Maternal smoking during pregnancy is associated with a variety of adverse neonatal outcomes including altered reproductive performance. Herein we provide molecular evidence for a pathway involved in the elimination of the female germline due to prepregnancy and/or lactational exposure to polycyclic aromatic hydrocarbons (PAHs), environmental toxicants found in cigarette smoke. We show that ovaries of offspring born to mice exposed to PAHs contained only a third of the ovarian follicle pool compared with offspring of unexposed female mice. Activation of the cell death pathway in immature follicles of exposed females was mediated by the aryl hydrocarbon receptor (Ahr), as ovarian reserve was fully rescued by maternal cotreatment with the Ahr antagonist, resveratrol, or by inactivation of the Ahr gene. Furthermore, in response to PAHs, Ahr-mediated activation of the harakiri, BCL2 interacting protein (contains only BH3 domain), was necessary for execution of cell death. This pathway appeared to be conserved between mouse and human, as xenotransplanted human ovarian cortex exposed to PAHs responded by activation of the identical cell death cascade. Our data indicate that maternal exposure to PAHs prior to pregnancy and/or during lactation compromises ovarian reserve of female offspring, raising the concern about the transgenerational impact of maternal smoking on ovarian function in the human.

There was a significant improvement in self-assessed health in parallel with a significant downward secular trend in the prevalence of menopause awareness among community-dwelling Japanese women. Women who felt themselves affected by menopause tended to perceive their own health as poor.

No abstract

In this study, we focused on the uctuation of the abdominal skin temperature (AST) during sleep as a second marker for determining the biphasic menstrual cycle, alongside the basal body temperature. The nocturnal AST was measured every 10 min using a wearable device mounted on the abdominal wall. With this system, the AST time-series data were recorded for a total of 1667, 1035, and 1690 days from seven participants for the menstrual/follicular, ovulatory, and luteal phases, respectively. First, the AST uctuation was evaluated by plotting the cumulative probability distribution (CPD) of changes in AST every 10 min from 0 to 0.7 C. The results showed that the CPD tted well with an exponential attenuation curve. Second, the mean attenuation coef cients obtained by exponential regression from the CPD data were compared among the three phases. For regular menstrual cycles, the attenuation coef cient was the highest in the menstrual/follicular phase (8.57; 95% con dence interval 8.44-8.70; R 2 = 0.983; P < 0.001), followed by the ovulatory phase (7.80; 95% con dence interval 7.65-7.96; R 2 = 0.985; P < 0.001) and then the luteal phase (7.24; 95% con dence interval 7.12-7.36; R 2 = 0.985; P < 0.001). Finally, we examined whether the attenuation coef cients can be used as an index to classify the three phases by long short-term memory (LSTM)-based deep learning. Consequently, the attenuation coef cient affected the prediction of the menstrual/follicular, ovulatory, and luteal phases with signi cantly higher F-measures of 0.603, 0.328, and 0.660, respectively. These results suggest that the thermoregulatory system may increase the AST uctuation in healthy women during the transition from the follicular phase to the ovulatory phase and then to the luteal phase.

No abstract

No abstract

No abstract