Describing The User Experience Of Wearable Fitness Technology Through Online Product Reviews

Regular exercise has many health benefits, however a major problem in the United States is that Americans do not exercise enough to reap these advantages. Although there are many ways that one can be motivated to exercise, the use of wearable technologies such as fitness tracking devices show great promise as an individual, and cost effective solution. On the other hand, many people who try out these devices return them leading to lower than idea acceptance rates for these devices. We examined online product reviews for wearable fitness devices in order to discover which factors led to product acceptance or rejection. We performed a qualitative analysis of user reviews across many websites and devices followed by a quantitative exploratory analysis using stepwise multiple regression predicting users\u27 experience. Overall, our results support that four high-level themes: usability, trust, motivation, and wearability determined a user\u27s experience

Gene Expression Profiling Identifies Important Genes Affected by R2 Compound Disrupting FAK and P53 Complex

Focal Adhesion Kinase (FAK) is a non-receptor kinase that plays an important role in many cellular processes: adhesion, proliferation, invasion, angiogenesis, metastasis and survival. Recently, we have shown that Roslin 2 or R2 (1-benzyl-15,3,5,7-tetraazatricyclo[3.3.1.1~3,7~]decane) compound disrupts FAK and p53 proteins, activates p53 transcriptional activity, and blocks tumor growth. In this report we performed a microarray gene expression analysis of R2-treated HCT116 p53+/+ and p53−/− cells and detected 1484 genes that were significantly up- or down-regulated (p < 0.05) in HCT116 p53+/+ cells but not in p53−/− cells. Among up-regulated genes in HCT p53+/+ cells we detected critical p53 targets: Mdm-2, Noxa-1, and RIP1. Among down-regulated genes, Met, PLK2, KIF14, BIRC2 and other genes were identified. In addition, a combination of R2 compound with M13 compound that disrupts FAK and Mmd-2 complex or R2 and Nutlin-1 that disrupts Mdm-2 and p53 decreased clonogenicity of HCT116 p53+/+ colon cancer cells more significantly than each agent alone in a p53-dependent manner. Thus, the report detects gene expression profile in response to R2 treatment and demonstrates that the combination of drugs targeting FAK, Mdm-2, and p53 can be a novel therapy approach