Impact of Small Monetary Incentives on Exercise in University Students.

OBJECTIVES: Research has demonstrated that health outcomes are significantly improved with the application of financial incentives. However, relatively larger incentives are not typically sustainable and removal of incentives tends to result in attrition of behavior. The feasibility of using relatively smaller incentives to improve physical activity is unclear. The aim of the present study is to determine whether small financial incentives (maximum $5.00 per week) can improve exercise-related energy expenditure of inactive individuals. METHODS: Twenty-two university students (20 ±1.6 years old) were randomized into incentive or non-incentive conditions. Exercise-related caloric expenditure was tracked over 10 weeks. RESULTS: The sample size yielded 62% power. The repeated measures ANCOVA, controlling for body mass index, indicated a main effect of condition (F = 5.50, p =.03) with no significant interaction (F = 2.25, p = .06). CONCLUSIONS: This pilot study demonstrates initial feasibility in implementing small financial incentives to promote exercise behavior in previously inactive young adults. Due to the small sample size, results should be interpreted with caution and further research is warranted to improve and maintain exercise behavior in response to relatively smaller incentives.

Deficiency of phospholipase A2 group 7 decreases intestinal polyposis and colon tumorigenesis in Apc(Min/+) mice.

Platelet-activating factor (PAF) is a naturally occurring phospholipid that mediates diverse effects such as physiological and pathological inflammation, immunosuppression, and cancer. Several lines of evidence support both positive and negative roles for PAF in carcinogenesis. PAF stimulates cell growth, oncogenic transformation, and metastasis, but can also limit proliferation and induce apoptosis. The biological context and microenvironment seem to define whether PAF has pro- or anticarcinogenic effects. To investigate the role of exacerbated PAF signaling in colon cancer, we conducted cell-based and in vivo studies using genetically engineered mice lacking expression of phospholipase A2 group 7 (PLA2G7), an enzyme that specifically metabolizes PAF and structurally related glycerophospholipids. Absence of Pla2g7 robustly decreased intestinal polyposis and colon tumor formation in Apc(Min)(/+) mice, suggesting an antitumorigenic role for PAF in settings characterized by aberrant function of the tumor suppressor Adenomatous polyposis coli (Apc). In colonic epithelial cells, exposure to a PAF analog led to dephosphorylation of Akt at serine-473 and induction of apoptosis. The mechanism of this response involved formation of a complex between ß-arrestin 1 and the Akt phosphatase PHLPP2, and activation of the intrinsic pathway of apoptosis. Our results suggest that strategies based on inhibiting PLA2G7 activity or increasing PAF-mediated signaling hold promise for the treatment of intestinal malignancies that harbor mutations in APC.