11 research outputs found

    Topological Characterization of Hamming and Dragonfly Networks and its Implications on Routing

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    Current HPC and datacenter networks rely on large-radix routers. Hamming graphs (Cartesian products of complete graphs) and dragonflies (two-level direct networks with nodes organized in groups) are some direct topologies proposed for such networks. The original definition of the dragonfly topology is very loose, with several degrees of freedom such as the inter- and intra-group topology, the specific global connectivity and the number of parallel links between groups (or trunking level). This work provides a comprehensive analysis of the topological properties of the dragonfly network, providing balancing conditions for network dimensioning, as well as introducing and classifying several alternatives for the global connectivity and trunking level. From a topological study of the network, it is noted that a Hamming graph can be seen as a canonical dragonfly topology with a large level of trunking. Based on this observation and by carefully selecting the global connectivity, the Dimension Order Routing (DOR) mechanism safely used in Hamming graphs is adapted to dragonfly networks with trunking. The resulting routing algorithms approximate the performance of minimal, non-minimal and adaptive routings typically used in dragonflies, but without requiring virtual channels to avoid packet deadlock, thus allowing for lower-cost router implementations. This is obtained by selecting properly the link to route between groups, based on a graph coloring of the network routers. Evaluations show that the proposed mechanisms are competitive to traditional solutions when using the same number of virtual channels, and enable for simpler implementations with lower cost. Finally, multilevel dragonflies are discussed, considering how the proposed mechanisms could be adapted to them

    The C-terminal region of Trypanosoma cruzi MASPs is antigenic and secreted via exovesicles.

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    Trypanosoma cruzi is the etiological agent of Chagas disease, a neglected and emerging tropical disease, endemic to South America and present in non-endemic regions due to human migration. The MASP multigene family is specific to T. cruzi, accounting for 6% of the parasite's genome and plays a key role in immune evasion. A common feature of MASPs is the presence of two conserved regions: an N-terminal region codifying for signal peptide and a C-terminal (C-term) region, which potentially acts as GPI-addition signal peptide. Our aim was the analysis of the presence of an immune response against the MASP C-term region. We found that this region is highly conserved, released via exovesicles (EVs) and has an associated immune response as revealed by epitope affinity mapping, IFA and inhibition of the complement lysis assays. We also demonstrate the presence of a fast IgM response in Balb/c mice infected with T. cruzi. Our results reveal the presence of non-canonical secreted peptides in EVs, which can subsequently be exposed to the immune system with a potential role in evading immune system targets in the parasite

    Algebraic and Computer-based Methods in the Undirected Degree/diameter Problem - a Brief Survey

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    This paper discusses the most popular algebraic techniques and computational methods that have been used to construct large graphs with given degree and diameter

    Processing of Leishmania dononvani by human dendritic cells

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    Leishmania parasites are intracellular protiststhat cause various human diseases ranging from self-healing cutaneous to fatal visceral leishmaniasis. The host cells are phagocytes, primarily neutrophils and macrophages, where the parasites neutralize innate immune defenses, proliferate and finally infect other cells. Despite that Leishmania induce vigorous T cell responses, which require antigen presentation and stimulation by phagocytes, importantly dendritic cells. So far it is not clear how to align the blockade of phagocyte functions with the efficient immune stimulation. We found that, in contrast to other phagocytes, human dendritic cells digest the parasites through an apoptotic process, granzyme B and maybe granulysin manage this killing, and digestion of parasites is delayed in granzyme B inhibited cells. The digested parasites co-localise with components of the MHC class I and II antigen processing pathways. Furthermore, the infection leads to enhanced activation of dendritic cells triggered by inflammatory cytokines. The data presented herein emphasize the need to address the DCs when developing anti-Leishmania vaccines or immunotherapies in order to induce efficient CD4+ helper and CD8 effector T cell responses. They may explain why leishmanization, i.e. immunization with life parasites, is efficient whereas subunit vaccines are not. However, leishmanization induces immunity through deliberate infection with subsequent disease, which may come with severe adverse effects. Alternative strategies may consider TLR agonists or inflammatory cytokines for in situ vaccination and immunotherapy to activate parasite-bearing DCs and thereby induce parasitocidal CD8 effector T cell and innate immune reaction

    Proceedings of the 3rd International Workshop on Optimal Networks Topologies IWONT 2010

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    Peer Reviewe

    Functional Investigation of Trypanosoma brucei Microtubule Associated Proteins and Their Role in Cellular Morphogenesis.

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    The Trypanosoma brucei cytoskeleton is generated by an elaborate array of subpellicular microtubules. This corset of microtubules requires extensive remodelling during cell growth and division. Microtubule nucleation/outgrowth and coordinated severing/re-establishment of inter-microtubule cross-links is orchestrated by microtubule associated proteins (MAPs). The T. brucei genome encodes a discrete set of trypanosomatid specific MAPs but functional data for most of these proteins is sparse. Through bioinformatic analysis we have identified a novel trypanosomatid-specific protein (GB4L). GB4L has a functional role in trypanosome morphogenesis and microtubule organisation in the procyclic and bloodstream form of the parasite. RNAi ablation of GB4L causes a cytokinetic defect, as does depletion of TCP86 (another novel and trypanosomatid-specific MAP recently identified in the McKean laboratory). Electron microscopy was used to examine both the GB4L and TCP86 RNAi cell lines, demonstrating that the phenotypes observed after GB4L and TCP86 protein depletion are very distinct. However, in both cases protein depletion causes morphological abnormalities at the posterior end of cells. ganisation of subpellicular microtubules was interrogated through localisation of canonical plus tip binding proteins (+TIPs) EB1 and XMAP215. Microtubule plus ends are organised in a highly reproducible pattern throughout the cell cycle. This organisation becomes disrupted when GB4L or TCP86 are depleted, showing that GB4L and TCP86 play critical yet distinct roles in orchestrating cytoskeletal remodelling. RNAi ablation of GB4L and TCP86 also has effects on other MAPs due the concerted roles these proteins play in cytoskeletal remodelling. Investigation into MAP interdependency relationships suggests that MAPs assemble as distinct complexes in a defined temporal order on subpellicular microtubules. This work provides further insight into the complexities of trypanosome morphogenesis and indicates that disruption of critical MAP interactions could conceivably provide valid targets for the development of novel chemotherapeutic strategies against human and animal trypanosomiasis

    Subject Index Volumes 1–200

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