Epidemiological literature regarding the effect of polycystic ovary syndrome (PCOS) as a risk factor for non-alcoholic fatty liver disease (NAFLD) remains inconsistent. Furthermore, it remains debatable whether NAFLD is associated with PCOS as a consequence of shared risk factors or whether PCOS contributes to NAFLD in an independent fashion. Therefore, this meta-analysis was conducted. This meta-analysis was conducted in accordance with the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Relevant studies published before May 2017 were identified and retrieved from PubMed and Web of Science databases. The data were extracted, and the pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. A total of 17 studies were included into the present analysis. Compared to the control group, the risk of NAFLD in the PCOS group was higher (OR = 2.25, 95% CI = 1.95–2.60). When stratified by BMI and geographic location, the results indicated that the frequency of NAFLD risk was significantly higher in obese subjects (OR = 3.01, 95% CI = 1.88–4.82), non-obese subjects (OR = 2.07, 95% CI = 1.12–3.85), subjects from Europe (OR = 2.00, 95% CI = 1.58–2.52), subjects from the Asia-Pacific Region, (OR = 2.32, 95% CI = 1.89–2.84) and subjects from America (OR = 2.96, 95% CI = 1.93–4.55). In addition, PCOS patients with hyperandrogenism (HA) had a significantly higher risk of NAFLD, compared with controls (OR = 3.31, 95% CI = 2.58–4.24). However, there was no association between PCOS patients without HA and higher risk of NAFLD (OR = 1.46; 95% CI =0.55–3.87). The results of this meta-analysis should be interpreted with caution due to the small number of observational studies and possible confounding factors. The meta-analysis results suggest that PCOS is significantly associated with high risk of NAFLD. Although this association was independent of obesity and geographic region, it might be correlated with HA.

Background: Endometrioid adenocarcinoma (EAC) is the most common subtype of endometrial cancer (EC) and is an estrogen-related cancer. In this study, we sought to investigate the expressions and mechanism of action of 17β-estradiol (E2) and long noncoding RNA (lncRNA) LINC01541 in G1/G2 EAC samples.Methods: The expressions of estrogen receptor β (ESR2), LINC01541, miR-200s, and VEGFA were evaluated using real-time PCR in human EAC tissues (n = 8) and adjacent normal tissues (n = 8). Two EC cell lines (Ishikawa and RL95-2) were selected for validation in vitro. Bioinformatics analyses and luciferase reporter analyses were performed to verify potential binding sites. qRT-PCR, Western blot, and CCK-8 were used to identify the regulatory mechanisms of related genes in cell biological behavior.Results: Compared with adjacent normal tissues, LINC01541 and miR-200s family (except miR-200c) were highly expressed in EAC tissues (n=8), while ESR2 and VEGFA were lowly expressed in EAC tissues (* P < 0.05; ** P < 0.01). In vitro: E2 inhibited the expression of LINC01541 and miR-429 in both cell lines, and estrogen antagonist (PHTPP) could reverse this effect, in addition, PHTPP could promote the proliferation of these two cancer cells, cell transfection LINC01541 also had this effect after overexpression of plasmid and miR-429 mimic. E2 promotes the expression of VEGFA in both cell lines, and PHTPP can also reverse this effect. LINC01541 interacts with miR-429 to promote the expression of each other, and both inhibit the synthesis of VEGFA in EAC cells after overexpression. Through the double validation of bioinformatics analysis and dual fluorescein reporter gene, it was confirmed that miR-429 targets the regulation of VEGFA expression (* P < 0.05; ** P < 0.01).Conclusion: E2 promotes the synthesis of VEGFA by altering the expression levels of LINC01541 and miR-429 in EAC, thereby affecting the angiogenesis process of EAC. Also, E2-mediated LINC01541/miR-429 expression may affect cell migration in EAC. In addition, we identified a reciprocal promotion between LINC01541 and miR-429.

Objective: The aim of this study was to investigate the effectiveness of ornidazole in inhibiting the progression of endometriosis in a rat model. Design: This was an in vivo experiment, including the ornidazole group (n = 16) and a control group (n = 14). Rats were provided with free access to water containing ornidazole (1 g/L) or drinking water only for 14 days. Materials and Methods: Surgical induction of endometriosis was performed in Sprague Dawley rats via autologous endometrial transplantation. Rats were provided with free access to water containing ornidazole (1 g/L) or drinking water only for 14 days. Once the rats were euthanized (ornidazole group, n = 16; control group, n = 14), histological signatures and the volumes of endometriosis lesions were assessed. Cells positive for the inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were counted. Angiogenesis was identified by assessing vascular endothelial growth factor (VEGF) and microvessel density. Results: The median lesion volume was lower in the ornidazole group (20.2 mm3; range, 5.7–53.3 mm3) than in the control group (81.3 mm3; range, 32.8–122.2 mm3; p = 0.007). Median IL-1β cell counts were 5.3 (range, 4.5–6.4) for ornidazole and 11.7 (range, 9.4–15.4) for control (p < 0.001). Mean IL-6 cell counts were 5.6 ± 1.8 for ornidazole and 11.3 ± 4.1 for control (p < 0.001). Median TNF-α cell counts were 5.7 (range, 4.5–7.2) for ornidazole and 12.1 (range, 10.0–15.9) for control (p < 0.001). Median VEGF cell counts were 8.1 (range, 6.5–11.4) for ornidazole and 18.3 (range, 14.2–21.0) for control (p = 0.001). Median microvessel density values were 11.3/HPF (range, 7.7–21.8) for ornidazole and 28.7/HPF (range, 13.1–48.2) for control (p = 0.012). Limitations: This study is a short period and small sample size experiment. In this study, multiple drug concentrations were not used. We did not use in vitro models to assess the anti-inflammatory and antiangiogenic effects of ornidazole on endometriosis, and the specific anti-inflammatory and antiangiogenic mechanisms associated with ornidazole need to be further investigated. Conclusion: Ornidazole restricts the growth of endometriosis in rats, possibly by exerting anti-inflammatory and antiangiogenic effects.

