Game theory framework for MAC parameter optimization in energy-delay constrained sensor networks

Optimizing energy consumption and end-to-end (e2e) packet delay in energy-constrained, delay-sensitive wireless sensor networks is a conflicting multiobjective optimization problem. We investigate the problem from a game theory perspective, where the two optimization objectives are considered as game players. The cost model of each player is mapped through a generalized optimization framework onto protocol-specific MAC parameters. From the optimization framework, a game is first defined by the Nash bargaining solution (NBS) to assure energy consumption and e2e delay balancing. Secondy, the Kalai-Smorodinsky bargaining solution (KSBS) is used to find an equal proportion of gain between players. Both methods offer a bargaining solution to the duty-cycle MAC protocol under different axioms. As a result, given the two performance requirements (i.e., the maximum latency tolerated by the application and the initial energy budget of nodes), the proposed framework allows to set tunable system parameters to reach a fair equilibrium point that dually minimizes the system latency and energy consumption. For illustration, this formulation is applied to six state-of-the-art wireless sensor network (WSN) MAC protocols: B-MAC, X-MAC, RI-MAC, SMAC, DMAC, and LMAC. The article shows the effectiveness and scalability of such a framework in optimizing protocol parameters that achieve a fair energy-delay performance trade-off under the application requirements

Fault‐Tolerant Prediction‐Based Scheme for Target Tracking in Wireless Sensor Networks

International audienceFault-tolerance is an important function in target tracking application using wireless sensor networks. We propose in this paper, an efficient fault-tolerant approach for target tracking that prevents the loss of the target. Instead of using a single prediction mechanism, our approach uses a multi-level incremental prediction technique that adjusts the prediction precision of the target movement. The responsible node of target detection uses multiple historical information pieces to calculate multi-level predictions which have different precision levels according to the number of information pieces used. Thanks to our parametric prediction model, our approach increases the prediction success rate and decreases the target loss frequency compared to basic approaches that use simple prediction models

Memo1-mediated tiling of radial glial cells facilitates cerebral cortical development

Polarized, non-overlapping, regularly spaced, tiled organization of radial glial cells (RGCs) serves as a framework to generate and organize cortical neuronal columns, layers, and circuitry. Here, we show that mediator of cell motility 1 (Memo1) is a critical determinant of radial glial tiling during neocortical development. Memo1 deletion or knockdown leads to hyperbranching of RGC basal processes and disrupted RGC tiling, resulting in aberrant radial unit assembly and neuronal layering. Memo1 regulates microtubule (MT) stability necessary for RGC tiling. Memo1 deficiency leads to disrupted MT minus-end CAMSAP2 distribution, initiation of aberrant MT branching, and altered polarized trafficking of key basal domain proteins such as GPR56, and thus aberrant RGC tiling. These findings identify Memo1 as a mediator of RGC scaffold tiling, necessary to generate and organize neurons into functional ensembles in the developing cerebral cortex

Memo1-mediated tiling of radial glial cells facilitates cerebral cortical development

Polarized, non-overlapping, regularly spaced, tiled organization of radial glial cells (RGCs) serves as a framework to generate and organize cortical neuronal columns, layers, and circuitry. Here, we show that mediator of cell motility 1 (Memo1) is a critical determinant of radial glial tiling during neocortical development. Memo1 deletion or knockdown leads to hyperbranching of RGC basal processes and disrupted RGC tiling, resulting in aberrant radial unit assembly and neuronal layering. Memo1 regulates microtubule (MT) stability necessary for RGC tiling. Memo1 deficiency leads to disrupted MT minus-end CAMSAP2 distribution, initiation of aberrant MT branching, and altered polarized trafficking of key basal domain proteins such as GPR56, and thus aberrant RGC tiling. These findings identify Memo1 as a mediator of RGC scaffold tiling, necessary to generate and organize neurons into functional ensembles in the developing cerebral cortex