Purpose. To explore risk factors of vulvovaginal candidiasis (VVC) among women of reproductive age in Xi'an district and then to offer reference for clinical prevention and treatment of VVC. Methods. Patients from the outpatient department of gynecology and obstetrics in the First Affiliated Hospital of Xi'an Jiaotong University from June 2016 to May 2017 were recruited strictly according to the inclusion and exclusion criteria. Participants diagnosed as simple VVC were assigned to the case group, while women who underwent routine gynecological examination and had normal vaginal microflora were assigned to the control group. Then we conducted a questionnaire survey of the two groups and used the logistic regression model to explore the related risk factors of VVC. Results. In the present study, ninety-seven cases were sample VVC patients and eighty-seven cases were healthy women. This cross-sectional study showed that occasionally or never drinking sweet drinks (odds ratio [OR] =0.161, 95% confidence interval [CI] =0.056-0.462, P=0.001), occasionally or never eating sweet foods (OR=0.158, 95%CI=0.054-0.460, P=0.001), and the use of condom (OR=0.265, 95%CI=0.243-0.526, P=0.001) were regarded as protective factors for VVC. In addition, sedentary life style (OR=7.876, 95%CI=1.818-34.109, P=0.006), frequently wearing tights (OR=6.613, 95%CI=1.369-27.751, P=0.018), frequent intravaginal douching (OR=3.493, 95%CI=1.379-8.847, P=0.008), having the first sexual encounter when under 20 years old (OR=2.364, 95%CI=1.181-7.758, P=0.006), the number of sexual partners being over two (OR=3.222, 95%CI=1.042-9.960, P=0.042), history of curettage (OR=3.471, 95%CI=1.317-9.148, P=0.012), history of vaginitis (OR=8.999, 95%CI=2.816-28.760, P<0.001), and not cleaning the vulva before or after sexual encounters (OR=13.684, 95%CI=2.843-65.874, P=0.001) were considered to be risk factors of VVC. Conclusion. In conclusion, risk factors of VVC are various, involving ages, hygienic habits, disease history, and other aspects.

Aim:The aim of the study is to evaluate the effects of metformin on pregnancy outcomes in women with polycystic ovary syndrome (PCOS).Methods:We searched electronic databases and bibliographies of relevant papers to identify studies comparing the pregnancy outcomes in the metformin group with those in the placebo or blank control group. Then, we did this meta-analysis based on the PRISMA guidelines. The primary outcomes included early pregnancy loss (EPL), preterm delivery, term delivery, and gestational diabetes mellitus (GDM). Secondary outcomes included pregnancy-induced hypertension (PIH), intrauterine growth restriction (IUGR), fetal malformation, vaginal delivery (VD), cesarean section (CS), and metformin's side effects, such as nausea or gastrointestinal discomfort. Certainly, data about neonatal death and macrosomia were analyzed if data available.Results:Finally, 13 studies including 5 randomized controlled trials (RCT) and 8 cohort studies involving 1606 pregnant women with PCOS were analyzed. The pooled OR of EPL was 0.19 with obvious statistical significance, manifesting that metformin help to lower the rate of EPL (95% CI 0.12–0.28, P < 0.00001). Simultaneously, metformin showed the advantage of reducing the prevalence of preterm delivery (OR 0.37, 95% CI 0.20–0.68, P = 0.002). In addition, metformin could promote term delivery greatly and the pooled OR was 5.23 with sharp statistical difference (95% CI 3.12–8.75, P < 0.00001).Conclusion:Metformin treatment in women with PCOS throughout pregnancy could increase the possibility of term delivery, VD and reduce the risk of EPL, preterm labor, pregnancy complications such as GDM and PIH, with no serious side effects. Moreover, metformin was not teratogenic based on the limited data. So we may recommend metformin treatment for women with PCOS during the whole pregnancy period for it is quite beneficial and safe for both mothers and babies.

