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Articles by J Kong
Total Records ( 2 ) for J Kong
  J Kong , X Li , Y Wang , W Sun and J. Zhang

Objective  To assess the impact of digital problem-based learning (PBL) cases on student learning in ophthalmology courses.

Methods  Ninety students were randomly divided into 3 classes (30 students per class). The first class studied under a didactic model. The other 2 classes were divided into 6 groups (10 students per group) and received PBL teaching; 3 groups studied via cases presented in digital form and the others studied via paper-form cases. The results of theoretical and case analysis examinations were analyzed using the 2 test. Student performance on the interval practice was analyzed using the Kruskal-Wallis test. Questionnaires were used to evaluate student and facilitator perceptions.

Results  Students in the digital groups exhibited better performance in the practice procedures according to tutorial evaluations compared with the other groups (P < .05). The 2 PBL classes had significantly higher mean results of theoretical and case analysis examinations (P < .001), but there was no significant difference between the 2 PBL classes. Ninety-three percent of students in the digital groups (vs 73% in the paper groups) noted that the cases greatly stimulated their interest.

Conclusions  Introducing PBL into ophthalmology could improve educational quality and effectiveness. Digital PBL cases stimulate interest and motivate students to further improve diagnosis and problem-handling skills.

  R. J Guo , S Funakoshi , H. H Lee , J Kong and J. P. Lynch

Cdx2 is an intestine-specific transcription factor known to regulate proliferation and differentiation. We have reported previously that Cdx2 limits the proliferation of human colon cancer cells by inhibiting the transcriptional activity of the β-catenin–T-cell factor (TCF) bipartite complex. Herein we further elucidate this mechanism. Studies with a classic Cdx2 target gene and a canonical Wnt/β-catenin/TCF reporter suggest that Cdx2 regulates these promoters by distinctly different processes. Specifically, inhibition of β-catenin/TCF activity by Cdx2 does not require Cdx2 transcriptional activity. Instead, Cdx2 binds β-catenin and disrupts its interaction with the DNA-binding TCF factors, thereby silencing β-catenin/TCF target gene expression. Using Cdx2 mutants, we map the Cdx2 domains required for the inhibition of β-catenin/TCF activity. We identify a subdomain in the N-terminus that is highly conserved and when mutated significantly reduces Cdx2 inhibition of β-catenin/TCF transcriptional activity. Mutation of this subdomain also abrogates Cdx2’s anti-proliferative effects in colon cancer cells. In summary, we conclude that Cdx2 binds β-catenin and disrupts the β-catenin–TCF complex. Considering the pivotal role of β-catenin/TCF activity in driving proliferation of normal intestinal epithelial and colon cancer cells, our findings suggest a novel mechanism for Cdx2-mediated regulation of Wnt/β-catenin signaling and cell proliferation.

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