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The combinatorics and topology of proper toric maps  [PDF]
M. A. de Cataldo,L. Migliorini,M. Mustata
Mathematics , 2014,
Abstract: We study the topology of toric maps. We show that if $f\colon X\to Y$ is a proper toric morphism, with $X$ simplicial, then the cohomology of every fiber of $f$ is pure and of Hodge-Tate type. When the map is a fibration, we give an explicit formula for the Betti numbers of the fibers in terms of a relative version of the $f$-vector, extending the usual formula for the Betti numbers of a simplicial complete toric variety. We then describe the Decomposition Theorem for a toric fibration, giving in particular a nonnegative combinatorial invariant attached to each cone in the fan of $Y$, which is positive precisely when the corresponding closed subset of $Y$ appears as a support in the Decomposition Theorem. The description of this invariant involves the stalks of the intersection cohomology complexes on $X$ and $Y$, but in the case when both $X$ and $Y$ are simplicial, there is a simple formula in terms of the relative $f$-vector.
Fuzzy algorithm to Mitigate Risk in the Assignment of Roles in a Wireless Network
A. K. Santra,Nagarajan S
International Journal of Computer Science Issues , 2012,
Abstract: This paper is presenting a method of defining a fuzzy membership function which helps in role assignment for wireless network. There is a risk involved in assigning roles dynamically as there can be a false negative or in other words an intruder is permitted into the system. The present proposal addresses this issue to mitigate the risk involved and overcome the false negative and false positive issues involved in assigning the roles.
Channel Assignment with Topology Preservation for Multi-radio Wireless Mesh Networks  [cached]
Hongju Cheng,Naixue Xiong,Guolong Chen,Xiaofang Zhuang
Journal of Communications , 2010, DOI: 10.4304/jcm.5.1.63-70
Abstract: Channel assignment is one of the most important issues in the multi-radio multi-channel wireless mesh networks. An improper channel assignment may lead to network partition or link failure. In this paper we focus on the channel assignment problem with the original topology preservation for the multi-radio mesh networks, and aim at minimizing the overall network interference. We have formulated an Integer Line Programming (ILP) which can be used to find the optimized solution for the channel assignment problem in small-size network. In this paper we also have developed a distributed algorithm for the channel assignment due to the NP-hardness of the ILP. Extensive simulation results have demonstrated that our algorithms have good performance in both dense and sparse networks compared with related works. The theoretic and experiment results have shown that the proposed algorithms serve as a practical solution to the channel assignment problem in the multi-channel multi-radio wireless mesh networks.
Cytokines and Their Roles in the Pathogenesis of Systemic Lupus Erythematosus: From Basics to Recent Advances
Desmond Yat Hin Yap,Kar Neng Lai
Journal of Biomedicine and Biotechnology , 2010, DOI: 10.1155/2010/365083
Abstract: Systemic lupus erythematosus (SLE) is a complex auto-immune disorder which involves various facets of the immune system. In addition to autoantibody production and immune complex deposition, emerging evidences suggest that cytokines may act as key players in the immunopathogenesis of SLE. These cytokines assume a critical role in the differentiation, maturation and activation of cells and also participate in the local inflammatory processes that mediate tissue insults in SLE. Certain cytokines such as the IL-6, IL-10, IL-17, BLys, type I interferons (IFN) and tumor necrosis factor- (TNF-) are closely linked to pathogenesis of SLE. The delineation of the role played by these cytokines not only fosters our understanding of this disease but also provides a sound rationale for various therapeutic approaches. In this context, this review focuses on selected cytokines which exert significant effect in the pathogenesis of SLE and their possible clinical applications.
Comprehensive Assignment of Roles for Salmonella Typhimurium Genes in Intestinal Colonization of Food-Producing Animals  [PDF]
Roy R. Chaudhuri equal contributor,Eirwen Morgan equal contributor,Sarah E. Peters,Stephen J. Pleasance,Debra L. Hudson,Holly M. Davies,Jinhong Wang,Pauline M. van Diemen,Anthony M. Buckley,Alison J. Bowen,Gillian D. Pullinger,Daniel J. Turner,Gemma C. Langridge,A. Keith Turner,Julian Parkhill,Ian G. Charles ?,Duncan J. Maskell ? ,Mark P. Stevens ?
