ABSTRACT
BACKGROUND: Several studies have revealed the frequency of family mealtimes to be inversely associated with depressive symptoms in adolescents. However, there have been few studies in older populations. This cross-sectional study investigated the association between family mealtime frequency and depressive symptoms in elderly Koreans. METHODS: This study analyzed 4,959 elderly men and women (aged 65 years or older) who participated in the Korea National Health and Nutrition Examination Survey. Self-administered questionnaires were used to assess depressive status, family mealtime frequency, and covariates. Multiple logistic regression analysis was performed to evaluate the association using the eating alone group as a reference. RESULTS: After adjusting for all covariates, participants who had family meals 3 times a day had fewer depressive symptoms than the eating alone group; adjusted odds ratios (ORs) (95% confidence intervals [CIs]) were 0.72 (0.58- 0.89) for point depressiveness/anxiety and 0.73 (0.56-0.94) for depressiveness lasting for at least 2 weeks. In suicidal ideation, the OR (95% CI) of eating with family twice a day was significant after full adjusting for covariates at 0.67 (0.50-0.88). CONCLUSION: Family mealtimes were closely associated with depressive symptoms in elderly Koreans, which suggests that maintaining intrafamilial bonding is important for mental health in an older population.
ABSTRACT
The deficiency of retinoblastoma (Rb) gene deregulates E2F transcription factors and thus induces E2F target genes directly or p53 target genes indirectly via mouse p19(Arf) (or p14(ARF) in humans), an E2F target gene. Here, we identified that etoposide-induced 2.4 mRNA (Ei24)/p53-induced gene 8 (Pig8), a p53 target gene involved in apoptosis and autophagy, was up-regulated in Rb(-/-) mouse embryonic fibroblasts (MEFs). The Ei24 promoter was activated by E2F1 via multiple E2F-responsive elements, independently of the previously reported p53-responsive element. Chromatin immunoprecipitation assays revealed that E2F1 directly acts on the mouse Ei24 promoter. We observed that Ei24 expression was suppressed in p53(-/-) MEFs upon UVC irradiation, which was exacerbated in p53(-/-) E2f1(-/-) MEFs, supporting the positive role of E2F1 on Ei24 transcription. Furthermore, Ei24 knockdown sensitized p53(-/-) MEFs against UVC irradiation. Together, our data indicate that Ei24 is a novel E2F target gene contributing to the survival of p53-deficient cells upon UVC irradiation and thus may have a potential significance as a therapeutic target of certain chemotherapy for treating p53-deficient tumors.
