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Background Polycystic ovary syndrome (PCOS) is a complex endocrinopathy, which leads to ovulation dysfunction and infertility, as well as metabolic and mental disorders. Women with PCOS exhibit several characteristic symptoms, with marked heterogeneity across different races and ethnicities. Methods In this review, the author outlines the phenotypic disparities of PCOS among various racial and ethnic populations. First, the prevalence of major symptoms in different racial and ethnic groups with PCOS is summarized. Next, the effects of four phenotypes, derived from the Rotterdam criteria for PCOS, on metabolic and reproductive features are recapitulated. Main Findings A growing body of evidence suggests that East Asian populations exhibit less hirsutism and adiposity compared with other groups. However, hirsutism is more prevalent in South Asian, Middle Eastern, and Hispanic populations. Hispanic and African American populations have more frequent obesity and insulin resistance. With regard to the association between mental disorders and racial and ethnic differences, limited studies exist; therefore, no conclusions can be drawn. Conclusion Race and ethnicity‐specific factors related to PCOS must be considered in clinical practice. The diagnostic criteria of PCOS should be specific to race and ethnicity to avoid missing treatment opportunities.

Inositol plays a crucial role in follicular development by regulating insulin signaling and ovarian function. However, its precise mechanism of action remains unclear. This study investigated the effects of myo-inositol (MI) and D-chiro-inositol (DCI) on the development of murine ovarian follicles in vitro. Follicles treated with DCI exhibited larger diameters than controls on Day 6 (275.20 ± 12.54 μm; p = 0.037) and Day 8 (277.47 ± 11.47 μm; p = 0.048), indicating a modest, marginally significant effect that was not maintained by Day 10. The rate of follicular antrum formation was significantly higher in the DCI-treated group on Day 6 (p < 0.05); however, no significant differences were observed on Days 8 and 10. In contrast, MI treatment did not affect follicular survival, diameter, or antrum formation compared with controls. Estradiol concentrations and the expression levels of follicle-stimulating hormone receptor and aromatase genes did not differ significantly among groups. Together, these data provide in vitro evidence that DCI can facilitate the transition from the secondary (preantral) to the early antral stage under these culture conditions. Given the small experimental sample size, the use of healthy murine follicles cultured under a high FSH concentration, and the absence of a PCOS-like ovarian milieu, these findings should be interpreted cautiously and cannot be directly generalized to infertility treatment in women with PCOS. Future studies using PCOS animal models and human follicle systems are needed to clarify translational relevance of these findings.

Early diagnosis is essential for the safer perinatal management of placenta accreta spectrum (PAS). We used transcriptome analysis to investigate diagnostic maternal serum biomarkers and the mechanisms of PAS development. We analyzed eight formalin-fixed paraffin-embedded placental specimens from two placenta increta and three placenta percreta cases who underwent cesarean hysterectomy at Sapporo Medical University Hospital between 2013 and 2019. Invaded placental regions were isolated from the uterine myometrium and RNA was extracted. The transcriptome difference between normal placenta and PAS was analyzed by microarray analysis. The PAS group showed markedly decreased expression of placenta-specific genes such as LGALS13 and the pregnancy-specific beta-1-glycoprotein (PSG) family. Term enrichment analysis revealed changes in genes related to cellular protein catabolic process, female pregnancy, autophagy, and metabolism of lipids. From the highly dysregulated genes in the PAS group, we investigated the expression of PSG family members, which are secreted into the intervillous space and can be detected in maternal serum from the early stage of pregnancy. The gene expression level of PSG6 in particular was progressively decreased from placenta increta to percreta. The PSG family, especially PSG6, is a potential biomarker for PAS diagnosis.

