Awareness and knowledge about human papillomavirus among high school students in China.

OBJECTIVE: To investigate awareness and knowledge of human papillomavirus (HPV) infection among high school students and to provide a basis for health education on HPV infection for high school students in China. STUDY DESIGN: A questionnaire on HPV awareness and knowledge was administered to 900 high school students in Xiangtan City of Hunan Province in China by layer cluster sampling. A total of 848 anonymous valid questionnaires were received from volunteers who completed the questionnaire correctly. RESULTS: Only 10.1% had heard of HPV, and of those only 18.6% knew that HPV could lead to cervical cancer. Single factor analysis indicated that home address, age, grade, academic achievement, sex history, gender, father's education level and mother's education level were impact factors for HPV knowledge of high school students. Multiple regression analysis showed 4 independent risk factors associated with HPV knowledge: academic achievement, sex history, gender, and mother's education level. The limited knowledge came primarily from television and radio broadcasts (59.3%), the Internet (57.0%), parents (25.6%), medical workers (20.9%), and teachers (18.6%). CONCLUSION: High school students lack HPV knowledge, which is affected by multiple factors. Targeted health education of all sorts must be provided. Both schools and families are responsible for reinforcing HPV education provided to high school students.

Overexpression of Helicobacter pylori VacA N-terminal fragment induces proinflammatory cytokine expression and apoptosis in human monocytic cell line through activation of NF-κB.

Vacuolating cytotoxin (VacA) is an important virulence factor in the pathogenesis of Helicobacter pylori-related diseases. The aim of this study was to investigate the function of the amino-terminal 476 residue fragment (p52) of VacA and the possible molecular mechanisms responsible for its induction of proinflammatory cytokines secretion and apoptosis. Human acute monocytic leukemia cell line THP-1 was used as an in vitro model to study proinflammatory cytokines secretion and apoptosis induced by transfection of a recombinant plasmid encoding the amino-terminal 476 residue fragment (p52) of VacA. The results showed that VacA p52 overexpression induced the production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1ß), nitric oxide, and reactive oxygen species in THP-1 cells in a time-dependent manner. VacA p52 overexpression also promoted THP-1 cells apoptosis. In addition, VacA p52 triggered the activation of nuclear factor kappa B (NF-κB), indicating a possible mechanism for its induction of proinflammatory cytokines secretion and cell apoptosis. Our study demonstrated that the induction of cytokines secretion and apoptosis by VacA p52 in THP-1 cells could be mediated through activation of nuclear factor kappa B.

Transcriptional repression of hDaxx enhanced by adenovirus 12 E1B 55-kDa oncoprotein interacting with hDaxx.

BACKGROUND: Daxx has been identified as a nuclear protein that involves in apoptosis and transcriptional repression. Daxx co-localizes with the promyelocytic leukemia (PML) protein and regulates transcription. Human Daxx (hDaxx) is a protein that functions as a transcriptional regulation through its interaction with some DNA-associated proteins. The aim of this study was to explore the transcriptional regulatory effect of hDaxx interacting with adenovirus (Ad) 12 E1B (Ad12E1B) 55-kDa oncoprotein. METHODS: The co-localization of hDaxx-Ad12E1B or hDaxx-PML protein in the nucleus was observed under a confocal microscope. Interaction of hDaxx and Ad12E1B was analyzed by yeast two-hybrid assay. Direct binding of hDaxx and Ad12E1B was analyzed using coimmunoprecipitation and Western blot in vivo and in vitro. The activity of a luciferase reporter gene, which was regulated by an hDaxx modulated thymidine kinase (TK) promoter, was detected in an automat luminometer. RESULTS: Ad12E1B, which co-localized with hDaxx in the nuclei of G401-CC3 cells, disrupted the co-localization of hDaxx and PML in the PML oncogenic domains (PODs). hDaxx bound directly to Ad12E1B in vivo and in vitro. hDaxx interacted with Ad12E1B along its full length. Ad12E1B enhanced transcriptional repression activity of hDaxx. CONCLUSION: Ad12E1B disrupts the co-localization of hDaxx with PML in PODs and enhances transcriptional repression activity of hDaxx.