PURPOSE: The purpose of this study was to investigate factors influencing college students' health promotion lifestyle. METHODS: The subject was 606 students. Statistical analysis with SPSS used descriptive statistics, t-test, one way ANOVA, Pearson correlation and Stepwise Multiple Regression. RESULTS: The average item score for health promotion lifestyle was 2.58. The subscale showing the highest score was interpersonal relationship (3.03), which was followed by spiritual growth (2.94), stress management (2.54), nutrition (2.52), physical activity (2.16) and health responsibility (2.15). There were significant differences according to age, gender, BMI, perceived health state, religion, economic state, live together, major and health promotion lifestyle. The most powerful predictors of health promotion lifestyle were the prior related behavior (51.8%) and self-efficacy (7.7%). The combination of prior related behavior, perceived self-efficacy, activity-related affect, social support, perceived stress, commitment to a plan of action accounted for 67.9% of the variance of health promotion lifestyle. CONCLUSION: Prior related behavior was the most powerful variable of health promotion lifestyle. Therefore, health promotion programs for changing and maintaining prior related behavior and increasing self-efficacy should be developed to promote a healthy lifestyle in college students.
Health Promotion* ; Humans ; Life Style* ; Motor Activity

Microglia are recognized as residential macrophageal cells in the brain. Activated microglia play a critical role in removal of dead or damaged cells through phagocytosis activity. During phagocytosis, however, microglia should survive under the harmful condition of self-producing ROS and pro-inflammatory mediators. TGF-beta has been known as a classic anti-inflammatory cytokine and controls both initiation and resolution of inflammation by counter-acting inflammatory cytokines. In the present study, to understand the self-protective mechanism, we studied time-dependent change of TNF-alpha and TGF-beta production in microglia phagocytizing opsonized-beads (i.e., polystyrene microspheres). We found that microglia phagocytized opsonized-bead in a time-dependent manner and simultaneously produced both TNF-alpha and TGF-beta. However, while TNF-alpha production gradually decreased after 6 h, TGF-beta production remained at increased level. Microglial cells pre-treated with lipopolysaccharides (a strong immunostimulant, LPS) synergistically increased the production of TNF-alpha and TGF-beta both. However, LPS-pretreated microglia produced TNF-alpha in a more sustained manner and became more vulnerable, probably due to the marked and sustained production of TNF-alpha and reduced TGF-beta. Intracellular oxidative stress appears to change in parallel with the microglial production of TNF-alpha. These results indicate TGF-beta contributes for the survival of phagocytizing microglia through autocrine suppression of TNF-alpha production and oxidative stress.
Brain ; Cytokines ; Inflammation ; Lipopolysaccharides ; Microglia ; Oxidative Stress ; Phagocytosis ; Polystyrenes ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusion-evoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-1beta in LPS-injected rat brains. However, simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-kappaB, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of IkappaB. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.
Animals ; Brain ; Corpus Callosum ; Inflammation ; Lipopolysaccharides ; Macrophages ; Meningitis, Bacterial ; Microglia ; Microinjections ; Monocytes ; NF-kappa B ; Oxidoreductases ; Rats ; Simvastatin* ; Stroke ; Vascular Diseases