Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

[Q]: Abstract: The cross-sectional relationship of endogenous androgens (testosterone, androstenedione, and dehydroepiandrosterone sulfate [DHEA-S]), estrogen (estradiol) and progestin (progesterone) to serum levels of lipoprotein cholesterol (very low-density [VLDL], low-density [LDL], and high-density lipoprotein [HDL]) and apolipoproteins (apo A-I and apo B) were studied in white (n = 251) and black (n = 258) adolescent boys, ages 11 to 17 years, as part of the Bogalusa Heart Study. Black boys had significantly higher levels of estradiol, HDL cholesterol, and apo A-I, and lower levels of androstenedione and VLDL cholesterol than white boys, independent of age and adiposity. Age was correlated strongly with testosterone and androstenedione, and moderately with DHEA-S and estradiol levels in both races. However, only in white boys was age consistently related to VLDL cholesterol (positively), HDL cholesterol (negatively), and apo A-I (negatively). Overall, testosterone was associated inversely with HDL cholesterol and apo A-I in white boys, while progesterone was related positively to apo A-I in both races after adjusting for age and adiposity. However, these relationships were found to differ with age. Partial correlations between levels of sex hormones and lipoproteins adjusted for age and adiposity showed no associations in the 11 to 12 year age group in boys of either race. A significant positive relation of testosterone to VLDL cholesterol, and inverse relations of testosterone to HDL cholesterol and apo A-I and DHEA-S to HDL cholesterol were apparent only in white boys in the 13 to 14 year age group.(ABSTRACT TRUNCATED AT 250 WORDS)
[A]: Racial (black-white) comparisons of the relationship of levels of endogenous sex hormones to serum lipoproteins during male adolescence: the Bogalusa Heart Study.

[Q]: Abstract: The effect of prolonged osmotic stimulation on the oxytocin (OT) mRNA levels of OT-producing neurons was investigated in separate hypothalamic nuclei of the rat. After drinking 2% NaCl for 2 weeks, a 2-fold increase in the OT mRNA content was found by Northern blot analysis of microdissected supraoptic nucleus (SON) and paraventricular nucleus (PVN). The same samples showed a similar change in vasopressin (VP) mRNA levels. This treatment resulted in a 70% depletion of both OT and VP from the neurointermediate lobe of the pituitary gland and a marked increase in OT and VP plasma levels. Analysis of the OT mRNA concentration by quantitative in situ hybridization showed that the SON, PVN, and anterior commissural nucleus responded similarly, with a 1.5-fold increase in OT mRNA after 7 days of osmotic stimulation. These results demonstrate that OT gene expression in the magnocellular neurons of the SON, PVN, and anterior commissural nucleus is sensitive to this osmotic stimulus, as is the VP gene of magnocellular neurons in the SON and PVN. The responsiveness of OT-producing neurons may point to a role for OT in the regulation of water and electrolyte balance.
[A]: Oxytocin gene expression in discrete hypothalamic magnocellular cell groups is stimulated by prolonged salt loading.

[Q]: Abstract: Electrocardiographic monitoring and provocative ventricular pacing were used to evaluate control and nadolol treatment groups 6 to 24 hours after left anterior descending coronary artery ligation in the dog. During the 6 to 24 hour period, the control group (n = 20) developed ventricular triplets at rates exceeding 270/min. Seven dogs spontaneously developed sustained monomorphic ventricular tachycardia (421 +/- 12 beats/min) at 13 +/- 2 hours. Sustained monomorphic ventricular tachycardia was present for 38 +/- 8 seconds before ventricular fibrillation developed. One dog developed recurrent monomorphic ventricular tachycardia, with six episodes lasting from 8 to 72 seconds (375 to 425 beats/min). At 24 hours, ventricular pacing produced sustained monomorphic ventricular tachycardia (378 +/- 12 beats/min) in 9 of 13 surviving animals. Nadolol administration 6 hours after coronary artery ligation (n = 19) lowered both the rate (241 +/- 8 versus 328 +/- 8 beats/min; p = 0.001) and the incidence (8 +/- 6 versus 198 +/- 61 per hour; p = 0.004) of rapid ventricular triplets and prevented sudden arrhythmic death (0%; p = 0.005). Nadolol failed to prevent sustained monomorphic ventricular tachycardia (88%; 365 +/- 12 beats/min) produced by ventricular pacing. The data suggest that nadolol prevents spontaneous sustained monomorphic ventricular tachycardia by selectively suppressing the arrhythmia trigger (rapid ventricular triplets) without altering the underlying arrhythmia substrate.
[A]:
Mechanism of prevention of sudden death by nadolol: differential actions on arrhythmia triggers and substrate after myocardial infarction in the dog.