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Biomedical subjects

G R Thompson

Publications and source records attributed to G R Thompson.

At least 127 records · Page 7Linked to original sources
PubMed1987

Kinetics of LDL subfractions.

After injecting 125I- or 131I-labeled lipoproteins, plasma was subjected to discontinuous density gradient centrifugation, which separates low-density lipoproteins (LDL) into three subfractions. Analysis of changes in apolipoprotein B-specific activity with time showed that light LDL is normally the product of intermediate-density lipoprotein and the precursor of heavy LDL, which is subsequently converted to heavier LDL. In hyperapobetalipoproteinemia these relationships are maintained but there is overproduction of light and heavy LDL secondary to increased synthesis of very low-density lipoprotein. In familial hypercholesterolemia, light LDL is produced normally but its conversion into heavy LDL is reduced and independent synthesis of the latter is apparent. These observations suggest that the LDL receptor normally plays a role in the conversion of light into heavy LDL. They also provide an explanation for previously documented differences in LDL composition between hyperapobetalipoproteinemia, in which there is a relative increase in cholesterol-depleted heavy and heavier subfractions, and familial hypercholesterolemia, in which there is a relative increase in the cholesterol-enriched light subfraction.

Animals↗
PubMed1987

Treatment of severe accidental hypothermia using the Clinitron bed.

Two cases of severe accidental hypothermia (core temperature less than 28 degrees C) rewarmed employing the Clinitron system are described. The physiological changes during hypothermia and rewarming are discussed and the current concepts of rewarming (active external versus internal) outlined. It is suggested that severely hypothermic patients can be successfully treated by rapid external rewarming using the Clinitron heated fluidised-bead bed. This method combines the advantages of rapid rewarming, minimal physiological disturbance and is non invasive.

Aged↗
PubMed1986

Clinical judgments of depression.

In an effort to reevaluate Gough's (1954) classic study of common misconceptions about neuroticism, an investigation was undertaken of the degree to which judges could simulate the Basic Personality Inventory (BPI) responses of a clinically depressed patient group. Judgments were recorded of the probability of responding to each of 240 BPI items by a total of 56 university student judges. Judges were assigned randomly to one of two information conditions, one that had only the label "clinical depression" and another that had, in addition, a more extensive definition. Judgmental profiles of depressed patients indicated very high reliabilities (.99) across information conditions, a high association with actual profiles of clinically depressed patients, and differentiation from other psychiatric patients and normal controls. Results were interpreted as supporting the accuracy of judgments of psychopathology, particularly when certain preconditions are met, namely, the use of a meaningful construct of psychopathology and the prediction of behavior relevant to that construct.

Depressive Disorder↗
PubMed1986

Paradoxical elevation of LDL apoprotein B levels in hypertriglyceridaemic patients and normal subjects ingesting fish oil.

Twenty-three hypertriglyceridaemic patients treated with 15 g/day of a fish oil concentrate (Maxepa) showed the expected reduction in serum triglyceride concentration but levels of LDL apoprotein B (apoB), measured by radial immunodiffusion, increased significantly. Increases in LDL apoB did not correlate with lipoprotein phenotype or changes in serum triglyceride. Studies in eight normal volunteers demonstrated that the effect of fish oil on LDL apoB was not restricted to hypertriglyceridaemic subjects. In view of the evidence that LDL apoB may be a risk factor for coronary heart disease these findings raise questions regarding the use of fish oil in the treatment of hypertriglyceridaemia.

Adult↗
PubMed1986

Binding and degradation of heavy and light subfractions of low density lipoprotein by cultured fibroblasts and macrophages.

The heavy and light subfractions of low density lipoprotein (LDL) were bound to the same extent and with the same affinity by the LDL receptors of cultured human fibroblasts, both when assayed at 4 degrees C and when assayed at 37 degrees C. They were also degraded similarly by the low affinity, LDL-receptor-mediated pathway exhibited by normal human monocyte-derived macrophages maintained in medium containing whole serum. Neither of the subfractions was taken up by the 'scavenger' pathway in mouse peritoneal or human monocyte-derived macrophages. Assuming that the LDL particles were not altered during isolation, the results provide no evidence to suggest that the higher fractional catabolic rate of light LDL observed in vivo can be explained by any preferential catabolism through LDL-receptor-mediated pathways.

Animals↗
PubMed1986

Metabolic basis of hyperapobetalipoproteinemia. Turnover of apolipoprotein B in low density lipoprotein and its precursors and subfractions compared with normal and familial hypercholesterolemia.

The turnover of apolipoprotein B (apo B) in very low density, intermediate density, and low density lipoproteins (VLDL, IDL, and LDL) and in the light and heavy fractions of LDL was determined in seven patients with hyperapobetalipoproteinemia (hyperapo B), six normolipidemic subjects, and five patients with heterozygous familial hypercholesterolemia (FH). After receiving an injection of 125I-VLDL, hyperapo B patients were found to have a higher rate of synthesis of VLDL-apo B than controls (40.1 vs. 21.5 mg/kg per d, P less than 0.05) but a reduced fractional catabolic rate (FCR) (0.230 vs. 0.366/h, P less than 0.01). After receiving an injection of 131I-LDL, hyperapo B patients had higher rates of LDL-apo B synthesis than controls (23.1 vs. 13.0 mg/kg per d, P less than 0.001), as did FH patients (22.7 mg/kg per d). The FCR of LDL was similar in hyperapo B patients and controls (0.386 vs. 0.366/d) but was markedly decreased in FH patients (0.192/d). Most subjects exhibited precursor-product relationships between VLDL and IDL, and all did between IDL and light LDL; an analogous relationship between light and heavy LDL was evident in most hyperapo B patients and controls but not in FH patients. Simultaneous injection of differentially labeled LDL fractions and deconvolution analysis showed increased light LDL synthesis with normal conversion into heavy LDL in hyperapo B, whereas in FH conversion of light LDL was reduced and there was independent synthesis of heavy LDL. These data show that the increased concentration of LDL-apo B in hyperapo B is solely due to increased LDL synthesis, which is secondary to increased VLDL synthesis; in contrast, in FH there is both an increase in synthesis of LDL (which is partly VLDL-independent) and reduced catabolism.

