BackgroundHepatitis B virus (HBV) infection is highly endemic in China and it threats human health seriously. The hepatitis B surface antigen (HBsAg) prevalence among women of childbearing age plays an important role in mother to child transmission of HBV, as 30% ~50% of chronic carriers can be attributed to maternal-infantile transmission. However, there are few studies which have reported on the prevalence of HBsAg among women of childbearing age in China. This study aimed to determine the prevalence of HBsAg and its associated risk factors among rural women of childbearing age in Hainan, which is the highest hepatitis B virus endemic province in China.MethodsA cross-sectional, population-based study, which included 12393 rural women aged 15 ~ 49 years, enrolled by a multistage stratified cluster sampling, was carried out in Hainan province, China, from November 2007 to December 2008. Blood samples were obtained from each study participant, and screened for HBsAg.ResultsThe overall HBsAg prevalence of childbearing age women was 9.51%. Risk factors for HBsAg positivity among rural women were: lower education level (OR=1.206), lower family monthly income (OR=1.233), having an HBsAg-positive family member (OR=1.300), without an immunization history (OR=1.243), tattooing (OR=1.190), body piercing (OR=1.293), vaginoscopy history (OR=1.103) and history of induced abortion (OR=1.142).ConclusionsThere is a high HBsAg seroprevalence rate among rural women of childbearing age in Hainan province. Hence, it is necessary to take preventive measures to reduce the seroprevalence of HBsAg and to control its associated risk factors.

MicroRNAs (miRNAs) play an important role in the tumorigenesis of ovarian cancer. Previously, we have reported the dysregulation of miR-203 in the ovarian cancer tissues. However, the biological functions and molecular mechanisms of miR-203 in ovarian cancer remain unknown. Here, we showed that the expression of miR-203 was increased in ovarian cancer tissues compared with the adjacent non-cancerous tissues and the transcription of miR-203 was inhibited by P53. Forced expression of miR-203 in ovarian cancer promoted cell growth and migration, while depletion of miR-203 inhibited the growth and migration of ovarian cancer cells. In addition, miR-203 promoted the metastasis of ovarian cancer cells in vivo and shorted the survival of the nude mice. Mechanically, miR-203 targeted the 3'-UTR of pyruvate dehydrogenase B (PDHB) and increased the consumption of glucose and the production of lactate. Overexpression of PDHB abolished the oncogenic effects of miR-203 on the growth of ovarian cancer cells. Together, our data suggested the oncogenic roles of miR-203 in ovarian cancer by promoting glycolysis, and miR-203 might be a therapeutic target for ovarian cancer.

The Hainan Province is confronted with the challenge to reduce the prevalence of birth defects. Interventions should focus on the rural areas where a higher prevalence of birth defects is observed.

Overcoming senescence is a feature of ovarian cancer cells; however, the mechanisms underlying senescence regulation in ovarian cancer cells remain largely unknown. In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. Taken together, the results of this study demonstrated the tumor suppressive roles of ITPKA in ovarian cancer and provided a good explanation for the oncogenic roles of miR-203.