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Because of the recent report by the Lipid Research Group showing that a lowering of total cholesterol and LDL cholesterol lowered mortality due to coronary heart disease (CHD) and other similar studies, there can no longer be any doubt that cholesterol is a causal factor in the development of CHD. Since total serum cholesterol and LDL cholesterol are produced by the body, those interested in the prevention of CHD must give greater attention to factors which are associated with raised endogenous cholesterol. The major factors are increased dietary and body fat, emotional arousal, and the inability of the liver to clear the serum of low density lipoprotein. The beneficial effect of exercise on lowering one's risk of CHD reported in the literature may be mediated by a rise in HDL cholesterol and/or weight loss. All patients should have their total cholesterol/HDL measured. Those with elevated serum cholesterols should be encouraged to eat a low saturated low fat diet, exercise, maintain proper weight and avoid undue distress. Cigarette smoking should be discouraged. Blood pressure elevations not responsive to diet and exercise should be treated with medication. Cholesterol elevations not responsive to life style change, should be treated with Cholestyramine.

To further understand the hormonal mechanisms linking behavior pattern and coronary artery disease (CAD), we investigated the relationship between 0930-hour plasma cortisol and cholesterol in relatively young males who had undergone coronary angiography and in a subgroup of individuals who had undergone the structured interview for classification of behavior pattern. A statistically significant association (p less than 0.05) was found between cortisol and cholesterol for individuals who had either minimal CAD (20% to 49% narrowing) or significant CAD (greater than or equal to 50% narrowing), but not for subjects without CAD. An association between cortisol and cholesterol was also found to be significant for the subgroup of individuals with Type A-1 behavior pattern, but not for those with Type A-2, X, or B behavior patterns. The findings suggest that hormonal mechanisms involving cortisol and cholesterol metabolism may be operative in individuals with CAD as well as in individuals with Type A-1 behavior.

The mitochondrial lipids from avocado fruit, cauliflower buds, and potato tubers, and the lipids of chloroplasts isolated from avocado fruit and from cauliflower leaves were identified and the concentrations were determined. The lipid composition was compared with that of beef heart mitochondria. Phospholipids constituted 50-56% of total lipids in plant mitochondria while this fraction made up 90% of the lipids in beef heart mitochondria. In both cases the chief phospholipids were phosphatidylcholine and phosphatidylethanolamine. A characteristic feature of plant mitochondria was the presence of monogalactosyl- and digalactosyldiglyceride and of sulfolipid. Potato mitochondria differed from the particles of other species investigated by their higher content of galactolipids, sterol glycosides, and carotenoids and lower content of phospholipids and of total lipids in the lipidprotein complex. The galactolipid content was markedly higher in chloroplasts from all sources than in mitochondria. The spectrum of lipids in the phospholipid fraction differed more strikingly between chloroplasts of the leaf and the mitochondria of the bud of cauliflower than between the two organelles of the avocado mesocarp. The fatty acid distribution of individual lipids and of classes of lipids was also more similar in the two organelles of the fruit tissue than in the cauliflower material.

The potential role of indoleactic acid (IAA)-oxidase as an in vivo abscission regulating system in the cotton (Gossypium hirsutum L.) cotyledonary explant was investigated. Phenols (usually monophenols), which are cofactors of cotton IAA-oxidase in vitro, accelerated abscission. Phenols (usually orthodihydroxyphenols), which inhibit cotton IAA-oxidase in vitro, inhibited abscission. Inhibition or stimulation of abscission was accomplished by phenols both with and without IAA. Results were similar when treatments were applied as lanolin pastes to the cut petiole ends or as solutions in which explants were submerged. An abscission accelerating phenol stimulated the decarboxylation of IAA-1-(14)C by explants and an abscission inhibiting phenol inhibited the decarboxylation of IAA-1-(14)C.The mechanism of abscission regulation by the phenolic compounds was concluded to involve auxin destruction via IAA-oxidase.In addition to the direct relationship of this study to abscission, the results support the more general hypothesis that IAA-oxidase acts in vivo to regulate auxin levels.