The appropriate timing of delivery for pregnancies has always been a concern for medical staff, and the timing of elective labor induction at 41 weeks in low-risk pregnant women has always been controversial. We compared maternal and fetal outcomes between gestational age at 40 0/7 to 40 6/7 and 41 0/7 to 41 6/7 weeks. This retrospective cohort study was conducted at the obstetrics department of Jiangsu Province Hospital from January 1^st to December 31^st in 2020. Maternal medical records and neonatal delivery data were collected. One-way analysis of variance, Mann–Whitney U test, χ² test, Fisher exact test and logistig regression analysis were performed. The study included 1569 pregnancies, with 1107 (70.6%) delivered at 40 0/7 to 40 6/7 weeks and 462 (29.4%) delivered at 41 0/7 to 41 6/7 weeks. Intrapartum cesarean section (8% vs 16%, P < .001), meconium-stained amniotic fluid (13% vs 19%, P = .004), episiotomy (41% vs 49%, P = .011), and macrosomia (13% vs 18%, P = .026) were significantly lower at 40 0/7 to 40 6/7 weeks. The premature rupture of membranes rate (22% vs 12%, P < .001), vaginal delivery rate of artificial rupture of membrane induction (83% vs 71%, P = .006) and balloon catheter combined with oxytocin induction (88% vs 79%, P = .049) were significantly higher at 40 0/7 to 40 6/7 weeks. Low-risk women who delivered at 40 0/7 to 40 6/7 weeks showed better outcomes in terms of the mother’s and baby’s health, such as decreased rates of intrapartum cesarean section, meconium-stained amniotic fluid, episiotomy, and macrosomia, compared with those who delivered at 41 0/7 to 41 6/7 weeks.

Introduction Endometrial cancer (EC) represents the most prevalent gynecological malignancy of the female reproductive tract, yet effective therapeutic strategies for advanced and recurrent EC remain limited. Cuproptosis is a copper-dependent form of regulated cell death with distinct molecular mechanisms separate from apoptosis and ferroptosis. To date, the cell-type-specific landscape of cuproptosis activity within the EC tumor microenvironment (TME), its regulatory crosstalk with T cell exhaustion, and its translational clinical value have not been systematically characterized. Methods In this study, we integrated multi-omics datasets, including single-cell RNA sequencing (scRNA-seq) profiles from 5 EC patients containing 32,182 cells (GSE173682), bulk transcriptomic data of 541 TCGA-UCEC cases, EPIC-based cellular deconvolution, and qRT-PCR as well as immunohistochemistry validation using 17 pairs of EC and matched adjacent normal tissues. Results Single-cell analyses revealed that T cells exhibited the lowest cuproptosis signature scores among all major cell populations in the EC TME, and cuproptosis activity gradually decreased as T cells progressed toward terminal exhaustion. As the core upstream regulator of the lipoylation pathway governing cuproptosis, FDX1 showed the strongest positive correlation with cuproptosis scores in intratumoral T cells (log₂FC = 0.53, p = 1.41 × 10⁻⁷). In the TCGA-UCEC cohort, elevated cuproptosis scores and high FDX1 expression independently predicted unfavorable overall survival (HR = 1.51 for cuproptosis signature, HR = 1.54 for FDX1, both p < 0.05). EPIC deconvolution further demonstrated that bulk-level cuproptosis signals primarily originated from tumor epithelial cells rather than infiltrating immune cells, explaining the contradictory prognostic trend observed between single-cell and bulk transcriptomic data. Consistent with computational predictions, our independent clinical tissue cohort verified significantly upregulated FDX1 expression at both mRNA and protein levels in EC lesions relative to paired normal endometrium (both p < 0.05). Discussion Collectively, FDX1 represents a central molecular hub linking cuproptosis metabolism, T cell dysfunction, and clinical prognosis in EC. This work uncovers the cell-type-specific heterogeneity of cuproptosis in the EC TME, identifies FDX1 as a promising prognostic biomarker, and provides a theoretical foundation for exploring cuproptosis-related strategies combined with tumor immunotherapy for EC.