Background: Prevalence rates of all anomalies classified as birth defects, including those identified before the 22nd gestational week, are limited in published reports, including those from the International Clearinghouse for Birth Defects Surveillance and Research (ICBDSR). In our birth cohort study, we collected the data for all birth defects after 12 weeks of gestation. Methods: Subjects in this study comprised 19,244 pregnant women who visited one of 37 associated hospitals in the Hokkaido Prefecture from 2003 through 2012, and completed follow-up. All birth defects after 12 weeks of gestation, including 55 marker anomalies associated with environmental chemical exposures, were recorded. We examined parental risk factors for birth defects and the association between birth defects and risk of growth retardation. Results: Prevalence of all birth defects was 18.9/1,000 births. The proportion of patients with birth defects delivered between 12 and 21 weeks of gestation was approximately one-tenth of all patients with birth defects. Among those with congenital malformation of the nerve system, 39% were delivered before 22 weeks of gestation. All patients with anencephaly and encephalocele were delivered before 22 weeks of gestation. We observed different patterns of parental risk factors between birth defect cases included in ISBDSR and cases not included. Cases included in ISBDSR were associated with an increased risk of preterm birth. Cases not included in ISBDSR were associated with an increased risk of being small for gestational age at term. Conclusions: Data from our study complemented the data from ICBDSR. We recommend that birth defects not included in ICBDSR also be analyzed to elucidate the etiology of birth defects.

BackgroundsJapanese studies on the association between maternal alcohol consumption and fetal growth are few. This study assessed the effect of maternal alcohol consumption on fetal growth.MethodsThis prospective birth cohort included 95,761 participants enrolled between January 2011 and March 2014 in the Japan Environment and Children’s Study. Adjusted multiple linear and logistic regression models were used to assess the association between prenatal alcohol consumption and infant birth size.ResultsConsumption of a weekly dose of alcohol in the second/third trimester showed a significant negative correlation with standard deviation (SD; Z) scores for body weight, body length, and head circumference at birth, respectively. Consumption of a weekly dose of alcohol during the second/third trimester had a significant positive correlation with incidences of Z-score ≤ −1.5 for birth head circumference. Associations between alcohol consumption in the second/third trimester and Z-score ≤ −1.5 for birth weight or birth length were not significant. Maternal alcohol consumption in the second/third trimester above 5, 20, and 100 g/week affected body weight, body length, and head circumference at birth, respectively.ConclusionLow-to-moderate alcohol consumption during pregnancy might affect fetal growth. Public health policies for pregnant women are needed to stop alcohol consumption during pregnancy.ImpactThis study examined the association between maternal alcohol consumption and fetal growth restriction in 95,761 pregnant Japanese women using the prospective birth cohort.Maternal alcohol consumption in the second/third trimester more than 5, 20, and 100 g/week might affect fetal growth in body weight, body length, and head circumference, respectively.The findings are relevant and important for educating pregnant women on the adverse health effects that prenatal alcohol consumptions have on infants.

Background: Low red blood cell folate concentrations during early pregnancy might cause neural tube defects. However, the association between folate concentrations and birth defects of other neural crest cell-derived organs remains unknown. We investigated the associations between birth defects and first-trimester serum folate concentrations in a birth-cohort study in Japan. Methods: In total, 14,896 women who were prior to 13 weeks of gestation were enrolled from 2003 through 2012. Birth defect information was obtained from medical records and questionnaires. The association between folate levels in the first trimester and birth defects categorized as ICD-10 cord defects and neural crest cell-derived organ defects was examined. The crude and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) per log-transformed folate concentration were calculated using logistic regression. Results: Blood samples were obtained at a mean of 10.8 weeks of gestation. Median serum folate level was 16.5 (interquartile range, 13.4–21.5) nmol/L, and the deficiency level (less than 6.8 nmol/L) was 0.7%. There were 358 infants with birth defects. The adjusted odds ratio for any birth defect, ventricular septal defects, and cleft lip was 0.99 (95% CI, 0.74–1.32), 0.63 (95% CI, 0.30–1.33), and 4.10 (95% CI, 0.96–17.58), respectively. There were no significant associations between first-trimester maternal serum folate and the risk of birth defects. Conclusions: We were unable to demonstrate a relationship between maternal serum folate in the first trimester and birth defects. Potential confounding factors may have influenced our results.

