Emotional symptoms, dietary patterns and dental caries: A cross-sectional study in adolescents.

OBJECTIVES: This study investigates the relationship between emotional symptoms and dental caries in adolescents and the role of dietary patterns as mediating variables. METHODS: This cross-sectional study used a multistage stratified random sample of schools, in Jiangsu, with a sample of 17,997 adolescents aged 11-19. Measures included emotional symptoms, dental caries, toothbrushing frequency, and dietary patterns. Logistic and Poisson regression models were conducted to test mediation hypotheses. RESULTS: The decayed, missing, and filled teeth index (DMFT) was related to depressive symptoms following adjustment for other variables (incidence rate ratios [IRR] = 1.09; p < 0.05), but not to anxiety symptoms level (IRR = 1.02; p > 0.05). The link between depressive symptoms and DMFT had a partial mediation impact on toothbrushing frequency (a, b, c' all p < 0.05). Sugary foods, but not fried foods, partially mediated the link between depressive symptoms and caries when toothbrushing frequency was adjusted. CONCLUSION: There are direct and indirect associations between emotional symptoms and caries; the latter may be due to changes in oral health behaviours that increase the risk of caries.

Sesamin induces cell cycle arrest and apoptosis through p38/C-Jun N-terminal kinase mitogen-activated protein kinase pathways in human colorectal cancer cells.

Sesamin, a lignan compound, exhibits a variety of biological activities and possesses potent anticancer properties on some human cancers. However, its effect on human colorectal cancer (CRC) remains to be elucidated. To investigate the effects of sesamin on CRC cells and further to explore the mechanisms, cell viability, cell cycle and apoptosis assays were performed in this study. We found that sesamin had a selective antiproliferation of CRC cell line HCT116 in a dose- and time-dependent manner, but no obvious effect on human normal colorectal mucosa epithelial cell FHC. Further study showed that sesamin-induced cell cycle arrest and decreased the expression of Cyclin D1 significantly and dose-dependently in HCT116 cells. Moreover, sesamin dose-dependently triggered apoptosis of HCT116 but not FHC, and promoted the expression levels of proapoptotic biomarkers Bax, cleaved caspase-3 and cleaved PARP-1 and inhibited the expression of antiapoptotic biomarker Bcl-2. Western blot analysis was used to reveal the possible signaling pathways, and we found that sesamin upregulated the phosphorylation expression levels of C-Jun N-terminal kinase (JNK) and p38 except ERK1/2 in a dose-dependent way in both HCT116 and another CRC cell line SW480. Moreover, we found that the apoptosis effect induced by sesamin was partially eliminated by inhibiting JNK or p38 activation. Finally, we showed that sesamin effectively reduced the growth of xenograft tumors derived from cell lines with limited toxicity. Taken together, the potential ability of sesamin to induce cell cycle arrest and apoptosis was shown to be via the p38 and JNK mitogen-activated protein kinase signaling pathways, which may be one of the mechanisms of the anticancer activity of this low-toxic agent.