Hybrid-Vehfog: A Robust Approach for Reliable Dissemination of Critical Messages in Connected Vehicles

Vehicular Ad-hoc Networks (VANET) enable efficient communication between vehicles with the aim of improving road safety. However, the growing number of vehicles in dense regions and obstacle shadowing regions like Manhattan and other downtown areas leads to frequent disconnection problems resulting in disrupted radio wave propagation between vehicles. To address this issue and to transmit critical messages between vehicles and drones deployed from service vehicles to overcome road incidents and obstacles, we proposed a hybrid technique based on fog computing called Hybrid-Vehfog to disseminate messages in obstacle shadowing regions, and multi-hop technique to disseminate messages in non-obstacle shadowing regions. Our proposed algorithm dynamically adapts to changes in an environment and benefits in efficiency with robust drone deployment capability as needed. Performance of Hybrid-Vehfog is carried out in Network Simulator (NS-2) and Simulation of Urban Mobility (SUMO) simulators. The results showed that Hybrid-Vehfog outperformed Cloud-assisted Message Downlink Dissemination Scheme (CMDS), Cross-Layer Broadcast Protocol (CLBP), PEer-to-Peer protocol for Allocated REsource (PrEPARE), Fog-Named Data Networking (NDN) with mobility, and flooding schemes at all vehicle densities and simulation times

Armed violence and poverty in Nigeria: a mini case study for the Armed Violence and Poverty Initiative

YesThis mini report on Nigeria is one of 13 case studies (all of the case studies can be found at www/bradford.ac.uk/cics). This research draws upon research studies, reports and evaluations commissioned by operational agencies, and survey data where this has been available. These sources have been complemented by interviews with government officers, aid policymakers and practitioners, and researchers. The analysis and opinions expressed in this report are those of the authors and do not necessarily represent the views or policy of DFID or the UK government

Dissemination of the apicomplexan parasite, Toxoplasma gondii

The parasitic protist Toxoplasma gondii is a common pathogen of rodents and felines that also infects humans. The most severe clinical manifestations of toxoplasmosis in humans derive from the systemic dissemination of T. gondii, during which the parasite penetrates biological barriers and accesses protected host compartments such as the central nervous system. T. gondii dissemination is enabled by the intrinsic gliding motility of extracellular parasites, which allows for travel to new host cells and tissues, and also powers the invasion of diverse host cells including migratory leukocytes. Dissemination is further advanced when migrating infected leukocytes shuttle intracellular parasites to new locations as they traffic throughout the host. All T. gondii gliding motility and host cell invasion was long presumed to be powered by the work of a parasite actin-myosin motor. The possibility of alternative gliding and invasion mechanisms was suggested by the development of inducible Cre-Lox technology that facilitated inducible disruption of genes thought to encode critical components of the T. gondii invasion machinery, including the parasite actin gene ACT1. To determine whether ACT1-independent invasion was likely, inducible Δact1 parasites were examined for uniformity of ACT1 protein depletion. Individual parasites with residual ACT1 protein persisted long after inducible ACT1 excision. Suggesting the residual ACT1 content of these parasites was functionally relevant, the invasion of Δact1 parasites was highly sensitive to an actin polymerization inhibitor. Parasite invasive ability was also found to negatively correlate with the length of time parasites were subjected to ACT1 depletion. Although the existence of ACT1-independent invasion mechanisms cannot be formally excluded, they do not appear to comprise robust alternatives to actin-dependent gliding and invasion in T. gondii. As the most abundantly infected circulating leukocyte during murine toxoplasmosis, monocytes have been theorized to be poised to deliver intracellular T. gondii across the blood-brain barrier and into the central nervous system. However, in vivo evidence supporting this theory was scarce. In vitro models had demonstrated that infection could alter the motility of monocytes when interacting with endothelial vasculature. However, whether infected monocytes could efficiently traverse the specialized endothelium that comprises the blood-brain barrier had not been tested, nor had the ability of infected monocytes to migrate through the tissue environments where T. gondii is first encountered. Models of peripheral and blood-brain barrier endothelium were used to show that infection markedly inhibited monocyte transendothelial migration. In contrast, infected monocytes and macrophages migrated through three-dimensional matrices in vitro and collagen-rich tissues in vivo with enhanced efficiency. Enhanced tissue migration relied on host Rho/ROCK and formin signaling, and the secreted T. gondii kinase ROP17. In a murine model, infection with Δrop17 parasites that fail to enhance tissue migration resulted in delayed dissemination and prolonged mouse survival. These results implicate monocytes in advancing the tissue spread of T. gondii during in vivo dissemination