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Smartphone adoption has increased significantly and, with the increase in smartphone capabilities, this means that users can access the Internet, communicate, and entertain themselves anywhere and anytime. However, there is growing evidence of problematic use of smartphones that impacts both social and heath aspects of users' lives. Currently, assessment of overuse or problematic use depends on one-time, self-reported behavioral information about phone use. Due to the known issues with self-reports in such types of assessments, we explore an automated, objective and repeatable approach for assessing problematic usage. We collect a wide range of phone usage data from smartphones, identify a number of usage features that are relevant to this assessment, and build detection models based on Adaboost with machine learning algorithms automatically detecting problematic use. We found that the number of apps used per day, the ratio of SMSs to calls, the number of event-initiated sessions, the number of apps used per event initiated session, and the length of non-eventinitiated sessions are useful for detecting problematic usage. With these, a detection model can identify users with problematic usage with 89.6% accuracy (F-score of .707).

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The United States Food and Drug Administration-approved antipsychotic drug, pimozide, has anticancer activities. However, the role of reactive oxygen species (ROS) in its effect on prostate cancer is not well-known. We examined cell proliferation, colony formation, migration, ROS production, and the expression of antioxidant-related genes after treatment of human prostate cancer PC3 and DU145 cells with pimozide. In addition, histopathology, ROS production, and superoxide dismutase (SOD) activity were analyzed after administering pimozide to TRAMP, a transgenic mouse with prostate cancer. Pimozide increased the generation of ROS in both cell lines and inhibited cell proliferation, migration, and colony formation. Oxidative stress induced by pimozide caused changes in the expression of antioxidant enzymes (SOD1, peroxiredoxin 6, and glutathione peroxidase 2) and CISD2. Co-treatment with glutathione, an antioxidant, reduced pimozide-induced ROS levels, and counteracted the inhibition of cell proliferation. Administration of pimozide to TRAMP mice reduced the progression of prostate cancer with increased ROS generation and decreased SOD activity. These results suggest that the antipsychotic drug, pimozide, has beneficial effects in prostate cancer in vivo and in vitro. The mechanism of pimozide may be related to augmenting ROS generation. We recommend pimozide as a promising anticancer agent.

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