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Foxhounds were made hypercholesterolemic by thyroidectomy and cholesterol feeding. Tracer cholesterol was administered orally, and i.v. and serum samples obtained sequentially for 30 to 89 days at which time the dogs were euthanized and necropsied. Serum and selected tissues were analyzed for cholesterol radioactivity. Kinetics of cholesterol metabolism were calculated. The hypercholesterolemic dogs had large concentrations of cholesterol in the liver. The only kinetic parameter which was correlated with degree of atherosclerosis was the size of pool 2. Absorption of cholesterol was not different in the hypercholesterolemic from control dogs. Tissue cholesterol disappearance rates suggest a third pool of cholesterol having T 1/2 of greater than 200 days. The bile cholesterol kinetics suggest that cholesterol excreted was derived from the very slow pool. Excretion rate and volume appear to be the factors which are most responsible for the inability of the whole animal to maintain homeostasis in cholesterol concentration when a large amount is consumed.

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The in vitro effect of 17 alpha-ethinylestradiol (E) and/or medroxy progesterone acetate (P) was determined on their abilities to alter conversion of glucose to lipid by porcine aorta. The combination of steroidal agents EP/HI (combination at high concentration) at a concentration of 9.5 X 10(-9) moles/ml caused a significant (p less than 0.01) reduction in 14C incorporation into total lipid. When the concentration of each hormone was reduced by one-half EP/LO (combination at low concentration) to give a final concentration of 4.8 X 10(-9) moles/ml the incorporation was also significantly reduced (p less than 0.05). The aforementioned reductions were subsequently found to be the result of depressed incorporation of the substrate glucose for the synthesis of phospholipid (PL), triacylglyceride (TG), a combined fraction of free cholesterol, diacylglyceride and free fatty acid (FC+DG+FFA), and cholesteryl ester (CE). The hormones individually had no effect on the incorporation of U14C-glucose into lipid. The study suggests that these oral contraceptives, when administered in pharmacological doses, can depress the conversion of glucose into arterial wall lipid.

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The use of oral hypoglycemic agents to treat adult-onset diabetes has been implicated in an increased incidence of cardiovascular mortality. Since it is likely that altered arterial wall metabolism plays an important role in the atherogenic process and in cardiovascular disease, the primary aim of the present study was to investigate the in vitro effects of two oral hypoglycemic agents (tolbutamide and glyburide) on glucose and acetate incorporation into aortic lipids of the dog. Tolbutamide resulted in a significantly increased incorporation of glucose in total lipids, phospholipids and fatty acids of aorta, but had no apparent effect on acetate incorporation into aortic lipids. In contrast, glyburide significantly decreased glucose incorporation into the total lipid, phospholipid and triglyceride fractions. Acetate incorporation into the triglyceride, free cholesterol, fatty acid and cholesterol ester fractions of aorta also was significantly decreased by glyburide. The data indicate that the oral hypoglycemic agents tolbutamide and glyburide can alter glucose and acetate utilization by arterial tissue. These observations on arterial lipid metabolism provide sufficient justification for further studies directed towards characterizing the effects of oral hypoglycemic agents on the various aspects of arterial wall metabolism.

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The effect of elevated glucose concentration on the incorporation of labeled glucose and acetate into aortic lipids of the dog was studied. Increased medium glucose concentration (80 mg p. 100-300 mg p. 100) resulted in: 1. an increased incorporation of glucose into aortic total lipids, phospholipids and triglycerides; 2. an increased incorporation of acetate into each lipid fraction studied. In addition, the effect of insulin on glucose incorporation into aortic lipid was assessed. At a concentration of 100 mU/ml, insulin had no effect on glucose incorporation into aortic lipids of the dog.

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The nature and frequency of cytopathologic changes in female mice genitally infected with type 2 herpes simplex virus have been investigated. The extent of virus infection in an individual mouse was assessed by a system of "plus scoring". Exfoliative cytology clearly provided a reliable evaluation of the extent of virus infection and a reliable prognostic index of mouse mortality. A composite index combining both cytologic and virologic information ('vircyt' value) was derived and shown to provide a convenient and precise prognostic index of mouse mortality.

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Patients with abnormal cervical cytology demonstrated a higher prevalence of type-specific complement-fixing antibody to type 2 herpes simplex virus than patients with negative cervical cytology and patients with carcinoma of other body sites. Case-control differences were apparent irrespective of age, socio-economic class and marital status. By contrast, case groups demonstrated a lower prevalence of subjects with type 1 specific antibody. This raises the possibility that pre-adolescent exposure to type 1 herpes simplex virus may offer some measure of protection against pre-malignant and malignant cervical pathology.

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Perfusion of ionophore A23187 (10 muM) in the isolated dog pancreas resulted in a monophasic release of insulin. Ionophore A23187 (10 muM) failed, however, to elicit insulin secretion when added to calcium deficient (0.1 mmoles/L) perfusate. Simultaneous reintroduction of calcium (1.27 mmoles/L) and discontinuance of ionophore A23187 following calcium deficient periods caused a monophasic secretion of insulin which was quantitatively very similar (41,400 +/- 13,800 muU) to that stimulated by ionophore during normocalcemic perfusion. With reference to the current literature, these results suggest that ionophore A23187 elicits insulin secretion in the perfused dog pancreas preparation by increasing the level of free intracellular calcium, a process which is dependent upon a normal extracellular ionic calcium concentration.

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Type-specific antigens for herpes simplex virus type 1 and 2 were prepared by rigorous absorption of cell extracts with heterotypic immune sera. Type-specificity was demonstrated by immunodiffusion and complement-fixation tests against immune sera prepared in rabbits. Specific type 1 complement-fixing reactivity was detected in eleven of fifteen sera from Roman Catholic nuns and in two convalescent sera from patients with recurrent herpes labialis; these sera had been previously shown to contain neutralising and complement-fixing antibody to herpes simplex virus. Three of the non-reacting sera contained low or absent levels of type-common complement-fixing reactivity and other contained no type-specific neutralising antibody. With the exception of three "acute" sera, specific type 2 complement-fixing reactivity was detected in every convalescent or interim serum obtained from patients with a virologically-proven history of type 2 herpes virus infection. It is suggested that complement-fixation testing using these absorbed type-specific antigens preparations may provide a convenient and rapid method for the identification of type-specific antibody in human sera.

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In the presence of a nonstimulatory concentration of glucose, a 60-min perfusion with 50 muM acetylcholine was shown to elicit a monophasic release of insulin in the isolated dog pancreas preparation. A decline in secretory response, which may be due to desensitization of the beta-cell to acetylcholine, was noted during the latter part of the perfusion interval. The potent insulin secretory response elicited by acetylcholine during the 60-min period was abolished 0y 25 muM atropine. Inhibition of the insulinotropic action of acetylcholine was also noted with administration of the mitotic spindle inhibitor, colchicine. When compared to 20-min control perfusions, addition of 1 mM colchicine resulted in a 50% reduction in acetylcholine-induced insulin release. These results suggest that insulin secretion stimulated by acetylcholine can be considered to be due to a muscarinic action of this agent which is dependent, at least in part, upon the microtubular system of the beta-cell.

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By treatment of herpes simplex virus-infected cells with virus antiserum with or without complement, the yield of infectious extracellular virus was significantly reduced. This was shown to be due to an immune alteration of the cell membrane which inhibited release of virus particles from the infected cells and not due to neutralization; both type-common and type-specific antigens of herpes simplex virus were involved. The phenomenon was also evident with antisera directed against cell determinants. The experimental findings are presented and their significance in the immunological defense mechanisms of the body and in viral immunotherapy is discussed.

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