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1003456
Abstract: Chickens, pigs, and cattle are key reservoirs of Salmonella enterica, a foodborne pathogen of worldwide importance. Though a decade has elapsed since publication of the first Salmonella genome, thousands of genes remain of hypothetical or unknown function, and the basis of colonization of reservoir hosts is ill-defined. Moreover, previous surveys of the role of Salmonella genes in vivo have focused on systemic virulence in murine typhoid models, and the genetic basis of intestinal persistence and thus zoonotic transmission have received little study. We therefore screened pools of random insertion mutants of S. enterica serovar Typhimurium in chickens, pigs, and cattle by transposon-directed insertion-site sequencing (TraDIS). The identity and relative fitness in each host of 7,702 mutants was simultaneously assigned by massively parallel sequencing of transposon-flanking regions. Phenotypes were assigned to 2,715 different genes, providing a phenotype–genotype map of unprecedented resolution. The data are self-consistent in that multiple independent mutations in a given gene or pathway were observed to exert a similar fitness cost. Phenotypes were further validated by screening defined null mutants in chickens. Our data indicate that a core set of genes is required for infection of all three host species, and smaller sets of genes may mediate persistence in specific hosts. By assigning roles to thousands of Salmonella genes in key reservoir hosts, our data facilitate systems approaches to understand pathogenesis and the rational design of novel cross-protective vaccines and inhibitors. Moreover, by simultaneously assigning the genotype and phenotype of over 90% of mutants screened in complex pools, our data establish TraDIS as a powerful tool to apply rich functional annotation to microbial genomes with minimal animal use.
Channel Assignment Strategy for Wireless Mesh Network Based on Topology-division
基于拓扑分割的无线Mesh网络信道分配策略

Yan Jun-rong,Zhang Shun-yi,Long Hua,Sun Yan-fei,
严军荣
,张顺颐,龙华,孙雁飞

电子与信息学报 , 2009,
Abstract: According to the characteristics of tree-topology aggregating traffic of wireless mesh network, this paper proposes a channel assignment strategy based on topology-division. Considering the effect of interference on different links, wireless interference is classified into vertical and horizontal interferences with determinate directions. An algorithm is proposed to divide the network topology into hop-by-hop subtopologies along the vertical interference. A channel assignment strategy for subtopologies is proposed including minimum channels to avoid vertical interference and additional channels to enhance the minimum throughput subtopology. A method is proposed based on channels to partition horizontal interference with channels within a subtopology. The collision domains within a subtopology and network performance bottleneck are analyzed, and the throughput and the order of channels assignment are simulated. The simulation results show that the proposed channel assignment strategy could effectively assure and enhance network throughout, and the method of horizontal interference partitioning outperforms the common channel framework multichannel mechanism defined in 802.11s.
Immunopathological Roles of Cytokines, Chemokines, Signaling Molecules, and Pattern-Recognition Receptors in Systemic Lupus Erythematosus
Shui-Lian Yu,Woon-Pang Kuan,Chun-Kwok Wong,Edmund K. Li,Lai-Shan Tam
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/715190
Abstract: Systemic lupus erythematosus (SLE) is an autoimmune disease with unknown etiology affecting more than one million individuals each year. It is characterized by B- and T-cell hyperactivity and by defects in the clearance of apoptotic cells and immune complexes. Understanding the complex process involved and the interaction between various cytokines, chemokines, signaling molecules, and pattern-recognition receptors (PRRs) in the immune pathways will provide valuable information on the development of novel therapeutic targets for treating SLE. In this paper, we review the immunopathological roles of novel cytokines, chemokines, signaling molecules, PRRs, and their interactions in immunoregulatory networks and suggest how their disturbances may implicate pathological conditions in SLE.