Objectives: The aim of this study was to investigate the feasibility and safety of the treatment of laparoscopic adenomyomectomy for severe adenomyoma. Study design: The study included 216 patients with severe adenomyoma, who underwent a laparoscopic adenomyomectomy between January 2008 and September 2012 in the Department of Gynecology, Second People’s Hospital of Changzhou, affiliated with Nanjing Medical University. Results: The mean age of the patients was 37 ( 3.3) years and the BMI was 26 ( 2.7). The volume of bleeding during surgery was 150.2 22.7 ml, the mean operative time was 60 48.6 minutes, the mean time for anal exhaust was one 1.8 days, and the mean time of hospital stay was five 1.2 days. During the surgeries, no bladder or bowel injuries occurred, and all the surgeries were completed successfully, with no conversions to open laparotomies. Of the 176 patients, 170 (96.6%) showed significant improvement in their dysmenorrheal symptoms after the surgeries, whereas six patients had a poor clinical outcome. Of the 157 patients,151 (96.2%) had an obvious effect on their menstrual cycle. Conclusions: Laparoscopic adenomyomectomy is feasible and safe for severe adenomyoma.

Objective To investigate the value of the combination of contrast-enhanced ultrasound (CEUS) and cancer antigen (CA) 125 in differentiating benign and malignant epithelial ovarian tumors (EOTs). Methods The study was performed in patients with pathology confirmed EOTs between June 2020 and April 2022 who underwent CEUS and serum CA125 measurements. The CEUS qualitative and quantitative features were evaluated. The accuracy of CEUS combined with CA125 for determining malignant and benign EOTs was analyzed. Results A total of 57 patients (mean age, 46.7 ± 14.2 years, 20 malignant EOTs and 37 benign EOTs) were included in the study. The sensitivity, specificity, positive and negative predictive values of CEUS for differentiating malignant EOTs from benign EOTs were 80.0%, 86.5%, 76.2% and 88.9%, respectively; those of CA125 were 70.0%, 62.2%, 50.0% and 79.3%, respectively. In addition, the sensitivity and specificity of CEUS combined with serum CA125 were 90.0% and 94.6%, which were significantly higher than those of CEUS (χ² = 8.889, 5.185, p = 0.003, 0.023) or serum CA125 alone (χ²=13.531, 4.405, p = 0.000, 0.036). The positive and negative predictive values of CEUS with serum CA125 in differentiating benign and malignant EOTs were also significantly higher than serum CA125 alone (χ²= 7.619, 4.163, p = 0.006, 0.041), but not significantly different (χ²=1.558, 0.725, p = 0.212, 0.394). Conclusion CEUS combined with serum CA125 can significantly improve the differential efficiency of benign and malignant EOTs.

Background: From an immunological perspective, changes in cytokine levels can shift the immune response, potentially affecting the development of endometrial polyps (EPs). The relationship between the balance of T helper 1 (Th1)/T helper 2 (Th2) and T helper 17 (Th17)/Regulatory T (Treg) cytokines and the pathogenesis of EPs is an area of ongoing research. This study aims to investigate the role of Th1/Th2 and Th17/Treg immune imbalances in the pathogenesis of EPs. Methods: A total of 79 patients were included in this prospective laboratory-based study. The experimental group included 20 patients with single EPs, 20 with multiple EPs, and 19 with postmenopausal EPs. The control group included 20 individuals with proliferative endometriums. Immunohistochemical staining was performed to investigate the expression of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-17 (IL-17), tumor necrosis factor-α (TNF-α), interferon-gamma (IFN-γ). Results: The levels of TNF-α, IFN-γ, IL-17 and transforming growth factor-β (TGF-β) in the single EP group were higher than in the control group (pTNF-α = 0.001, pIFN-γ < 0.001, pIL-17 < 0.001, pTGF-β < 0.001), while the level of IL-6 in the stroma was lower than in the control group (pIL-6 < 0.001). The levels of IL-2, IFN-γ, IL-4, IL-17 and TGF-β in the glands of the multiple EPs group were higher than in the glands of the control group (pIL-2 = 0.041, pIFN-γ < 0.001, pIL-4 = 0.044, pIL-17 < 0.001, pTGF-β < 0.001). The levels of IL-4, IL-6, TNF-α, and IL-17 in the postmenopausal single polyp group were lower than in the total control group (pIL-4 = 0.020, pIL-6 = 0.002, pTNF-α < 0.001, pIL-17 = 0.006), while the levels of IL-2, IFN-γ and TGF-β in the glands were higher than in the control group (pIL-2 = 0.002, pIFN-γ = 0.002, pTGF-β = 0.005). Conclusion: Th1/Th2 and Th17/Treg immune imbalances are one of the causes of EPs.