Understanding the Lifestyle Correlates with Chronic Constipation and Self-Rated Health

The objective of this study is to evaluate the healthy and unhealthy behaviors as risk factors for chronic constipation and self-rated health status. Eight hundred tenth students enrolled from a university in Miaoli city, Taiwan. Chronic constipation was assessed using Chinese questionnaire. Information of unhealthy and healthy lifestyles was interviewed by constructed questionnaire. Thirty-six percentage of university students were assessed as chronic constipation. Using multivariate logistic regression adjusted for age, sex, race and BMI, we found chronic constipation significantly correlated with frequency of consumption from snack, fast food, fried food, daily consumption of water, physical activity and junk food used as regular food. Moreover, these unhealthy behaviors significantly correlated with self-rated health status. Students with chronic constipation had poor self-rated health status. It is urgent to create healthy behaviors to reduce the risk for chronic constipation or upgrade self-rated health status in university students.

Comparative transcriptomic analysis reveals adriamycin-induced apoptosis via p53 signaling pathway in retinal pigment epithelial cells

Objective: This paper applied a transcriptomic approach to investigate the mechanisms of adriamycin(ADR) in treating proliferative vitreoretinopathy(PVR) using ARPE-19 cells. Methods: The growth inhibitory effects of ADR on ARPE-19 cells were assessed by sulforhodamine B(SRB) assay and propidium iodide(PI) staining using flow cytometry. The differentially expressed genes between ADR-treated ARPE-19 cells and normal ARPE-19 cells and the signaling pathways involved were investigated by microarray analysis. Mitochondrial function was detected by JC-1 staining using flow cytometry and the Bcl-2/Bax protein family. The phosphorylated histone H2 AX(γ-H2 AX), phosphorylated checkpoint kinase 1(p-CHK1), and phosphorylated checkpoint kinase 2(p-CHK2) were assessed to detect DNA damage and repair. Results: ADR could significantly inhibit ARPE-19 cell proliferation and induce caspasedependent apoptosis in vitro. In total, 4479 differentially expressed genes were found, and gene ontology items and the p53 signaling pathway were enriched. A protein–protein interaction analysis indicated that the TP53 protein molecules regulated by ADR were related to DNA damage and oxidative stress. ADR reduced mitochondrial membrane potential and the Bcl-2/Bax ratio. p53-knockdown restored the activation of c-caspase-3 activity induced by ADR by regulating Bax expression, and it inhibited ADR-induced ARPE-19 cell apoptosis. Finally, the levels of the γ-H2 AX, p-CHK1, and p-CHK2 proteins were up-regulated after ADR exposure. Conclusions: The mechanism of ARPE-19 cell death induced by ADR may be caspase-dependent apoptosis, and it may be regulated by the p53-dependent mitochondrial dysfunction, activating the p53 signaling pathway through DNA damage.