55 research outputs found

    TWEAK/Fn14 Activation Participates in Skin Inflammation

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    Joint QoS multicast routing and channel assignment in multiradio multichannel wireless mesh networks using intelligent computational methods

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    Copyright @ 2010 Elsevier B.V. All rights reserved.In this paper, the quality of service multicast routing and channel assignment (QoS-MRCA) problem is investigated. It is proved to be a NP-hard problem. Previous work separates the multicast tree construction from the channel assignment. Therefore they bear severe drawback, that is, channel assignment cannot work well with the determined multicast tree. In this paper, we integrate them together and solve it by intelligent computational methods. First, we develop a unified framework which consists of the problem formulation, the solution representation, the fitness function, and the channel assignment algorithm. Then, we propose three separate algorithms based on three representative intelligent computational methods (i.e., genetic algorithm, simulated annealing, and tabu search). These three algorithms aim to search minimum-interference multicast trees which also satisfy the end-to-end delay constraint and optimize the usage of the scarce radio network resource in wireless mesh networks. To achieve this goal, the optimization techniques based on state of the art genetic algorithm and the techniques to control the annealing process and the tabu search procedure are well developed separately. Simulation results show that the proposed three intelligent computational methods based multicast algorithms all achieve better performance in terms of both the total channel conflict and the tree cost than those comparative references.This work was supported by the Engineering and Physical Sciences Research Council (EPSRC) of UK under Grant EP/E060722/1

    A multipopulation parallel genetic simulated annealing based QoS routing and wavelength assignment integration algorithm for multicast in optical networks

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    Copyright @ 2008 Elsevier B.V. All rights reserved.In this paper, we propose an integrated Quality of Service (QoS) routing algorithm for optical networks. Given a QoS multicast request and the delay interval specified by users, the proposed algorithm can find a flexible-QoS-based cost suboptimal routing tree. The algorithm first constructs the multicast tree based on the multipopulation parallel genetic simulated annealing algorithm, and then assigns wavelengths to the tree based on the wavelength graph. In the algorithm, routing and wavelength assignment are integrated into a single process. For routing, the objective is to find a cost suboptimal multicast tree. For wavelength assignment, the objective is to minimize the delay of the multicast tree, which is achieved by minimizing the number of wavelength conversion. Thus both the cost of multicast tree and the user QoS satisfaction degree can approach the optimal. Our algorithm also considers load balance. Simulation results show that the proposed algorithm is feasible and effective. We also discuss the practical realization mechanisms of the algorithm.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of UK under Grant EP/E060722/1, the National Natural Science Foundation of China under Grant nos. 60673159 and 70671020, the National High-Tech Research and Development Plan of China under Grant no. 2006AA01Z214, Program for New Century Excellent Talents in University, and the Key Project of Chinese Ministry of Education under Grant no. 108040

    Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling

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    Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor–inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis
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