filtered platelets derived from normolipidaemic controls with identical concentrations of lipoproteins derived from either nomolipidaemic controls or hypercholesterolaemic patients very-low- and low-density lipoproteins from the patients caused significantly greater thrombin-induced platelet aggregation (P less than 0.01). High-density lipoprotein from normal subjects reduced platelet release by 22%, whereas the patients' high-density lipoprotein had no significant effect on platelet release. Lipoprotein-deficient plasma from both groups augmented platelet function to a similar extent. Lipoprotein composition has an important effect on platelet function in vitro. The abnormal lipid and protein composition of the lipoproteins derived from hypercholesterolaemic patients appears to be the cause of platelet hyperactivity observed in these patients.

Adult↗
PubMed1984

Plasma cholesterol concentration and extra lipid band in monoclonal gammopathies.

Plasma lipids and lipoproteins were studied in 21 patients with benign monoclonal gammopathy, 21 patients with multiple myeloma and seven patients with Waldenström's macroglobulinaemia. Results were compared with those of a control group, age and sex matched. Low plasma cholesterol levels in all three patient groups were associated with low HDL-cholesterol concentrations. Apo A-I, but not apo B, was significantly reduced. Sixty per cent of the patients exhibited an extra lipid band on plasma lipoprotein electrophoresis, which could be an immunoglobulin-lipid complex. In these patients plasma and LDL-cholesterol levels were significantly lower than in those patients in whom this band was absent. No correlation was found between the severity of the disease and plasma lipid pattern.

Aged↗
PubMed1984

High dose of L-carnitine increases platelet aggregation and plasma triglyceride levels in uremic patients on hemodialysis.

Uremic patients undergoing chronic hemodialysis demonstrate a secondary systemic carnitine deficiency. We studied the effect of carnitine replacement with high doses (L-carnitine, 3 g/day) similar to those used in the treatment of primary systemic carnitine deficiency. 10 uremic patients on hemodialysis were randomly selected into a control group (4 patients) treated by placebo and a treatment group (6 patients) treated by L-carnitine. Plasma lipoprotein concentration and composition as well as platelet aggregation were studied before and after treatment. Following carnitine administration, a paradoxical rise in plasma triglyceride concentration from 180 +/- 66 to 219 +/- 88 mg% (p less than 0.05) was noted. No other significant changes in lipoprotein concentration and composition or in plasma apoprotein A-I and B concentration were observed. Carnitine treatment caused a significant rise in platelet aggregation induced by epinephrine, ADP, and thrombin. These findings suggest a harmful effect of L-carnitine replacement therapy when given in high doses, causing aggravation of uremic hypertriglyceridemia and increased platelet aggregation in patients predisposed to thromboembolic phenomena.

Adult↗
PubMed1983

Plasma lipoprotein separation by discontinuous density gradient ultracentrifugation in hyperlipoproteinemic patients.

Quantitative plasma lipoprotein separation is usually performed by sequential ultracentrifugation which because of the necessity of repeated ultracentrifugation is extremely time consuming and results in changes in lipoprotein composition. We describe a simple, reliable, and rapid method for quantitative plasma lipoprotein separation which is based on ultracentrifugation of the plasma in a discontinuous density gradient media consisting of a saline solution of different densities placed over a plasma solution of 1.250 g/ml (with potassium bromide). After 48 hr of ultra-centrifugation in a swinging bucket rotor excellent lipoprotein separation was demonstrated. The lipoproteins were pure and there was significantly less loss of high density lipoprotein protein to the lipoprotein deficient plasma (d greater than 1.210 g/ml) when compared to the losses incurred during the sequential flotation method. The results of separating the plasma lipoproteins from subjects with dyslipoproteinemias by this method were demonstrated. We conclude that discontinuous density gradient ultra-centrifugation is the method of choice for quantitative plasma lipoprotein separation for both clinical and research use.

Adult↗
PubMed1983

High density lipoprotein in octogenarians.

