Objective. The relationship between metabolic risk and ovarian function is ambiguous. This retrospective study analyzed the medical records of 461 PCOS patients collected between January 2019 and June 2020 to investigate the relationship between serum anti-Müllerian hormone (AMH) and parameters of metabolic risk in the population with polycystic ovary syndrome (PCOS). Methods. A total of 461 PCOS patients aged 2040 years were included and stratified into four groups according to the AMH level. The association between AMH and the parameters related to metabolic risk in these groups was compared, and the discrepancies were further explored. Binary logistic regression was performed to examine the risk factors of HOMA-IR. The values of AMH that best predicted the risk of HOMA-IR were also analyzed by ROC curves. Results. AMH was negatively associated with HOMA-IR (odds ratio (OR) 0.279, 95 confidence interval (CI) 0.36 to 0.20), fasting insulin (OR 0.282, 95 CI 0.36 to 0.20), 1-hour postprandial insulin (OR 0.184, 95 CI 0.28 to 0.11), 2-hour postprandial insulin (0.180, 95CI 0.28 to 0.11), 3-hour postprandial insulin (OR 0.198, 95 CI 0.30 to 0.13), waist-hip ratio (OR 0.235, 95 CI 0.31 to 0.14), and body mass index (OR 0.350, 95 CI 0.43 to 0.27). There was no statistically significant relationship between blood pressure, serum glucose profile, or lipid levels and AMH. Binary logistic regression showed that AMH protected against the occurrence of PCOS patients (OR: 0.835, 0.776, and 0.898). For the prediction of HOMA-IR, AMH had an AUC-ROC of 0.704 (95 CI 0.6520.755) with a cutoff value of 7.81mmol/L, a sensitivity of 70.3, and a specificity of 70.1. Conclusions. Higher AMH levels were significantly associated with a lower insulin profile and might be a useful predictor for HOMA-IR in PCOS patients.

Previous studies have suggested that the trophoblast cells inhibit the proliferation of peripheral natural killer (pNK) cells and the level of pNK cells decrease in middle and late pregnancy stage among healthy women. The change of pNK cells level during early pregnancy and the relationship between the change of pNK level and pregnancy outcomes in women with unexplained recurrent pregnancy loss (URPL) has not been sufficiently explored. This study aims to characterize the level of pre-pregnancy pNK to early pregnancy among women with URPL and whether the change in the level of pNK cells in early pregnancy from pre-pregnancy can predict pregnancy outcomes. In this prospective cohort study, 1758 women with recurrent pregnancy loss were recruited between January 2017 and December 2021, of which 252 URPL women had pre-pregnancy and early pregnancy (4-6 weeks gestation) pNK measurements. These 252 women were divided into two groups: those with a lower gestational pNK levels (Group 1) compared to pre pregnancy, and those without (Group 2). Their respective outcomes on live birth and pregnancy loss were comparatively analyzed using Chi-square and Student's t test. Candidate influence factors for live birth were selected using the Akaike information criterion (AIC). Then the participates were randomly divided into training and testing groups. Multivariable logistic regression model was performed, and nomogram was calculated to assess the possibility of live birth. Predictive accuracy was discriminated by area under the receiver operating characteristic curve (ROC), validated by plotting the predicted probabilities and the observed probabilities. Hosmer-Lemeshow test was used to assess the goodsess of fit. When early gestational pNK cells levels were compared with pre pregnancy pNK cells levels, 61.5% (154) women had a comparatively lower early gestational pNK cells levels versus 38.9% (98) women with increase or no change of their pNK cells levels. The live birth rate in Group 1 was 89.0% (137/154), which was significantly higher than 49.0% (48/98) of Group 2 (p<0.001). Decrease of pNK cells level (odds ratio [OR]=1.36, 95% CI 1.22-1.55, p<0.001) and anti-Muellerian hormone (AMH) (OR=1.41, 95% CI 1.14-1.81, p=0.003) were important predicting factors for higher live birth. Female BMI (OR=0.97, 95% CI 0.82-1.15, p=0.763) and parity (OR=1.61, 95% CI 0.71-4.12, p=0.287) were also predicting factors. Furthermore, the area under the ROC curve of the model to diagnose of live birth was 0.853 with a sensitivity of 81.6% and specificity of 78.0% using the training dataset. And the Hosmer-Lemeshow test showed that the model was a good fit (p = 6.068). We report a comparative decrease in pNK cells levels in over 60% URPL women at 4-6 weeks of gestation, when compared to their pre-pregnancy pNK cells level. Compared to pre pregnancy pNK cells levels, a decrease pNK cells level during early pregnancy might be a useful predictor for LBR in women with URPL.

