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1.
BMC Med Educ ; 22(1): 138, 2022 Mar 02.
Artigo em Inglês | MEDLINE | ID: mdl-35236332

RESUMO

BACKGROUND: This study was aimed to evaluate the application of WeChat-based flipped classroom in root canal filling teaching in a preclinical endodontic course. METHODS: A two-group comparative study was designed. The pre-class test, on-site quiz, and root canal filling on extracted premolars were performed by students from a lecture-based classroom group (LG, n = 30) and a WeChat-based flipped classroom group (WFG, n = 30). Results of the Pre-class test and on-site quiz were analyzed by independent samples t-test. Post-filling radiographs were taken and evaluated by a specialist in oral radiology who was blinded to grouping. Results of root canal fillings were analyzed by the Pearson chi-square test. Student responses in questionnaires were analyzed by Fisher's exact test. RESULTS: The students in WFG could get significantly higher scores in the on-site test and make better performances in root canal filling than those in LG. In terms of questionnaires, students from WFG were perceived to be more motivated to learn, better to understand the knowledge, better to improve communication and clinical skills, easier to perform root canal filling but spending more time. CONCLUSION: The WeChat-based flipped classroom teaching can have a better effect than lecture-based teaching on root canal filling learning for students with limited endodontic experiences.


Assuntos
Cavidade Pulpar , Radiologia , Competência Clínica , Humanos , Aprendizagem , Aprendizagem Baseada em Problemas/métodos , Obturação do Canal Radicular , Ensino
2.
Front Mol Biosci ; 8: 720370, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34568426

RESUMO

Purpose: Despite considerable efforts to improve treatment modalities for cholangiocarcinoma, a common form of malignant tumor, its long-term survival rate remains poor. Hydroxychloroquine (HCQ) is a 4-aminoquinoline derivative antimalarial drug that has antimalarial and autophagy inhibition effects and exhibits comprehensive therapeutic effects on various cancers. In this study, we aimed to explore the anticancer potential and the underlying molecular mechanism of HCQ in cholangiocarcinoma treatment in vitro and in vivo. Methods: Autophagy-related genes (ARGs) were obtained from the Human Autophagy Database and Molecular Signatures Database, and the expression profiles of ARGs were downloaded from the database of The Cancer Genome Atlas. Different expression gene sets were performed using R software. The Gene Ontology and KEGG enrichment analyses were performed to reveal significantly enriched signaling pathways and to identify differentially expressed genes in cholangiocarcinoma tissues. HuCCT-1 and CCLP-1 cells were exposed to different concentrations of HCQ. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8), colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) assays. Cell apoptosis and cycle arrest were detected by the Live/Dead cell assay and flow cytometry (FCM). The inhibition of autophagy was observed using fluorescence microscopy. The reactive oxygen species levels were assessed by fluorescence microscopy and flow cytometry. The protein levels were determined by western blot. A cholangiocarcinoma cell line xenograft model was used to evaluate the antitumor activity of HCQ in vivo. Results: Compared with normal tissues, there were 141 ARGs with an aberrant expression in cholangiocarcinoma tissues which were mainly enriched in autophagy-related processes. Inhibition of autophagy by HCQ effectively suppressed cholangiocarcinoma in vitro and in vivo. HCQ inhibited cell proliferation and induced apoptosis and cycle arrest in vitro by increasing ROS accumulation, which was involved in autophagy inhibition. The ROS scavenger reduced l-glutathione distinctly weakened HCQ-induced cell apoptosis and viability inhibition in cholangiocarcinoma cells. In addition, HCQ inhibited growth of cholangiocarcinoma cell line xenograft tumors. Conclusion: HCQ could inhibit cell proliferation and induce apoptosis in cholangiocarcinoma by triggering ROS accumulation via autophagy inhibition, which makes HCQ a potential antitumor drug candidate for cholangiocarcinoma treatment.

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