High density lipoprotein (HDL) cholesterol, total cholesterol, and total triglyceride levels were assayed in the plasma of 42 octogenarians. No differences were found in the levels of HDL cholesterol and total triglycerides when comparing subjects with and without ischemic heart disease. The average lipid profile of males in this age group shows significantly lower levels of triglycerides and total cholesterol when compared with the females. HDL cholesterol levels were 10% higher in the females. The distribution pattern of HDL cholesterol levels in this age group suggests a bimodal distribution with 85% of the population distributed around a low peak of 53 mg% and 15% around a high peak of greater than 70 mg%. This pattern suggests that the hyperalphalipoproteinemia phenotype does exist as a separate entity in a population demonstrating longevity, but its low incidence cannot provide an explanation for longevity in the majority of subjects. Subfractionation of HDL was performed by preparative ultracentrifugation and the subfraction profile of 17 female octogenarians was compared with a group of young controls. The younger individuals had greater fat to protein ratios in the HDL-1 and HDL-2 subfractions. This was only difference in lipoprotein composition. We conclude that neither the total level of HDL particles nor the distribution of lipoprotein components among the subfractions can account for the longevity of the majority of the study population.

Aged↗
PubMed1983

Accumulation of lipoprotein remnants in patients with chronic renal failure.

The composition and concentration of remnant lipoprotein particles accumulating in the plasma of patients with chronic renal failure (CRF) was determined. Ten patients on chronic hemodialysis were compared with 8 controls. The patients' very low density lipoproteins (VLDL) were abnormal and contained more of the dense VLDL subfraction (VLDL3). The concentration of intermediate density lipoproteins (IDL) was increased 3-fold in CRF plasma, whereas the amount of low density lipoprotein (LDL) was decreased by 25%. On electrophoresis of plasma lipoproteins the beta-band from the patients' samples demonstrated increased anodal mobility, indicating an abnormality in composition of the patients' LDL. These abnormalities were present regardless of whether patients were hyperlipidemic or not. These findings suggest defective conversion of VLDL to LDL in CRF, allowing for the accumulation of lipoprotein particles usually absent from plasma. The latter may account for the accelerated atherosclerosis reported in patients with CRF.

Adult↗
PubMed1983

Platelet interaction with high and low density lipoproteins.

Gel-filtered platelets (GFP) from normal human subjects bound both low density lipoproteins (LDL) and high density lipoproteins (HDL). This binding was saturable and 125I-labelled lipoprotein uptake was inhibited by plasma. Platelets are also able to degrade lipoproteins but only to a limited extent. LDL appeared to compete with 125I-labelled HDL for platelet uptake, whereas the ability of HDL to displace 125I-LDL was limited. Cyclohexanedione-treated LDL (CHD-LDL), unlike CHD-HDL, did not compete with [125I]LDL for platelet accumulation, suggesting that arginine residues are necessary for LDL but not HDL binding. Addition of HDL or LDL to GFP did not alter platelet aggregation. However, in the presence of thrombin (0.5 U/ml), 1 mg/ml LDL incubated for 1 h at 23 degrees C enhanced platelet aggregation (215% increase) whereas HDL under similar conditions decreased aggregation by 53%. LDL also shortened the time of maximal aggregation whereas HDL had the opposite effect.

Blood Platelets↗
PubMed1983

Changes in lipoproteins and subfractions following oophorectomy and oestrogen replacement in peri-menopausal women.

Serum cholesterol concentrations in lipoprotein fractions and subfractions were determined in 11 peri-menopausal women both before and after bilateral oophorectomy, as well as 60 days after commencement of oral oestradiol replacement therapy. Pre-operatively, all subjects were found to have normal lipid and lipoprotein concentrations. There was a post-operative increase in the total cholesterol level, which was attributed to a raised very-low-density lipoprotein (VLDL) cholesterol. Changes in high-density lipoprotein (HDL) subfractions HDL-2 and HDL-3 were noted but since these were compensatory little difference in total HDL cholesterol was observed. Following oral oestrogen replacement, the cholesterol level decreased as a result of a drop in both VLDL and low-density lipoprotein (LDL) cholesterol. The oestradiol-induced HDL cholesterol increment reflected an increase in the levels of both HDL subfractions.

Castration↗