ABSTRACT
OBJECTIVE: Observe the effect of Tai Chi exercise on the rehabilitation of elder patients suffered from the anxiety disorder. METHODS: 32 elder patients suffered from the anxiety disorder are randomly divided into the experimental group and the control group and each of them consists of 16 patients. The control group only receives the drug therapy, while the experimental group is treated with Tai Chi exercise in addition to the drug therapy. When they are chosen and 45 days after treatment, they are respectively evaluated by Hamilton Anxiety Scale (HAMA) and Generic Quality of Life Inventory-74 (GQOLI-74). The cured patients stop the drug therapy, but the cured patients in the experimental group continue to do Tai Chi exercise after stopping the drug therapy. After tracing and investigating each cured patient for 2 months, test and evaluate whether their disease reoccurs within the 2 months. RESULTS: After 45 days' treatment, it is found that HAMA and GQOLI-74 scores of the patients in the experimental group are improved significantly in comparison with those in the time of their selection and those in the control group (P<0.05); upon tracing and investigation of the cured patients, it is found that the recurrence rate is 42.86% in the control group, while that of the experimental group is only 9.09%. CONCLUSION: After the elder patients suffered from the anxiety disorder are treated with Tai Chi exercise in addition to the drug therapy, their effect is more significant than those who only are treated by the drug. Meanwhile, if the patients are only treated by the drug, their disease is easy to reoccur after curing. However, if they insist on Tai Chi exercise, the recurrence rate is low and the effect is significant.
ABSTRACT
BACKGROUND: Glucagon-like peptide-1 (GLP-1) reduces fatty acid-induced beta-cell lipotoxicity in diabetes; however, the explicit mechanisms underlying this process are not fully understood. This study was designed to investigate the involvement of microRNA, which regulates gene expression by the sequence-specific inhibition of mRNA transcription in the GLP-1 mediation of beta-cell function. METHODS: The cell viability and apoptosis were determined using an methyl thiazoleterazolium (MTT) assay and flow cytometry. The expression of genes involved in beta-cell function, including microRNA-34a and sirtuin 1, were investigated using real-time PCR. The underlying mechanisms of microRNA-34a were further explored using cell-transfection assays. RESULTS: A 24-hours incubation of INS-1 cells with palmitate significantly decreased cell viability, increased cell apoptosis and led to the activation of microRNA-34a and the suppression of sirtuin 1. A co-incubation with GLP-1 protected the cells against palmitate-induced toxicity in association with a reduction in palmitate-induced activation of microRNA-34a. Furthermore, palmitate-induced apoptosis was significantly increased in cells that were infected with microRNA-34a mimics and decreased in cells that were infected with microRNA-34a inhibitors. CONCLUSION: MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.
