Mobility-Aware Privacy-Preserving Mobile Crowdsourcing.

The increasing popularity of smartphones and location-based service (LBS) has brought us a new experience of mobile crowdsourcing marked by the characteristics of network-interconnection and information-sharing. However, these mobile crowdsourcing applications suffer from various inferential attacks based on mobile behavioral factors, such as location semantic, spatiotemporal correlation, etc. Unfortunately, most of the existing techniques protect the participant's location-privacy according to actual trajectories. Once the protection fails, data leakage will directly threaten the participant's location-related private information. It open the issue of participating in mobile crowdsourcing service without actual locations. In this paper, we propose a mobility-aware trajectory-prediction solution, TMarkov, for achieving privacy-preserving mobile crowdsourcing. Specifically, we introduce a time-partitioning concept into the Markov model to overcome its traditional limitations. A new transfer model is constructed to record the mobile user's time-varying behavioral patterns. Then, an unbiased estimation is conducted according to Gibbs Sampling method, because of the data incompleteness. Finally, we have the TMarkov model which characterizes the participant's dynamic mobile behaviors. With TMarkov in place, a mobility-aware spatiotemporal trajectory is predicted for the mobile user to participate in the crowdsourcing application. Extensive experiments with real-world dataset demonstrate that TMarkov well balances the trade-off between privacy preservation and data usability.

AngII-induced glomerular mesangial cell proliferation inhibited by losartan via changes in intracellular calcium ion concentration.

This study investigated the changes in intracellular [Ca(2+)](i) (intracellular calcium ion concentration) and TRPC6 (transient receptor potential channel 6) expression during angiotensin II (AngII)-induced glomerular mesangial cell (GMC) proliferation, as well as the inhibitory effect of losartan. GMC cultures were split into four groups treated for 24 h: Group N (blank control group), Group A (10(-7 )mol/L AngII), Group LT (10(-7 )mol/L AngII and 10(-5 )mol/L losartan), and Group Pred (10(-7 )mol/L AngII and 10(-5 )mol/L prednisone). GMCs proliferation was measured by the MTT and trypan blue assays. The distribution of TRPC6 was monitored by immunofluorescence, the expression of TRPC6 was detected by RT-PCR and Western blotting, and [Ca(2+)](i) was measured by laser scanning confocal microscopy. The results showed that the maximal proliferation of GMCs was induced by treatment with 10(-7 )mol/L AngII for 24 h. In Group A, the distribution of TRPC6 was not uniform in the cell membrane, there was increased accumulation of this protein within the cytoplasm, and the increased expression of TRPC6 and [Ca(2+)](i) was consistent with the proliferation of cells. In Group LT, losartan inhibited the proliferation of GMCs significantly, the levels of TRPC6 and [Ca(2+)](i) were diminished, and the distribution of TRPC6 was improved. Prednisone also significantly inhibited the proliferation of GMCs and had no effects on the expression of TRPC6 and [Ca(2+)](i) in Group Pred. These findings suggested that AngII could enhance the expression of TRPC6, increase [Ca(2+)](i,) and demonstrate a time-dose-response relationship with the proliferation of GMCs, while losartan reversed the effect of AngII on GMC proliferation.