Association between bacterial vaginosis with human papillomavirus in the United States (NHANES 2003-2004).

BACKGROUND: The balance of vaginal microecology is closely related to human papillomavirus (HPV) infection and cervical lesions. This study aims to investigate the relationship between bacterial vaginosis (BV) and HPV infection. METHODS: In total, 1,310 individuals from the National Health and Nutrition Examination Survey (NHANES, 2003-2004) were included in this study. Logistic regression and subgroup analyses were used to examine the association between BV and HPV infection. RESULTS: A significant positive association was observed between BV and HPV infection in women after adjustment for other confounders (OR = 1.47, 95% confidence interval [CI]: 1.15-1.88). In subgroup analyses, we have found this positive correlation was most prominent among Mexican Americans (OR = 1.83, 95% CI: 1.08-3.08) and non-Hispanic blacks (OR = 1.81, 95% CI: 1.08-3.04). CONCLUSIONS: This cross-sectional study demonstrated a positive association between BV and HPV infection in women.

MiR-193a-5p serves as an inhibitor in ovarian cancer cells through RAB11A.

Ovarian cancer is often not diagnosed until it is in advanced stages and its cure rate is relatively low. Thus, this investigation is concerned about the pathogenesis of this cancer. Differential expression analysis was undertaken on messenger RNA (mRNA) and microRNA (miRNA) data of ovarian cancer in Gene Expression Profiling Interactive Analysis and Gene Expression Omnibus databases. RAB11A mRNA and miR-193a-5p expression levels were tested by quantitative polymerase chain reaction. The targeting relationship between RAB11A and miR-193a-5p was verified by dual-luciferase assay. Cell behaviors of ovarian cancer were tested by Cell-Counting-Kit-8, colony formation and transwell assays. Expression of RAB11A protein and the proteins associated with Wnt/ß-catenin was tested by western blot. RAB11A high expression and miR-193a-5p low expression were found in ovarian cancer cells. RAB11A was targeted by miR-193a-5p. Cellular function experiments proved that RAB11A facilitated Wnt/ß-catenin signaling activation and deteriorated ovarian cancer progression. Rescue experiments exhibited two results: miR-193a-5p hindered proliferation, migration and invasion of ovarian cancer cells, and this suppression was counteracted by overexpression of RAB11A and miR-193a-5p. Furthermore, miR-193a-5p repressed RAB11A-mediated Wnt/ß-catenin activation. Altogether, miR-193a-5p served as a modulator in ovarian cancer cells via targeting RAB11A.

Estrogen Exerts Neuroprotective Effects in Vascular Dementia Rats by Suppressing Autophagy and Activating the Wnt/ß-Catenin Signaling Pathway.

Vascular dementia (VD) is a clinical syndrome of acquired cognitive dysfunction caused by various cerebrovascular factors. Estrogen is a steroid hormone involved in promoting neuronal survival and in regulating many signaling pathways. However, the mechanism by which it confers neuroprotective effects in VD remains unclear. Here, we aimed to investigate the effect of estrogen on neuronal injury and cognitive impairment in VD rats. Adult female rats were randomly divided into four groups (sham, model, estrogen early and estrogen later treatment) and received sham surgery or bilateral ovariectomy and permanent occlusion of bilateral common carotid arteries (BCCAO). The early treatment group received daily intraperitoneal injections of 17ß-estradiol (100 µg/kg/day) for 8 weeks starting the day after BCCAO. The later treatment group was administered the same starting 1 week after BCCAO. Learning and memory functions were assessed using the Morris water maze. Morphological changes within the hippocampal CA1 region were observed by hematoxylin/eosin staining and electron microscopy. Expression of proteins associated with autophagy and signaling were detected by immunohistochemical staining and Western blot. We found that estrogen significantly alleviated cognitive damage and neuronal injury and reduced the expression of Beclin1 and LC3B, indicating a suppression of autophagy. Moreover, estrogen enhanced expression of ß-catenin and Cyclin D1, while reducing glycogen synthase kinase 3ß, suggesting activation of Wnt/ß-catenin signaling. These results indicate that estrogen ameliorates learning and memory deficiencies in VD rats, and that this neuroprotective effect may be explained by the suppression of autophagy and activation of Wnt/ß-catenin signaling.

The expression levels and clinical significance of MFG-E8 and CD133 in epithelial ovarian cancer.

The aim of our study was to test whether there is an association between high expression of milk fat globule EGF factor 8 (MFG-E8) and CD133 presence or clinical outcomes of patients with epithelial ovarian cancer (EOC). MFG-E8 and CD133 expression levels were analyzed by immunohistochemistry in 88 EOC tumor specimens. High expression of MFG-E8 directly and significantly correlated with the presence of CD133 immunostaining (R = 0.353, p=.001), whereas immunostaining of MFG-E8 and CD133 significantly correlated with FIGO stage, tumor grade, debulking status, the dualistic model, ascites status, and nonresponse to chemotherapy (p<.05). It was also found that high expression of MFG-E8 and CD133 presence is a potent predictor of poor clinical outcomes among patients with EOC. Our study is the first to show that high expression of MFG-E8 in EOCs positively correlates with CD133 presence. Further research on MFG-E8 in EOC is needed to determine whether MFG-E8 is a new tumor marker of ovarian cancer and a new target for anticancer therapy as well as whether it can interact with cancer stem cell inhibitors for the treatment of refractory tumors.

Insulin-like growth factor 1 regulates growth of endometrial carcinoma through PI3k signaling pathway in insulin-resistant type 2 diabetes.

Previous studies have shown that insulin-like growth factor 1 (IGF-1) may be responsible for the higher risk for developing endometrial carcinoma (EMC) in insulin-resistant type 2 diabetes mellitus (T2DM) patients. However, the underlying mechanisms are not understood. Here, we compared T2DM patients with or without EMC. We did not find difference in the serum levels of IGF-1, insulin-like growth factor 2 (IGF-2), IGF-1 binding protein 3, as well as the activation of IGF-1 receptor (IGF1R) in endometrial cells between T2DM patients with or without EMC. However, the levels of IGF2R activation and activation of PI3k, an IGF1R downstream factor, were significantly higher in endometrial cells in T2DM patients with EMC. In vitro analyses of activation of IGF1R, IGF2R, PI3k and CCND1 in EMC cells or IGF2R-overexpressing EMC cells by IGF-1 or IGF-2 suggest that increases in IGF2R in endometrial cells in T2DM may increase PI3k/CCND1-dependent cell growth through loss of competitive binding of IGF-2 to IGF1R, as a possible explanation for the higher risk for developing EMC in T2DM.