Fetal well-being measures included umbilical artery Dopplers, fetal heart tracing and rate, and biophysical profile.

Measures were obtained at rest and immediately postexercise.

RESULTS: Groups were similar in age, body mass index, and gestational age. Maternal resting heart rate in the highly active group (61.6 +/- 7.2 beats per minute [bpm]) was significantly lower than the nonexercise (79.0 +/- 11.6 bpm) and regularly active (71.9 +/- 7.4 bpm) groups (P<.001). Treadmill time was longer in highly active (22.3 +/- 2.9 minutes) than regularly active (16.6 +/- 3.4) and nonexercise selleck (12.1 +/- 3.6) groups (P<.001), reflecting higher fitness. With moderate exercise, all umbilical artery Doppler indices were similar pre-exercise and postexercise among groups. With vigorous exercise, Dopplers were similar in regularly and highly active women with statistically significant decreases postexercise (P<.05). The group x time interaction was not significant. Postexercise fetal heart tracings met criteria for reactivity within 20 minutes

after all tests. Biophysical profile scores were reassuring.

CONCLUSION: GNS-1480 mw This study supports existing guidelines indicating pregnant women may begin or maintain an exercise program at moderate (inactive) or vigorous (active) intensities. (Obstet Gynecol 2012;119:603-10) DOI: 10.1097/AOG.0b013e31824760b5″
“The enzymes and pathways of steroidogenesis are central to an understanding of adrenarche. The quantitative regulation of steroidogenesis occurs Sapitinib concentration at the first step, the conversion of cholesterol to pregnenolone. Chronic quantitative regulation

is principally at the level of transcription of the CYP11A1 gene encoding P450scc, which is the enzymatically rate-limiting step. Acute regulation is mediated by the steroidogenic acute regulatory protein (StAR), which facilitates the rapid influx of cholesterol into mitochondria, where P450scc resides. Qualitative regulation, which determines the type of steroid produced in a cell, is principally at the level of P450c17 (CYP17). In the absence of P450c17 in the zona glomerulosa, C21 deoxy steroids are produced, leading to the mineralocorticoid, aldosterone. In the presence of the 17 alpha-hydroxylase but not the 17,20 lyase activity of P450c17 in the zona fasciculata, C21, 17-hydroxy steroids are produced, leading to the glucocorticoid, cortisol. When both the 17 alpha-hydroxylase and 17,20 lyase activities of P450c17 are present in the zona reticularis, the androgen precursor DHEA is produced. The discrimination between 17 alpha-hydroxylase and 17,20 lyase activities is regulated by two post-translational events, the serine phosphorylation of P450c17 and the allosteric action of cytochrome b(5), both of which act to optimize the interaction of P450c17 with its obligatory electron donor, P450 oxidoreductase.