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Subcutaneous co-administration of 75 IU lutropin alfa with follitropin alfa is safe and effective in inducing follicular development in women with profound gonadotrophin deficiency.

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Insulin resistance occurs frequently in metabolic syndrome components, obesity, and the polycystic ovary syndrome, and is partly due to impaired glucose transport into skeletal muscle, but underlying mechanisms are uncertain. Atypical protein kinase C and protein kinase B, operating downstream of phosphatidylinositol 3-kinase, mediate insulin effects on glucose transport, but their importance in these syndromes is poorly understood. Presently, we examined these signaling factors in muscle biopsies obtained during euglycemic/hyperinsulinemic clamp studies. In lean subjects, insulin provoked approximately twofold increases in muscle atypical protein kinase C activity. In obese subjects and obese subjects who had evidence of the polycystic ovary syndrome, insulin-stimulated glucose disposal and atypical protein kinase C activation were diminished, whereas activation of insulin receptor substrate-1-dependent phosphatidylinositol 3-kinase and protein kinase B trended lower, but not significantly. Interestingly, direct activation of atypical protein kinase C by phosphatidylinositol-3,4,5-(PO(4))(3), the lipid product of phosphatidylinositol 3-kinase, was readily apparent in immunoprecipitates prepared from muscles of lean subjects, but to a lesser degree or poorly if at all in subjects who were obese or had the obesity/polycystic ovary syndrome. Our findings suggest that activation of muscle atypical protein kinase C by insulin and phosphatidylinositol-3,4,5-(PO(4))(3) is defective and may contribute to skeletal muscle insulin resistance in women who are obese, or have obesity associated with the polycystic ovary syndrome.

A case-control study, using data abstracted between 1983 and 1987 from a large perinatal registry, was conducted to explore the relationship between smoking and ectopic pregnancy. Women with ectopic pregnancy (n = 634) seen at University of Illinois Perinatal Network Hospitals were compared to women who were delivered of a single live-bom infant (n = 4287). Adjusted for age and race, women who reported smoking during pregnancy had a greater than twofold risk of ectopic pregnancy (Odds Ratio = 2.5, 95% confidence interval = 1.9, 3.2) compared to women who never IntroductionAlthough ectopic pregnancy is a relatively uncommon occurrence, its incidence has quadrupled from a rate of 5/1000 live births in 1970.1 Simultaneously, maternal mortality rates from other causes have fallen, making ectopic pregnancy the primary cause of maternal mortality during the first trimester of pregnancy. Known risk factors for ectopic pregnancy include pelvic inflammatory disease, prior tubal surgery, contraceptive history, and a history of infertility.2 As the rise in incidence of ectopic pregnancy has paralleled the increase in cigarette smoking among women, it is reasonable to examine smoking as a potential risk factor.Most of the evidence for the positive association of smoking and ectopic pregnancy derives from studies in which smoking was not a primary hypothesis (Odds Ratios = 1.5 to 3.9).3-Recently Chow, et al, investigated the potential etiologic relationship between cigarette smoking at the time of conception and ectopic pregnancy, considering the effect of age at initiation, smoking duration, and intensity on this event. An overall association of smoking with ectopic pregnancy was evident (OR = 2.2), but a dose-response was not demonstrated, possibly due to an inadequate number of cases. To permit more stable estimates of the risk of ectopic pregnancy by level of smoking, a case-control study using data from a large perinatal registry was conducted.

Lower ff NO3/NO2 levels at the time of oocyte retrieval are associated with adequate fertilization and embryo cleavage rates. In our IVF model, no correlation was found between ff IL-1beta levels and ff NO3/NO2, fertilization, or embryo cleavage rates.