Apolipoproteins B↗
PubMed1986

Efficacy of mevinolin as adjuvant therapy for refractory familial hypercholesterolaemia.

Mevinolin, a potent inhibitor of cholesterol synthesis, was used as a therapeutic adjuvant in patients with refractory familial hypercholesterolaemia for an average period of 13 months. Sustained decreases in serum cholesterol of 23 and 31 per cent were achieved by doses of 20 mg and 40 mg/day respectively in 13 heterozygotes already on cholestyramine or after partial ileal bypass. Administration of 80 mg/day to three patients undergoing plasma exchange reduced peak serum cholesterol levels by 11.5 per cent in two homozygotes and by 17 per cent in a double heterozygote for familial hypercholesterolaemia and type III hyperlipoproteinaemia. The decrease in cholesterol was largely confined to low-density lipoprotein and no significant changes occurred in serum triglyceride or high-density lipoprotein cholesterol. Mevinolin was well-tolerated except in one patient who developed myositic symptoms; asymptomatic, transient elevations of serum enzymes were observed in five others. Short and long Synacthen tests showed no evidence that the drug impaired adrenocortical response to ACTH. These results indicate that mevinolin provides a safe and highly effective means of reducing LDL levels in patients with heterozygous familial hypercholesterolaemia refractory to conventional treatment but is less useful in homozygotes.

Adult↗
PubMed1985

Improved survival of patients with homozygous familial hypercholesterolaemia treated with plasma exchange.

Plasma exchange was undertaken in five patients with homozygous familial hypercholesterolaemia at intervals of two weeks for a mean of 8.4 years. These patients had survived an average of 5.5 years longer than their five respective homozygous siblings (p = 0.3), each of whom must have had a matching genetic defect but who died untreated. The 37% decrease in peak serum cholesterol concentrations maintained by plasma exchange presumably reduced progression of atherosclerosis in the treated patients and thus lessened their risk of premature death.

Adolescent↗
PubMed1985

Failure of experimental atherosclerosis to sensitize coronary arteries to spasm in hypercholesterolemic rabbits.

Since hypercholesterolemia sensitizes isolated rabbit coronary arteries to vasoconstrictor stimuli, we assessed the possibility of reproducing occlusive coronary spasm both in vitro and in vivo in atherosclerotic rabbits. In Langendorff-perfused hearts from nine atherosclerotic rabbits (2% cholesterol diet for 18 weeks), despite a threefold increase of cholesterol concentration in the coronary wall compared with nine control rabbits, ergonovine and serotonin did not produce any increase of coronary vascular resistances; the increase produced by pitressin was significantly less in atherosclerotic than in normal hearts (56 +/- 13% vs 138 +/- 28%, p less than 0.05, respectively), whereas that produced by phenylephrine was similar (10.1 +/- 1.8% vs 8.5 +/- 2.4%, p = n.s.). In eight other unanesthetized rabbits we recorded the ECG during ergonovine administration (0.05 mg/kg) and during hypothalamic stimulation before and at regular intervals during the 2% cholesterol diet; rabbits survived for periods ranging from 1 to 22 weeks (mean 9.6 weeks). Only one animal had ST depression during episodes of marked tachycardia; no ischemic ECG changes were ever observed in the other rabbits despite the diffuse subintimal coronary deposition of cholesterol found postmortem. Thus, in atherosclerotic rabbits with chronic marked hypercholesterolemia, coronary arteries do not develop occlusive coronary spasm as observed in patients with variant angina.

Animals↗
PubMed1985

Coronary artery disease and haemostatic variables in heterozygous familial hypercholesterolaemia.

Haemostatic variables were measured in 61 patients with heterozygous familial hypercholesterolaemia, 32 of whom had evidence of coronary heart disease. Age adjusted mean concentrations of plasma fibrinogen and factor VIII were significantly higher in these patients than in the 29 patients without coronary heart disease, but there were no significant differences in serum lipid concentrations between the two groups. Comparisons in 30 patients taking and not taking lipid lowering drugs showed lower values for low density lipoprotein cholesterol, high density lipoprotein cholesterol and antithrombin III, and a higher high density lipoprotein ratio while receiving treatment. The results suggest that hypercoagulability may play a role in the pathogenesis of coronary heart disease in patients with familial hypercholesterolaemia.

Adult↗
PubMed1985

Experience with plasma-exchange in homozygous familial hypercholesterolaemia.

Reduction of plasma cholesterol and apolipoprotein B concentrations can be expected and may appear to slow the rate of progression of the atherosclerotic process (Thompson, 1980). The usefulness of plasma exchange to the treatment of homozygous FH patients has been extended recently by Stoffel et al. (1981), who perfused plasma through an on-line anti-LDL sepharose column, which selectively removes LDL. Having theoretical advantages over plasma-exchange, this procedure avoids the loss of HDL and of other important plasma proteins. In short, plasma-exchange has proved to be a remarkably safe, well tolerated and effective means of treating homozygous FH.

Apolipoproteins B↗