parkITsmart: minimization of cruising for parking

Finding a parking space in urban areas is a daily challenge for drivers across the world, due to the increasing amount of vehicles and the limited amount of parking spaces. Drivers who are looking for a parking space in peak hours are often forced to drive around city blocks until they spot a free parking space. This process is termed in literature “cruising for parking” and is proven to (a) cost a lot of time and gas for drivers, (b) generate unnecessary traffic load, and (c) affect the environment negatively due to increased vehicle emissions. This work proposes a Parking Monitoring and Management System (PMMS) that collects, processes, and presents data about available parking spaces and their tariffs within a geographical region. The end-user application of the PMMS, parkITsmart, delivers at drivers bird’s-eye view concerning the parking availability. To facilitate this, the PMMS gathers data from drivers’, vehicles, their mobile phones, and Parking Inspectors (PIs). This work shows that in the Internet-of-Things (IoT) environment, “pairing” cars and drivers’ mobile phones, collecting data from their sensors, and from PIs in a parking monitoring and management system, can decrease significantly cruising times for parking and can increase the time demands of the parking controlling process

IL-3 but not monomeric IgE regulates FcεRI levels and cell survival in primary human basophils.

Binding of allergen-specific IgE to its primary receptor FcεRI on basophils and mast cells represents a central event in the development of allergic diseases. The high-affinity interaction between IgE and FcεRI results in permanent sensitization of these allergic effector cells and critically regulates their release of pro-inflammatory mediators upon IgE cross-linking by allergens. In addition, binding of monomeric IgE has been reported to actively regulate FcεRI surface levels and promote survival of mast cells in the absence of allergen through the induction of autocrine cytokine secretion including interleukin-3 (IL-3). As basophils and mast cells share many biological commonalities we sought to assess the role of monomeric IgE binding and IL-3 signaling in FcεRI regulation and cell survival of primary human basophils. FcεRI cell surface levels and survival of isolated blood basophils were assessed upon addition of monomeric IgE or physiologic removal of endogenous cell-bound IgE with a disruptive IgE inhibitor by flow cytometry. We further determined basophil cell numbers in both low and high serum IgE blood donors and mice that are either sufficient or deficient for FcεRI. Ultimately, we investigated the effect of IL-3 on basophil surface FcεRI levels by protein and gene expression analysis. Surface levels of FcεRI were passively stabilized but not actively upregulated in the presence of monomeric IgE. In contrast to previous observations with mast cells, monomeric IgE binding did not enhance basophil survival. Interestingly, we found that IL-3 transcriptionally regulates surface levels of FcεRI in human primary basophils. Our data suggest that IL-3 but not monomeric IgE regulates FcεRI expression and cell survival in primary human basophils. Thus, blocking of IL-3 signaling in allergic effector cells might represent an interesting approach to diminish surface FcεRI levels and to prevent prolonged cell survival in allergic inflammation