Background Letrozole has been reported to be effective in treating anovulation, preventing ovarian hyperstimulation syndrome (OHSS), and retrieving oocytes in breast cancer patients. However, the role and mechanism of letrozole in follicular development remain unclear. Results We treated mouse preantral follicles with various treatments; we found no significant difference in follicle survival rates in the letrozole (LET) group compared with the control group, but the average diameter of follicles in the LET group tended to be larger (CTRL vs. LET 30, p  = 0.064; CTRL vs. LET 100, p  = 0.025). The estradiol concentrations in culture media of the LET group were significantly lower than those observed in the control group (CTRL vs. LET 30, p  = 0.038; CTRL vs. LET 100, p  = 0.025). We further found a marked increase in follicle-stimulating hormone receptor (FSHR) gene expression in response to letrozole treatment (CTRL vs. LET 30, p  = 0.075; CTRL vs. LET 100, p  = 0.034). This result suggested that increased FSHR expression promotes follicle development. Letrozole inhibited aromatase activity, but the effect was limited. Letrozole did not significantly reduce vascular endothelial growth factor (VEGF) gene expression. Conclusions Letrozole may promote follicle development by increasing the expression of FSHR. Letrozole may be useful for fertility preservation of patients with estrogen-dependent cancers such as breast cancer and various other cancers. Whether letrozole has a direct effect in reducing OHSS requires further investigation.

Aim To understand the preferences of individuals with gender incongruence (GI) regarding gender‐affirming surgery (GAS), including gonadectomy. Methods A prospective, multicenter survey was conducted in Japan targeting individuals aged 18 years or older with GI who had not yet undergone GAS. Participants completed a questionnaire about their GAS preferences, desired surgical procedures, the reasons for their preferences, and willingness to undergo gonadectomy even if it was not legally required. Results In total, 107 participants (82 assigned female at birth [AFAB] and 25 assigned male at birth [AMAB]; median age: 31) participated in the study. Of those, 69% desired GAS, 29% did not, and 2% were undecided. The primary reasons for desiring GAS were the need for legal gender change (positive feelings: 62%, unavoidable: 24%), mental stability (56%), and reducing gender dysphoria (54%). Conversely, the main reasons for not wanting GAS were difficulty in securing funds for surgery (58%), followed by resistance to gonadectomy (41%). Of the 53 AFAB participants, 52 individuals desired hysterectomy and oophorectomy, and 26 wanted only this surgery. Among the 22 AMAB participants, 13 individuals desired vaginoplasty; however, five withdrew due to concerns about costs or postoperative complications. Even without legal requirements, 47% said they would choose gonadectomy. Conclusion Reforming legal requirements for gonadectomy may alter the demand for or details of GAS in Japan, yet half of the participants still desire surgery. The primary reason for not undergoing surgery is the difficulty in securing funds, which is a significant finding. Preferences for gender‐affirming surgery in Japan were shaped by legal and psychological factors, with financial difficulty as the main barrier.

This study examined the risk of intrauterine infection associated with radical trachelectomy (RT) in early‐stage cervical cancer patients. This procedure preserves fertility but is linked to increased risk of intrauterine infection due to cervical defects during pregnancy. DNA was extracted from the formalin‐fixed paraffin‐embedded (FFPE) placental specimens of 23 pregnant post‐RT patients and 16S rRNA gene sequencing was used for bacterial identification. The prevalence of Lactobacillus crispatus and Burkholderia stabilis was significantly higher in the non‐chorioamnionitis group. In contrast, alpha diversity analysis using the PD index showed significantly higher diversity in the chorioamnionitis group (P = 0.04). The demonstrated relationship between chorioamnionitis and microbial diversity affirms the importance of controlling the genital bacterial flora in pregnancies following RT. The study investigates the risk of intrauterine infections during pregnancy following radical trachelectomy (RT) in early‐stage cervical cancer patients. Using 16S rRNA sequencing on FFPE placental specimens, the research highlights a correlation between microbial diversity and chorioamnionitis, emphasizing the need for careful management of genital bacterial flora in pregnancies post‐RT.

Hyperandrogenism is one of the cardinal symptoms in polycystic ovary syndrome and plays a key role in the pathogenesis of polycystic ovary syndrome. However, the precise effects and mechanisms of excess androgen during follicular development are still unclear. Here we investigated the effects of androgen on mouse follicle development in vitro. Androgen did not affect the growth of follicles smaller than 160–180 μm in the presence of follicle-stimulating hormone (FSH). However, in the presence of low FSH, androgen supported the growth of follicles larger than 160–180 μm, a size at which growing follicles acquire FSH-dependency. Androgen did not change the mRNA expression of various growth-promoting factors but did increase mRNA expression of the FSH receptor. We suggest that androgen has a positive impact on follicle development by augmentation of the actions of FSH. Therefore, FSH-responsive but FSH-independent follicles grow in the presence of a certain level of FSH or androgen, and androgen compensates for FSH deficiency in FSH-dependent follicles.