Radioimmunoassay (RIA) data on concentrations of circulating steroids in normal prepubertal and adult male and female humans, chimpanzees, rhesus monkeys, rats, mice, and hamsters have been collated from the literature. Few reports include data for both sexes, for age groups, or for more than one species. In selecting references for inclusion in the tables, efforts were made to choose data only from RIA procedures that were adequately validated. A number of similarities can be found by reviewing the tables. Levels of estradiol appear somewhat similar for humans, chimpanzees, and rhesus monkeys of both sexes. Among the notable differences are the levels of estradiol and progesterone in primates and rodents, the apparently high level of aldosterone in mice, and the patterns of progesterone secretion in mice and rats. All values in the tables have been converted to picograms for easy comparison between steroids and species. Data for humans are fairly complete, but there is a significant lack of information for several other species.
After catecholamine depletion by reserpine, the capacity of the digitalis materials to induce ventricular arrhythmia is diminished. In papillary muscles from cats pretreated with reserpine, the incidence of ouabain-induced extra beats is reduced. The dose of ac. stroph. necessary to induce ventricular arrhythmia in combination with vagal stimulation is increased by reserpine pretreatment. Threshold doses comparable to those in cats not pretreated with reserpine produced arrhythmia after the catecholamine stores were repleted with norepinephrine or isoproterenol. In dogs with A-V block, βTM 10, an agent which prevents the release of catecholamines, markedly reduces the response of the ventricular pacemaker to ac. stroph. Since the arrhythmias induced by large doses of ac. stroph. are not affected by reserpine pretreatment, it is concluded that while catecholamine release is the primary mechanism involved in the arrhythmia produced by small doses, another mechanism also plays a role in this action after larger doses. Only in the dose of 10 mg/kg did it appear that catecholamine depletion did not account entirely for the action of reserpine. The ac. stroph. threshold dose was not increased to the same degree as with the smaller doses of reserpine, and the incidence of ventricular fibrillation induced by the large dose of ac. stroph was reduced. Hypotension produced by reserpine and βTM 10 did not seem to be an important factor in depression of the responsiveness of the ventricular pacemaker to ac. stroph. While the incidence of ouabain-induced extra beats was reduced by reserpine pretreatment, the action of ouabain to increase the tension developed by isolated papillary muscles was not affected.
Aims: (a) To measure infant angiotensin converting enzyme (ACE) activity in healthy term infants at birth and during the first three months of life. (b) To determine the relation between serum ACE activity and infant feeding practice during this period. (c) To investigate the relation between serum ACE activity and birth weight and other potential contributing factors including acid-base status at birth, gestation, and maternal ACE genotype. Methods: Prospective study of term infants, with clinical and feeding data collected from parents and medical records, and serum ACE measured in the infant at birth and 1 and 3 months of age, and in the mother at the time of birth and one to three months after birth. Results: At birth and 1 and 3 months of age, infant serum ACE activity was twice that of maternal ACE activity. Infant ACE activity at birth and 1 and 3 months did not significantly differ between breast and formula fed infants. There was a highly significant negative correlation between infant ACE activity at 3 months and birth weight (r = 20.52; p , 0.001). This persisted after the conversion of birth weights to z scores (r = 20.34; p = 0.03). ACE activity at 3 months was also related to placental weight (r = 20.30; p = 0.02) and maternal age (r = 20.30; p = 0.05). The strong correlation between serum ACE activity and birth weight z score persisted after adjustment for maternal age and placental weight (r = 20.34; p = 0.03). Conclusion: As ACE is increasingly identified as a risk factor for cardiovascular disease, serum ACE activity in infancy may contribute to the link between low birth weight and later cardiovascular events.T here are numerous reports of low birth weight being associated with coronary heart disease, hypertension, stroke, and non-insulin dependent diabetes. 1 These associations are thought to be the consequence of a stimulus or an insult occurring at a critical period of early life and resulting in permanent effects on structure and metabolism. 2 There is evidence that this concept of ''programming'' may not be exclusive to intrauterine life, and nutritional interventions during the postnatal period may also influence later health.3 For example, recent data indicate that children who are breast fed in infancy have lower blood pressures during later childhood and adolescence than children who are formula fed. [4][5][6] Although there are several constituents of breast milk that are possible causes, including hormones, nutrients, and trophic substances, 5 the underlying mechanisms remain uncertain.Angiotensin converting enzyme (ACE) not only has a key role in the regulation of peripheral blood pressure, 7 but it is now increasingly being identified as a major risk factor for cardiovascular disease.8 9 There is some evidence that ACE activity may be increased in preterm infants especially those with respiratory distress syndrome in the newborn period. 11Infant lung capillaries are a rich source of ACE, and hypoxic mice are known to have raised serum ACE activity at birth. 11Whether this increase...
The residual acidity is taken as acetic acid 56-5 % by weight, and butyric acid 43-5 % by weight. The non-volatile portion is recorded as butyric acid for the purpose of calculation. (See Table III, p. 232, and pp. 246-7.) Calculated as Percentage of Starch Fermented. 100g. starch gives 111 1 g. hexose and contains 44*4 g. carbon g. Carbon 100 g. starch gives 10-77 acetone
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