Effect of glucagon on hepatic malonyl coenzyme A concentration and on lipid synthesis.
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Biomedical subjects
Publications and source records attributed to G A Cook.
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Fatty acid and cholesterol synthesis in isolated rat hepatocytes were strongly inhibited by 5-(tetradecyloxy)-2-furoic acid. With either 3H2O or [2(-14)C] acetate as the labeled precursor, the concentrations of inhibitor causing 50% decrease in fatty acid and cholesterol synthesis were, respectively, less than 0.005 mM and 0.020 mM. At 0.1 mM inhibitor, citrate concentration in cells from fed rats was increased by 75%; lactate and pyruvate concentrations were decreased by 30%; ethanol oxidation was decreased by 20%; with cells from starved rats, the mitochondrial [NAD+]/[NADH] was decreased. Other parameters were unaffected. Both its potency and its specificity indicate that 5-(tetradecyloxy)-2-furoic acid will be useful in studies on the regulation of lipid biosynthesis.
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This paper seeks to clarify those conceptual foundations of G.H. Mead's social behaviorism which are assumed, but not made explicit, in that writer's well-known volume Mind, Self and Society. These foundations are shown to be an outgrowth of Mead's early commitment to the organic conception of conduct underlying the psychological functionalism of the Chicago School. Further light is shed upon Mead's position by pointing out the fundamental differences between his model of conduct and that characteristic of the behaviorist tradition in American psychology.
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Long-term observations of a 35-year-old woman who died from refractory congestive heart failure due to Takayasu's aortoarteritis are reported. Severe systolic hypertension was documented in the pre-pulseless phase. After the loss of all limb pulses, but relative sparing of carotid vessels, serial ophthalmodynamometric retinal pressures suggested that central aortic pressure remained high during her terminal cardiac illness. Postmortem pathologic examination showed a narrowed, severely atherosclerotic aorta with variable occlusions of all branch vessels. The loss of capacitance and volume of the aorta appears to be the cause of systolic hypertension and refractory pump failure of the left ventricle.
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