The endometrium is a highly dynamic tissue central to female reproductive function, undergoing nearly 500 cycles of proliferation, differentiation, shedding, and regeneration throughout a woman’s reproductive life. This remarkable regenerative capacity is driven by a reservoir of endometrial stem/progenitor cells (ESCs), which are crucial for maintaining tissue homeostasis. Dysregulation of these cells is linked to a variety of clinical disorders, including menstrual abnormalities, infertility, recurrent pregnancy loss, and serious gynecological conditions such as endometriosis and endometrial cancer. Recent advancements in organoid technology and lineage-tracing models have provided insights into the complex cellular hierarchy that underlies endometrial regeneration and differentiation. This review highlights the latest breakthroughs in endometrial stem cell biology, focusing particularly on 3D in vitro platforms that replicate endometrial physiology and disease states. By integrating these cutting-edge approaches, we aim to offer new perspectives on the pathogenesis of endometrial disorders and establish a comprehensive framework for developing precision regenerative therapies.

Thin endometrium (TE), affecting 1.5 %-9.1 % of reproductive-aged women, emerges as a disturbed decidua microenvironment underpinning implantation failure and recurrent pregnancy loss. Through integrated single-cell transcriptomics with histopathology and multiplex immunofluorescence (TSA) validation, we delineated TE as a disease of coordinated repairment impairment and pro-fibrotic remodeling across stromal and immune compartments. Key findings revealed a pathological imbalance in stromal subsets, including the decrease of regenerative IGFBP3 + Stromal_1 cells and expansion of fibrogenic Stromal_2 populations, driving collagen-dominant extracellular matrix remodeling. Concurrently, immune dysfunction was unmasked. NK cells decreased and shifted from immune surveillance to a pro-inflammatory phenotype, T cells transitioned from immune regulation to extracellular matrix remodeling effectors and macrophages adopted a pro-fibrotic phenotype with lipid metabolic collapse. CellChat analysis pinpointed suppression of GZMA-PARD3 and APOE-TREM2 axes as drivers of stromal dysfunction, while the hyperactivated adhesion (LAMA3) and collagen pathways served as central mediators of the fibro-inflammatory cascade. These findings, based on single-cell RNA-seq and spatial verification, suggest therapeutic targets for restoring endometrial homeostasis in TE. These findings suggested that TE as a disease of progressive stromal-immune fibrosis dysregulation, offering novel therapeutic targets to restore endometrial repairment and microenvironmental homeostasis.

Background: This aim of this study was to evaluate the effect of human menopause gonadotropin (HMG) on pregnancy outcomes of infertility patients with intrauterine insemination (IUI) treatments.Methods: This retrospective cohort study analyzed couples using 75 IU HMG as initiate ovarian stimulation method for IUI from January 2015 to December 2019. Couples were divided into four groups according to a total dose of HMG: 189 cycles with a dose <500 IU, 601 with a dose 500 to1000 IU, 199 with a dose 1000 to 1500 IU and 241 with a dose ＞1500 IU. The differences in baseline characteristics and pregnancy outcomes including among the four groups were investigated. We used a logistic regression model to further study the association between various doses of HMG and pregnancy outcomes and adjusted for confounding factors.Results: The study included 792 couples with 1230 cycles, and pregnancy was achieved in 212 (17.2%) cycles, while live birth was achieved in 176 (14.3%) cycles. Stratified analyses revealed that a higher dose of HMG was associated with increased pregnancy rate (PR), live birth rate (LBR), endometrial thickness (EMT) on insemination day, number of follicle ≥18 mm, serum estrogen 2( E2) level, and EMT on the trigger day among four groups, which were all statistically different (P＜0.05). The logistic regression indicated that both PR and LBR were positively associated with the total dose and day of HMG, which were statistically different (P＜0.05).Conclusion: Increasing the total dose and day of HMG may benefit the serum E2 level, EMT, follicle development, and pregnancy outcomes in 75IU HMG stimulated IUI cycles.

Introduction: Recurrent pregnancy loss (RPL), defined as two or more pregnancy losses, affects 1%–2% of women of reproductive age. Approximately 50% of cases remain unexplained recurrent pregnancy loss (uRPL). Antinuclear antibodies (ANAs) are detected in about 22% of women with uRPL, but whether ANA status predicts subsequent pregnancy outcomes is unclear. Aims: This study aimed to investigate the correlation between pre-pregnancy ANA positivity and subsequent pregnancy outcomes in women with uRPL. Methods: In this prospective cohort study, 386 women with uRPL underwent pre-pregnancy ANA screening via magnetic chemiluminescence immunoassay. Participants were followed for 2 years, with documentation of conception methods, any immunomodulatory treatments received, and pregnancy outcomes. Results: Of the 386 participants, 77 (20.0%) were ANA-positive and 309 were ANA-negative. During follow-up, 300 women in the ANA-negative group and 64 in the ANA-positive group achieved a pregnancy. No significant differences were observed in pregnancy outcomes (early pregnancy loss or live birth) between the ANA-positive and ANA-negative groups, nor when ANA-positive women were stratified by titre level (low vs. high). Conclusions: Pre-pregnancy ANA positivity was not associated with an increased risk of early pregnancy loss in women with uRPL, regardless of the titre cut-off used. A history of prior live birth emerged as a significant protective factor. Future research should focus on the dynamics of ANA levels during pregnancy and their prognostic implications.