Objective To compare the ease of cervical entry after administration of vaginal misoprostol at 2 different intervals before vaginoscopic hysteroscopy. Methods In this randomized, double-blinded study, 140 women undergoing vaginoscopic hysteroscopy were allocated into two groups: 1) short-interval: placebo tablet administered vaginally 12 hours before the procedure, followed by 200 mcg vaginal misoprostol 3 hours before, and 2) long-interval: 200 mcg vaginal misoprostol 12 hours before the procedure and a placebo tablet 3 hours before. The primary outcome was the ease of cervical entry, evaluated using a 5-point Likert scale, and the secondary outcomes included 1) time interval to cervical entry and completion of the procedure, 2) pain assessment using a visual analog scale (VAS), and 3) any adverse effects associated with the drug or procedure. Results All except two patients with cervical stenosis underwent vaginoscopic hysteroscopy. The proportion of patients who reported "easy" or "very-easy" cervical entry was similar in both groups (64.3% [95% confidence interval [CI], 53.1-75.5%], vs. 72.9% [95% CI, 62.4-83.3%]; P=0.275). Pain perception was lower in the long-interval group than in the short-interval group (P=0.024). However, the temporal change in the pain score was not significantly different between the groups. The side effects of misoprostol were mild, self-limiting, and similar in both groups. Conclusion Vaginal misoprostol administration 12 hours before vaginoscopic hysteroscopy was associated with a similar ease of entry but a lower perception of pain using the VAS than misoprostol administration 3 hours before the procedure.
Objective Approximately 15% of couples of reproductive age experience infertility. In vitro fertilization (IVF) is the most useful treatment for patients with infertility. However, repeated implantation failure (RIF) is one of the most difficult challenges for the success of IVF, caused by poor endometrial receptivity due to decreased endometrial cell proliferation. This study aimed to investigate the mechanism regulating endometrial cell proliferation to overcome RIF. Methods Hub genes involved in RIF were identified by RNA sequencing for endometrial tissues. The regulatory effects of circular RNA (circRNA) and microRNA (miRNA) in human endometrial stromal cells (hESCs) were determined using miRNA pulldown and dual-luciferase reporter gene assays. Cell proliferation was detected using a Cell Counting Kit-8 assay. Results G protein-coupled estrogen receptor 1 (GPER1) expression was dramatically downregulated in endometrial tissues obtained from patients with RIF, suggesting that GPER1 might be a hub gene involved in RIF. Additionally, circRNA SNX11 increases GPER1 expression via hsa-miR-1343-3p in hESCs. Additionally, circRNA SNX11 promotes cell proliferation, reduces apoptosis, and modulates RIF-related pathways through GPER1 by sponging hsa-miR-1343-3p in hESCs. Conclusion This study reveals that circRNA SNX11 facilitates endometrial cell proliferation by upregulating GPER1 by sponging hsa-miR-1343-3p, providing novel therapeutic targets to overcome RIF.
Cerebral palsy (CP) has long been associated with intrapartum hypoxia; however, contemporary evidence indicates that acute hypoxic-ischemic events during labor account for only a minority of cases. This narrative review summarizes the current evidence regarding the epidemiology, pathophysiology, and causation assessment of CP, focusing on the limitations of electronic fetal monitoring, umbilical cord pH, low Apgar scores, and cesarean delivery as predictors or preventive measures for CP. Prematurity, intrauterine infection and inflammation, placental pathology, perinatal arterial ischemic stroke, and genetic factors are important associated factors or contributory pathways in CP, although their population-attributable contributions remain uncertain. Recent genomic studies have identified pathogenic or likely pathogenic variants in approximately one-quarter to one-third of affected children, challenging the traditional assumption that unexplained CP is attributable to intrapartum events. Current evidence indicates that isolated fetal heart rate abnormalities, acidemia, or neonatal encephalopathy alone are insufficient to establish intrapartum hypoxia as the cause of CP. The Korean Society for Maternal Fetal Medicine emphasizes that causation assessments should rely on strict criteria, exclusion of alternative etiologies, and integrated interpretation of antenatal, intrapartum, neonatal, neuroimaging, placental, and genetic findings. A multifactorial and evidence-based approach is essential for rational clinical assessment, appropriate counseling, and avoidance of unnecessary defensive obstetric practices.
The role of human epidermal growth factor receptor 2 (HER2) in gynecological oncology has evolved from a histotype-restricted biomarker to a central component of molecular stratification, particularly within the p53-aberrant subgroup of Müllerian malignancies. HER2 amplification and overexpression are strongly enriched in this molecular class across diverse histologies, including serous carcinoma, carcinosarcoma, and high-grade endometrioid carcinoma. However, accurate assessment remains challenging owing to the presence of distinct basolateral staining patterns and marked intratumoral heterogeneity, both of which differ from canonical breast cancer paradigms and contribute to clinically significant diagnostic discordance. The therapeutic landscape has simultaneously undergone a major transition, moving beyond monoclonal antibodies that require high HER2 expression to antibody-drug conjugates capable of targeting tumors with low-level expression. This shift has established the clinically actionable "HER2-low" category, substantially expanding the population eligible for targeted therapy. More recently, the emerging concept of "HER2-ultralow" expression (defined as immunohistochemistry 0 with faint/incomplete membrane staining in ??0% of tumor cells) has further challenged traditional binary classification systems and may have therapeutic implications. The efficacy of these agents is driven by the bystander effect, which enables their activity in heterogeneous tumors. This review summarizes the current understanding of HER2 biology in Müllerian cancers, outlines the diagnostic pitfalls and scoring challenges, and discusses evolving therapeutic strategies, with emphasis on integrating molecular classification and optimized testing to ensure accurate patient selection.
