Serum steroid levels following a large intravenous dose of a steroid sulfate precursor during the second trimester of human pregnancy. II. Pregnenolone sulfate.
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Biomedical subjects
Publications and source records attributed to J E Buster.
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PROBLEM: This study measured platelet-activating factor (PAF) production of in vitro and in vivo fertilized murine embryos to ascertain whether site of fertilization impacted subsequent embryonic PAF production. METHOD: Oocytes and embryo were collected from stimulated B6D2F1 mice. PAF production throughout the preimplantation phase from the two-celled stage through expanded blastocysts was measured and compared among normally developing embryos with the only difference being site of fertilization. RESULTS: A striking increase in PAF production was noted for both in vivo and in vitro fertilized embryos over the four days of culture. Significantly higher (P < .001) levels of PAF production were noted with development from the two-celled stage (47.22 +/- 4.13; 44.30 +/- 2.43) to expanded blastocysts (254.31 +/- 24.01; 255.11 +/- 5.35 ng/embryo/24 h) for both in vitro and in vivo fertilized embryos, respectively. There was no significant difference (P > .05) in PAF production between the two groups of embryos. CONCLUSIONS: Embryonic PAF production in the mouse increases in a stage-specific manner, and specifically the site of fertilization in vitro versus in vivo does not affect PAF production in normally developing embryos.
OBJECTIVE: We hypothesized that intravenous dehydroepiandrosterone (DHEA) would decrease insulin resistance in normal and insulin-resistant women. METHODS: Five insulin-resistant women diagnosed as having polycystic ovaries (PCO) with elevated testosterone and normal dehydroepiandrosterone sulfate (DHEAS) with amenorrhea were recruited. Obese controls (OC) with normal menses and normal testosterone and DHEAS were recruited and matched to each PCO woman for age and weight. The PCO women had a mean testosterone of 3.2 +/- 0.4 nmol/L, fasting serum insulin level of 330 +/- 55 pmol/L, and DHEAS level of 3.4 +/- 1.3 mumol/L. An oral glucose tolerance test (OGTT) was performed at 8 AM after an overnight fast. A DHEA infusion (1 mg/hour for 17 hours) was begun at 6 PM and continued until the completion of the second OGTT performed the following morning at 8 AM. T-lymphocytes were drawn at 8 AM each morning. RESULTS: The DHEA infusion had no significant effect on any of the in vivo indices of insulin sensitivity, ie, basal and OGTT insulin, C-peptide, and ratios of insulin/glucose. In vitro, DHEA significantly increased insulin binding to T-lymphocytes of PCO women but caused no significant change in OC women. There was, however, marked enhancement of T-lymphocyte pyruvate dehydrogenase (PDH) activities in both groups of study subjects following DHEA. CONCLUSION: We conclude that a 17-hour infusion of DHEA enhanced T-lymphocyte insulin binding and PDH activity while producing no detectable improvements in in vivo indices of insulin sensitivity.
Five unruptured isthmic tubal pregnancies diagnosed at laparoscopy were treated with either methotrexate/citrovorum factor rescue (MTX/CF) (n = 4) or observation alone (n = 1). Entry criteria required that the ectopic be fully visualized, no greater than 3 cm in diameter, with intact serosa, and without active bleeding. Treatment selection was based upon preoperative levels of beta-hCG with MTX/CF given to subjects exhibiting a plateaued or rising pattern and observation alone given those with falling levels. Subjects were followed with serial measurements of beta-hCG, complete blood counts, and liver function tests. In all subjects the ectopic pregnancy resolved without further surgery. Time to resolution (first day of treatment to undetectable beta-hCG) ranged from 12 to 55 days. Of the five subjects studied, follow-up hysterosalpingograms in four demonstrated tubal patency on the side of the ectopic gestation.
Two clinically healthy pregnant women were studied in a single 24-h span during the third trimester. Blood drawn every 20 min was assayed for cortisol (F), dehydroepiandrosterone sulfate (DHEA-S), estriol (E3), and prolactin (PRL). Blood drawn hourly was assayed for progesterone (P), human placental lactogen (HPL) and 15alpha-hydroxyestriol (E4). Breast temperature (BT) was continuously monitored. Single cosinor analysis demonstrated statistically significant circadian rhythms for plasma concentrations of F, DHEA-S, and BT for both subjects, and of E3 for one subject. Statistically significant circadian rhythms in plasma concentrations of P, HPL, E4 or PRL could not be demonstrated in our third trimester subjects. However, analysis of data from subjects sampled at earlier gestational ages revealed highly significant PRL circadian rhythms. These results suggest that plasma concentrations of PRL show a progressive decrease in circadian amplitude despite a progressive increase in mesor with advancing gestational age. Frequent sampling and cosinor data analysis permit identification of circadian rhythms in BT. The use of BT as a potential marker for rhythms in plasma concentration of certain hormones awaits further scrutiny. The demonstration of several circadian endocrine rhythms in individual subjects in the third trimester of human pregnancy facilitates the usefulness of such marker rhythms.