Effectiveness of a Workplace Walking Program Using a Fitness Tracker Including Individual Counseling and Tailored Text Messaging

PURPOSE: This study is designed as a non-equivalent, control group pre/post-test for identifying effectiveness of a workplace walking program using a fitness tracker including individual counseling and tailored text messaging. METHODS: Seventy-nine employees from two large companies were allocated into an intervention group (n=39) and a control group (n=40). Participants were asked to wear a fitness tracker (Fitbit Charger HR) during 24-hour, 5-days per week, for 10 weeks. The intervention group was provided with daily walking steps measured by Fitbit, weekly counseling with a specifically designed workbook, and seven weekly text messaging, and the control group with the fitness tracker only. RESULTS: At the week 10 measurement, there were significant differences between the intervention and control groups in physical activity self-efficacy (p<.001), physical activity behavior (p<.001), daily walking steps (p<.001), systolic blood pressure (p=.033), and wellness (p<.001). CONCLUSION: These results suggest that the workplace walking program using a fitness tracker including individual counseling and tailored text messaging is more effective for persons with 10,000 steps/day. Therefore, it is recommended to actively apply this workplace walking program to inactive employees for encouraging regular physical activities and improving their wellness.

Transcriptional induction of DLC-1 gene through Sp1 sites by histone deacetylase inhibitors in gastric cancer cells

We previously reported that trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, induced DLC-1 mRNA expression and accumulated acetylated histones H3 and H4 associated with the DLC-1 promoter in DLC-1 non-expressing gastric cancer cells. In this study, we demonstrated the molecular mechanisms by which TSA induced the DLC-1 gene expression. Treatment of the gastric cancer cells with TSA activates the DLC-1 promoter activity through Sp1 sites located at -219 and -174 relative to the transcription start site. Electrophoretic mobility-shift assay (EMSA) revealed that Sp1 and Sp3 specifically interact with these Sp1 sites and showed that TSA did not change their binding activities. The ectopic expression of Sp1, but not Sp3, enhances the DLC-1 promoter responsiveness by TSA. Furthermore, the TSA-induced DLC-1 promoter activity was increased by p300 expression and reduced by knockdown of p300. These results demonstrated the requirement of specific Sp1 sites and dependence of Sp1 and p300 for TSA-mediated activation of DLC-1 promoter.