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In spite of the importance of the corpus luteum in human reproduction, little is known about its formation after ovulation and during regression in the absence of conception. This is largely due to constraints on the availability of normal human tissue: therefore an appropriate model which could be studied and provide information applicable to the human was sought. The baboon (Papio), a non-human primate, has been determined to be one such model. Thus, in the past several years our studies have examined the role of luteal peptides in corpus luteum function, and, when possible, we have attempted to examine corpora lutea from the human and baboon in parallel. Although a milk-ejection factor was recognized to be present in luteal tissue in 1910 (Ott and Scott, Proc. Soc. Exp. Biol. Med., Vol. 8, p 49), the role of oxytocin in luteal physiology has not been easy to ascertain. This is in part due to the methodologies employed to assess its role. Our studies summarized below suggest that oxytocin does not directly affect luteal steroidogenesis, but that it may play a role in cell to cell communication involving the expression of the gap junction proteins, the connexins. In view of the fact that oxytocin, its receptor, gap junctions and associated proteins are not unique to the human and non-human primates, the model of luteal development and demise proposed may be applicable to most species. [ABSTRACT FROM PUBLISHER]

Objective: This study was undertaken to investigate the effects of 17beta-estradiol (E2) on G1 cell cycle progression and proliferation in uterine fibroid and myometrial cells and the roles of phosphatidylinositol-3 kinase and mammalian target of rapamycin in mediating these estrogen effects.Study Design: The human uterine smooth muscle-derived cells (UtSM) and uterine leiomyoma-derived cells (UtLM) were treated with varying doses of E2 with or without pretreatment with LY294002, a phosphatidylinositol-3 kinase inhibitor, or rapamycin, a mammalian target of rapamycin inhibitor. The effects of E2 on cell cycle progression and proliferation and the roles of phosphatidylinositol-3 kinase and mammalian target of rapamycin in E2-induced effects were studied.Results: Compared with controls, E2 significantly induced G1 cell cycle progression and proliferation in uterine smooth muscle-derived cells and uterine leiomyoma-derived cells. These effects, however, were significantly blocked when LY294002 or rapamycin was used.Conclusion: E2 significantly induces G1 cell cycle progression and cell proliferation in uterine smooth muscle-derived cells and uterine leiomyoma-derived cells, in which phosphatidylinositol-3 kinase and mammalian target of rapamycin are essentially required. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of this study was to compare acetaminophen with ibuprofen for pain relief and menstrual fluid prostaglandin F2alpha (PGF2alpha) suppression in primary dysmenorrhea. STUDY DESIGN: Twelve subjects were randomized to placebo, acetaminophen (1000 mg orally, 4 x daily for 3 days) or ibuprofen (400 mg orally, 4 x daily for 3 days), once during each cycle in a prospective, double-blinded, crossover study. Using preweighed super absorbent tampons, menstrual fluid was collected, extracted, and PGF2alpha radioimmunoassayed. RESULTS: Ten patients completed the study. Ibuprofen (P = .002) and acetaminophen (P = .022) were rated significantly better than placebo. Total menstrual fluid PGF2alpha with placebo was 36.2 + 6.1 microg but were 14.8 + 3.0 microg with ibuprofen (P = .001) and 21.4 + 3.4 microg with acetaminophen (P = .008). PGF2alpha concentrations with placebo were 0.34 + 0.054 microg/mL, with ibuprofen 0.16 + 0.026 microg/mL (P = .001), and with acetaminophen 0.23 + 0.029 microg/mL (P = .016). CONCLUSION: Both ibuprofen and acetaminophen were superior to placebo for pain relief and menstrual fluid PGF2alpha suppression, with ibuprofen being more potent. [ABSTRACT FROM AUTHOR]