Lack of physical activity has been shown to increase disease and reduce life expectancy. In response, mobile devices are increasingly being used to support people's health and fitness by tracking physical activity. Prior work shows that the type of feedback, either ambient or via notification, affects users' behavior towards their physical activity. Yet, these phone- and watch-based interactions and notifications have primarily been visual in nature. Inspired by prior research, we explored the impact of feedback modality (visual, tactile, and hybrid: visual/tactile) on 44 participants' behavior and exercise mindset in a 6-week field study. We present the differences between modalities and the notion of push vs. pull for interface feedback and notifications. Across 1,662 days of study data, we found statistically significant impacts of feedback modality and, in particular, the positive effects of push feedback on participants' mindset about the process of exercise. Our results also highlight design guidelines for wearables and multimodal notification systems.

Chronic constriction injury (CCI) of the rodent sciatic nerve causes light touch mechanical sensitivity (allodynia) and leads to activation of spinal astrocytes and microglia. The endocannabinoid system includes the cannabinoid receptor 1 (CB1R) present on neurons and the cannabinoid receptor 2 (CB2R) present mostly on immune cells. CB2R agonists, like AM1710, believed to exert analgesic effects through CB2R actions, are effective in controlling pathological pain states in animal models. However, activation of CB1R could be partly responsible for the analgesic effects of AM1710 through non-specific binding. We sought to determine whether AM1710 could lead to anti-allodynia and produce changes in spinal pro-and anti-inflammatory protein IR in mice lacking functional CB1R (CB1R-/-). We first characterized the allodynia profile of CB1R+/+, CB1R+/-and CB1R-/-mice. Following CCI, CB1R-/-mice displayed allodynia similar to wild-type and heterozygous littermates, with reliable 27-day chronic allodynia. Following baseline threshold assessment, mice underwent sham or CCI surgery, and thresholds were reassessed 5 and 12 days later. Mice were given an intraperitoneal (i.p.) injection of either AM1710 (25 mg/kg/ml) or equivolume vehicle. Following behavioral reassessment at 25 min after injection, spinal tissues were harvested. AM1710, given i.p. reversed CCI-induced allodynia in CB1R-KO mice to control levels. Next, we sought to determine an effective timecourse for AM1710 (5 mg) delivered intrathecally (i.t.) to reverse allodynia in wild type mice. Allodynia reversal occurred 2 hours after administration. Finally, we sought to determine if spinal CB1R were responsible for intrathecal AM170 effects. We found AM1710 robustly reversed chronic allodynia in CB1R-/-mice. Ongoing studies using spectral analysis of IR will examine glial activation, and pro-and anti-inflammatory cytokine changes in these tissues.