Clinical guidelines for obstetrical practice were first published by the Japan Society of Obstetrics and Gynecology (JSOG) and the Japan Association of Obstetricians and Gynecologists (JAOG) in 2008, and a revised version was published in 2011. The aims of this publication include the determination of current standard care practices for pregnant women in Japan, the widespread use of standard care practices, the enhancement of safety in obstetrical practice, the reduction in burdens associated with medico-legal and medico-economical problems, and a better understanding between pregnant women and maternity-service providers. These guidelines include a total of 87 Clinical Questions followed by several Answers (CQ&A), a Discussion, a List of References, and some Tables and Figures covering common problems and questions encountered in obstetrical practice. Each answer with a recommendation level of A, B or C has been prepared based principally on "evidence" or a consensus among Japanese obstetricians in situations where "evidence" is weak or lacking. Answers with a recommendation level of A or B represent current standard care practices in Japan. All 87 CQ&As are presented herein to promote a better understanding of the current standard care practices for pregnant women in Japan.

Melatonin plays a critical role in a variety of mammalian reproductive processes not only acting on the central nervous system but also behaving as a peripheral physiologic regulator. To address the relevance of melatonin to the maintenance of pregnancy at the feto-maternal interface, we investigated the expression of two types of membrane melatonin receptors, MT1 and MT2, as well as arylalkylamine N-acetyltransferase (AA-NAT) and hydroxyindole-O-methyltransferase (HIOMT), the two enzymes required for the conversion of serotonin to melatonin, in the human placenta and the effect of melatonin on the release of human chorionic gonadotropin (hCG) from cultured human trophoblast cells. RT-PCR analysis and DNA sequencing revealed that transcripts of MT1, MT2, AA-NAT, and HIOMT were present in the first-trimester human placenta. We also found that melatonin significantly potentiated hCG secretion at optimal concentrations. These results suggest that melatonin may regulate human placental function in a paracrine/autocrine manner, providing evidence for a novel role in human reproduction.

The present study was undertaken to investigate the effects of GH on follicular growth, oocyte maturation, ovulation, and production of insulin-like growth factor-I (IGF-I) in the in vitro perfused rabbit ovaries. Ovulation did not occur in any ovaries perfused with GH at a concentration of 1, 10, 100, or 200 ng/ml, but the addition of GH to the perfusate increased the follicle diameter in a dose-dependent manner. The production of IGF-I by ovaries perfused with medium alone was very low throughout the perfusion period. The addition of 100 ng/ml GH to the perfusate significantly increased ovarian production of IGF-I at 4, 6, 8, and 12 h compared with the contralateral control ovaries. Changes in the tissue concentrations of IGF-I in ovaries perfused with 100 ng/ml GH paralleled those triggered by exposure to 50 IU human CG (hCG). When the effect of GH on the tissue concentration of IGF-I was determined at 4 h, GH stimulated the tissue concentration of IGF-I in perfused rabbit ovaries in a dose-dependent manner. The percent increase in follicle diameter in ovaries treated with GH was significantly correlated with the intraovarian IGF-I content. The mean number of ovulations per ovary and the ovulatory efficiency were significantly reduced in ovaries perfused with 5 IU hCG, compared with those in ovaries perfused with 50 IU hCG. The addition of 100 ng/ml GH to the perfusate significantly increased the ovulatory efficiency and follicle diameter in the 5 IU hCG-treated ovaries. Exposure to GH significantly stimulated the resumption of meiosis in the follicular oocytes compared with that in ovaries perfused with medium alone. Furthermore, GH significantly stimulated the resumption of meiosis in ovulated ova and follicular oocytes in ovaries treated with 5 IU hCG. Thus, exposure to GH-stimulated follicular growth, oocyte maturation, and production of IGF-I in the in vitro perfused rabbit ovaries, which indicates that the ovary is in fact a site of GH reception and action. Additionally, GH enhanced the effects of gonadotropins, acting synergistically to promote the ovulatory process. These observations suggest that GH may amplify gonadotropin actions in the process of follicular development and ovulation, at least in part, by stimulating ovarian IGF-I production.

We examined the effects of insulin-like growth factor (IGF)-I on follicular growth, oocyte maturation, and ovarian steroidogenesis and plasminogen activator (PA) activity in vitro, using a perfused rabbit ovary preparation in order to determine whether the follicle-stimulating effects of growth hormone (GH) are mediated by IGF-I. The addition of IGF-I to the perfusate stimulated follicular growth and the resumption of meiosis in follicular oocytes in a dose-dependent manner. There was no significant difference in the production of progesterone by perfused rabbit ovaries between IGF-I-treated and control ovaries, whereas IGF-I increased the production of estradiol (E2) by perfused rabbit ovaries in a dose-dependent manner. The concomitant addition of a monoclonal antibody recognizing the type I IGF receptor, alpha IR-3, to the perfusate significantly blocked IGF-I-stimulated follicular growth, oocyte maturation, and E2 production. Intrafollicular PA activity increased significantly 4 h after exposure to 10 or 100 ng/ml of IGF-I and reached maximal levels at 6 h. The percentage increase in follicle diameter at 6 h after exposure to IGF-I was significantly correlated with the intrafollicular PA activity. Treatment with GH resulted in a 2.7-fold increase in intrafollicular levels of IGF-I mRNA. The binding of [125I]-IGF-I to rabbit ovarian membrane preparations was inhibited by unlabeled IGF-I and IGF-II in a concentration-dependent manner. The relative affinity of the IGF-I receptor for IGF-I, IGF-II, and insulin was typical of type I binding (IGF-I > IGF-II > insulin). Affinity cross-linking of ovarian membranes with [125I]-IGF-I revealed a radiolabeled band corresponding to a molecular weight of 135,000, the alpha subunit of the type I IGF receptor. This band was totally displaced by IGF-I and alpha IR-3. It was concluded that IGF-I stimulated follicular development, E2 production, and oocyte maturation by interacting with its specific receptor located in rabbit ovarian membranes.

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