Topology and Phase Transitions: towards a proper mathematical definition of finite N transitions  [PDF]
Marco Pettini,Roberto Franzosi,Lionel Spinelli
Physics , 2001,
Abstract: A new point of view about the deep origin of thermodynamic phase transitions is sketched. The main idea is to link the appearance of phase transitions to some major topology change of suitable submanifolds of phase space instead of linking them to non-analyticity, as is usual in the Yang-Lee and in the Dobrushin-Ruelle-Sinai theories. In the new framework a new possibility appears to properly define a mathematical counterpart of phase transitions also at finite number of degrees of freedom. This is of prospective interest to the study of those systems that challenge the conventional approaches, as is the case of phase transitions in nuclear clusters.
How big is too big? Critical Shocks for Systemic Failure Cascades  [PDF]
Claudio J. Tessone,Antonios Garas,Beniamino Guerra,Frank Schweitzer
Quantitative Finance , 2012, DOI: 10.1007/s10955-013-0723-y
Abstract: External or internal shocks may lead to the collapse of a system consisting of many agents. If the shock hits only one agent initially and causes it to fail, this can induce a cascade of failures among neighoring agents. Several critical constellations determine whether this cascade remains finite or reaches the size of the system, i.e. leads to systemic risk. We investigate the critical parameters for such cascades in a simple model, where agents are characterized by an individual threshold \theta_i determining their capacity to handle a load \alpha\theta_i with 1-\alpha being their safety margin. If agents fail, they redistribute their load equally to K neighboring agents in a regular network. For three different threshold distributions P(\theta), we derive analytical results for the size of the cascade, X(t), which is regarded as a measure of systemic risk, and the time when it stops. We focus on two different regimes, (i) EEE, an external extreme event where the size of the shock is of the order of the total capacity of the network, and (ii) RIE, a random internal event where the size of the shock is of the order of the capacity of an agent. We find that even for large extreme events that exceed the capacity of the network finite cascades are still possible, if a power-law threshold distribution is assumed. On the other hand, even small random fluctuations may lead to full cascades if critical conditions are met. Most importantly, we demonstrate that the size of the "big" shock is not the problem, as the systemic risk only varies slightly for changes of 10 to 50 percent of the external shock. Systemic risk depends much more on ingredients such as the network topology, the safety margin and the threshold distribution, which gives hints on how to reduce systemic risk.
Urokinase-type plasminogen activator and arthritis progression: contrasting roles in systemic and monoarticular arthritis models
Christine M De Nardo, Jason C Lenzo, Jarrad Pobjoy, John A Hamilton, Andrew D Cook
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar3171
Abstract: To determine how the different pathogenic mechanisms leading to arthritis development in the different models may explain the contrasting requirement for u-PA, the systemic, polyarticular, immune complex-driven K/BxN arthritis model was modified to include an i.a. injection of saline as a local trauma in u-PA-/- mice. This modified model and the antigen-induced arthritis (AIA) model were also used in u-PA-/- mice to determine the requirement for u-PA in joint destruction. Disease severity was determined by clinical and histologic scoring. Fibrin(ogen) staining and the matrix metalloproteinase (MMP)-generated neoepitope DIPEN staining were performed by immunohistochemistry. Gene expression of inflammatory and destructive mediators was measured in joint tissue by quantitative PCR.In our modified arthritis model, u-PA-/- mice went from being resistant to arthritis development following K/BxN serum transfer to being susceptible following the addition of an i.a. injection of saline. u-PA-/- mice also developed more sustained AIA compared with C57BL/6 mice, including reduced proteoglycan levels and increased bone erosions, fibrin(ogen) deposition and DIPEN expression. Synovial gene expression of the proinflammatory mediators (TNF and IL-1β), aggrecanases (ADAMTS-4 and -5) and MMPs (MMP3 and MMP13) were all sustained over time following AIA induction in u-PA-/- mice compared with C57BL/6 mice.We propose that u-PA has a protective role in arthritis models with 'wound healing-like' processes following local trauma, possibly through u-PA/plasmin-mediated fibrinolysis, but a deleterious role in systemic models that are critically dependent on immune complex formation and complement activation. Given that cartilage proteoglycan loss and bone erosions were present and sustained in u-PA-/- mice with monoarticular arthritis, it is unlikely that u-PA/plasmin-mediated proteolysis is contributing directly to this tissue destruction/remodeling.Urokinase-type plasminogen activator (u-P
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