Social-Loc: Improving indoor localization with social sensing

Location-based services, such as targeted advertisement, geo-social networking and emergency services, are becoming in-creasingly popular for mobile applications. While GPS pro-vides accurate outdoor locations, accurate indoor localiza-tion schemes still require either additional infrastructure support (e.g., ranging devices) or extensive training before system deployment (e.g., WiFi signal fingerprinting). In or-der to help existing localization systems to overcome their limitations or to further improve their accuracy, we propose Social-Loc, a middleware that takes the potential locations for individual users, which is estimated by any underlying indoor localization system as input and exploits both so-cial encounter and non-encounter events to cooperatively calibrate the estimation errors. We have fully implemented Social-Loc on the Android platform and demonstrated its performance on two underlying indoor localization systems: Dead-reckoning and WiFi fingerprint. Experiment results show that Social-Loc improves user’s localization accuracy of WiFi fingerprint and dead-reckoning by at least 22 % and 37%, respectively. Large-scale simulation results indicate Social-Loc is scalable, provides good accuracy for a long du-ration of time, and is robust against measurement errors

HMF: Heatmap and WiFi Fingerprint-based Indoor Localization with Building Layout Consideration

International audienc

A Comparative Study of Location-sharing Privacy Preferences in the U.S. and China (CMU-CyLab-12-003)

While prior studies have provided us with an initial understanding of people's location-sharing privacy preferences, they have been limited to Western countries and have not investigated the impact of the granularity of location disclosures on people’s privacy preferences. We report findings of a three-week comparative study collecting location traces and location-sharing preferences from two comparable groups in the U.S. and China. Results of the study shed further light on the complexity of people’s location-sharing privacy preferences and key attributes influencing willingness to disclose locations to others and to advertisers. While our findings reveal many similarities between U.S. and Chinese participants, they also show interesting differences, such as differences in willingness to share location at 'home' and at 'work' and differences in the granularity of disclosures people feel comfortable with. We conclude with a discussion of implications for the design of location-sharing applications and location-based advertising.</p

AT1R/GSK-3β/mTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo

Objective. The focus of the present study is to evaluate the effects of Angiotensin II (Ang II) on neuronal apoptosis after HIE and the potential underlying mechanisms. Methods. Primary neonatal rat cortical neurons were used to study the oxygen-glucose deprivation (OGD) cell model. The expressions of Ang II, AT1R, GSK-3β, p-GSK-3β, mTOR, p-mTOR, Bax, Bcl-2, and cleaved caspase-3 were detected via western blot. IF and flow cytometry were used to evaluate neuronal apoptosis. Hypoxic-ischemic encephalopathy (HIE) was established to evaluate the therapeutic effects of Ang II in vivo. Cerebral infarction areas were detected by 2,3,5-Triphenyltetrazolium chloride staining. The righting and geotaxis reflexes were also recorded. In addition, Fluoro-Jade C staining and TUNEL staining were performed to evaluate neuronal degeneration and apoptosis. Results. Ang II significantly increased the rate of neuronal apoptosis, upregulated the expression of cleaved caspase-3, and downregulated Bcl-2/Bax ratio after OGD insult. For vivo assay, the expressions of endogenous Ang II and AT1R gradually increased and peaked at 24 h after HIE. Ang II increased NeuN-positive AT1R cell expression. In addition, Ang II increased the area of cerebral infarction, promoted neuronal degeneration and apoptosis, aggravated neurological deficits on righting and geotaxis reflexes, and was accompanied by increased expressions of phosphorylated GSK-3β and mTOR. The application of valsartan (Ang II inhibitor) or SB216763 (GSK-3β inhibitor) reversed these phenomena triggered by Ang II following HIE. Conclusion. Ang II increased neuronal apoptosis through the AT1R/GSK-3β/mTOR signaling pathway after experimental HIE both in vitro and in vivo, and Ang II may serve as a novel therapeutic target to ameliorate brain injury after HIE