Fu Jen Catholic University

About: Fu Jen Catholic University is a education organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Hazard ratio. The organization has 6842 authors who have published 9512 publications receiving 171005 citations. The organization is also known as: FJU & Fu Jen.

A recommendation mechanism for contextualized mobile advertising

Abstract: Mobile advertising complements the Internet and interactive television advertising and makes it possible for advertisers to create tailor-made campaigns targeting users according to where they are, their needs of the moment and the devices they are using (ie contextualized mobile advertising) Therefore, it is necessary that a fully personalized mobile advertising infrastructure be made In this paper, we present such a personalized contextualized mobile advertising infrastructure for the advertisement of commercial/non-commercial activities We name this infrastructure MALCR, in which the primary ingredient is a recommendation mechanism that is supported by the following concepts: (1) minimize users' inputs (a typical interaction metaphor for mobile devices) for implicit browsing behaviors to be best utilized; (2) implicit browsing behaviors are then analyzed with a view to understanding the users' interests in the values of features of advertisements; (3) having understood the users' interests, Mobile Ads relevant to a designated location are subsequently scored and ranked; (4) Top-N scored advertisements are recommended The recommendation mechanism is novel in its combination of two-level Neural Network learning, Neural Network sensitivity analysis, and attribute-based filtering This recommendation mechanism is also justified (by thorough evaluations) to show its ability in furnishing effective personalized contextualized mobile advertising

Coping with racial discrimination: the role of substance use.

Abstract: Three studies tested the hypothesis that the relation between perceived racial discrimination and substance use reported in previous research is moderated by use of substances as a coping mechanism. Studies 1 and 2 were experimental studies of African American adolescents' and young adults' reactions to a discrimination experience. Results revealed that those who endorsed substance use-as-coping reported more willingness to use substances after experiencing discrimination. Study 3 was a prospective study of the relation between perceived discrimination and substance use over an 8-year period in African American adolescents. Results demonstrated that discrimination is associated with increases in substance use, but only among adolescents who endorse substance use-as-coping. Together, these three studies provide evidence that experiencing discrimination has both short- and long-term detrimental effects on African Americans' substance use, but significantly more so for those who adopt a pattern of using substances as a coping mechanism.

TOPK/PBK promotes cell migration via modulation of the PI3K/PTEN/AKT pathway and is associated with poor prognosis in lung cancer.

Abstract: We integrated four gene expression profile data sets, namely two different pair-matched stage I lung adenocarcinoma data sets, secondary metastatic tumors vs benign tumors and lung tumor metastasizes to the brain, and we identified one kinase, T-LAK Cell-Originated Protein Kinase (TOPK), as a putative gene that promotes metastasis. To delineate the role of TOPK in lung cancer, we showed that overexpression of TOPK, but not a catalytically inactive form of TOPK, can enhance the migration and invasion of lung fibroblasts or cells with low TOPK expression. In addition, TOPK-induced cell migration was shown to be a PI3K/AKT-dependent event. TOPK concurrently promoted AKT phosphorylation at Ser(473) and decreased the phosphatase and tensin homolog (PTEN) levels, whereas TOPK knockdown had the reverse effects. LY294002, a PI3K inhibitor, did not inhibit the TOPK-induced decrease in PTEN, and co-expression of PTEN significantly reduced TOPK-induced AKT phosphorylation in a dose-dependent manner; these results indicate that the TOPK-mediated PTEN decrease has an upstream role in regulating PI3K/AKT-stimulated migration. Using immunohistochemical analysis of lung cancer tissue samples, we showed that a high TOPK expression level correlates strongly with reduced overall and disease-free survivals. Moreover, an inverse correlation between TOPK and PTEN expression was present and is consistent with the biochemical findings. Finally, a combination of high TOPK and low PTEN expression was inversely correlated with overall and disease-free survivals, independent of other pathologic staging factors. Our results suggest that TOPK is a potential therapeutic target in lung cancer that promotes cell migration by modulating a PI3K/PTEN/AKT-dependent signaling pathway; they also suggest that high TOPK expression, either alone or in combination with a low level of PTEN, may serve as a prognostic marker for lung cancer.

Infertility with defective spermatogenesis and steroidogenesis in male mice lacking androgen receptor in Leydig cells

Abstract: Androgen and the androgen receptor (AR) have been shown to play critical roles in male fertility. Our previous data demonstrated that mice lacking AR (AR(-/y)) revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in Leydig cells remain largely unknown. Using a Cre-LoxP conditional knockout strategy, we generated a tissue-specific knockout mouse (L-AR(-/y)) with the AR gene deleted by the anti-Mullerian hormone receptor-2 (Amhr2) promoter driven Cre expressed in Leydig cells. Phenotype analyses show that the outside appearance of L-AR(-/y) mice was indistinguishable from wild type mice (AR(+/y)), but with atrophied testes and epididymis. L-AR(-/y) mice were infertile, with spermatogenic arrest predominately at the round spermatid stage and no sperm could be detected in the epididymis. L-AR(-/y) mice also have lower serum testosterone concentrations and higher serum leuteinizing hormone and follicle-stimulating hormone concentrations than AR(+/y) mice. Further mechanistic studies demonstrated that hypotestosteronemia in L-AR(-/y) mice is not caused by reducing numbers of Leydig cells, but instead by the alterations of several key steroidogenic enzymes, including 17beta-HSD3, 3beta-HSD6, and P450c17. Together, L-AR(-/y) mice provide in vivo evidence that functional AR in Leydig cells is essential to maintain normal spermatogenesis, testosterone production, and required for normal male fertility.