Abstract. Choriocarcinoma (CC) is the highest malignant gestational trophoblastic tumor which causes high mortality without timely treatment. HIF-1α is a very important molecule promoting neoplasm aggressiveness, metastasis through the induction of the epithelial to mesenchymal transition (EMT). Several researches have shown that Notch signaling is necessary for coupling hypoxia to the EMT. However, the pathway in choriocarcinoma remains undetermined. In this study, overexpression of HIF-1α inhibited epithelial index E-cadherin, cytokeratin 18 (CK18) and cytokeratin 19 (CK19) in two choriocarcinoma cell lines (JAR and JEG-3, respectively). The reciprocal changes associated with the EMT phenotypic transformation. The migration and invasive capability was significantly enhanced. HIF-1α overexpression was positively correlated with Notch1 and Hes1 (P<0.01; respectively). Using DAPT (Notch1 inhibitor) to knock down Notch1 expression, morphological and molecular typical changes of the EMT were detected in vitro. Knockdown of Notch1 prominently reduced MMP2 and MMP9 activities, and increased E-cadherin, CK18 and CK19 expression in JAR and JEG-3 cells (P<0.01). In vivo, serum-free suspension containing 5x10 6 JAR cells (lv-HIF-1α and lv-NC, respecticely) were implanted subcutaneously or injected intravenously into female NOD SCID mice, which were injected with DAPT or DMSO six times at 3-day intervals. Mice with subcutaneous nodules were injected i.v. fluorine-18 fluorodeoxyglucose ( 18 F-FDG) and then scanned in small animal PET/CT (SA-PET/ CT), and mice with lung metastasis were monitored by using the in vivo imaging system (IVIS). The in vivo data showed that inhibition of Notch signaling by DAPT treatment effectively suppressed metastatic tumor growth, metabolic activity and invasion. In summary, overexpression of HIF-1α promotes choriocarcinoma cell aggressiveness and metastasis through the regulation of the EMT dependenting on Notch signaling pathway.

Purpose: Fluzoparib (PARP inhibitor) showed promising antitumor activity for advanced ovarian cancer in a phase I study. This study aimed to assess the efficacy and safety of fluzoparib in patients with germline BRCA1/2-mutated recurrent ovarian cancer. Patients and Methods: This open-label, multicenter, single-arm, phase II study enrolled patients with platinum-sensitive recurrent ovarian cancer and germline BRCA1/2 mutation who had previously received two to four lines of platinum-based chemotherapy. Fluzoparib 150 mg was administered orally twice daily. The primary endpoint was independent review committee (IRC)-assessed objective response rate per RECIST v1.1. Results: A total of 113 patients were enrolled and received at least one dose of fluzoparib. As of data cutoff on March 21, 2020, the median follow-up period was 15.9 months (interquartile range, 13.5–18.5). The IRC- and investigator-assessed objective response rates were 69.9% [95% confidence interval (CI), 60.6–78.2] and 70.8% (95% CI, 61.5–79.0), respectively. The objective response rates were similar across all prespecified subgroups. The median IRC- and investigator-assessed progression-free survival was 12.0 months (95% CI, 9.3–13.9) and 10.3 months (95% CI, 9.2–12.0), respectively. The 12-month survival rate was 93.7% (95% CI, 87.2–96.9). Grade ≥3 adverse events occurred in 63.7% (72/113) of the patients, with the most common one being anemia/decreased hemoglobin. Adverse events that led to treatment interruption, dose reduction, and discontinuation occurred in 39.8%, 34.5%, and 0.9% of patients, respectively. One treatment-related death occurred. Conclusions: Fluzoparib demonstrated promising antitumor activity and acceptable safety profile in germline BRCA1/2-mutated, platinum-sensitive relapsed ovarian cancer. Thus, fluzoparib might be a novel treatment option for this population.

Background: Tumor-infiltrating lymphocytes (TILs) are involved in the antitumor immune response. The association between prognosis in patients with TILs and high-grade serous ovarian cancer (HGSOC) remains obscure, with some studies reporting conflicting results. Methods: We conducted an extensive literature search of electronic databases and retrieved prognostic data of each selected subtype of TILs, including CD3+, CD4+, CD8+, CD103+, and PD-1+ TILs. The fixed-effects model was applied to derive the pooled hazard ratio (HR) and 95% confidence interval (CI) of these markers. Results: The systematic review process yielded 19 eligible studies comprising 6004 patients with HGSOC. We compared TIL-positive and TIL-negative patients, and the pooled HRs from the multivariate analysis revealed that intraepithelial CD8+ TILs were positively correlated with progression-free survival (PFS, HR 0.46, 95% CI 0.25–0.67) and overall survival (OS, HR 0.90, 95% CI 0.86–0.9); stromal CD8+ TILs were positively correlated with OS (HR 0.61, 95% CI 0.36–0.87). Furthermore, the pooled HRs from univariate analysis demonstrated that intraepithelial CD3+, CD4+, CD8+, and CD103+ TILs were positively associated with OS (HR 0.58, 95% CI 0.44–0.72; HR 0.37, 95% CI 0.16–0.59; HR 0.51, 95% CI 0.42–0.60, and HR 0.59, 95% CI 0.44–0.74, respectively); stromal CD4+ and CD8+ TILs were significantly associated with OS (HR 0.63, 95% CI 0.32–0.94 and HR 0.78, 95% CI 0.58–0.97, respectively). However, the pooled HR from the multivariate analysis revealed that PD-1+ TILs were not associated with the OS of patients with HGSOC (HR 0.97, 95% CI 0.90–1.04). Conclusion: This meta-analysis provided evidence of the association of CD3+, CD4+, CD8+, and CD103+ TILs with the survival benefits (OS and PFS) of patients with HGSOC.