Self-stabilizing algorithms for Connected Vertex Cover and Clique decomposition problems

In many wireless networks, there is no fixed physical backbone nor centralized network management. The nodes of such a network have to self-organize in order to maintain a virtual backbone used to route messages. Moreover, any node of the network can be a priori at the origin of a malicious attack. Thus, in one hand the backbone must be fault-tolerant and in other hand it can be useful to monitor all network communications to identify an attack as soon as possible. We are interested in the minimum \emph{Connected Vertex Cover} problem, a generalization of the classical minimum Vertex Cover problem, which allows to obtain a connected backbone. Recently, Delbot et al.~\cite{DelbotLP13} proposed a new centralized algorithm with a constant approximation ratio of $2$ for this problem. In this paper, we propose a distributed and self-stabilizing version of their algorithm with the same approximation guarantee. To the best knowledge of the authors, it is the first distributed and fault-tolerant algorithm for this problem. The approach followed to solve the considered problem is based on the construction of a connected minimal clique partition. Therefore, we also design the first distributed self-stabilizing algorithm for this problem, which is of independent interest

Early and reversible changes to the hippocampal proteome in mice on a high-fat diet

Funding LMW, FMC, CG, ACM and C-DM were funded by the Scottish Government’s Rural and Environment Science and Analytical Services Division (RESAS). FHM was supported by an EASTBIO DTP BBSRC studentship. DS was supported by a SULSA studentship.Peer reviewedPublisher PD

0.9 eV POTENTIAL BARRIER SCHOTTKY DIODE ON 0.75-0.5 eV GAP GaxIn1-xAS\a-Si:H\Pt

Les courbes I(V,T) de ces structures pour 1000 Å de a-Si : H et x = 0.2 et 0.47 sont similaires à celles des diodes Pt/a-Si : H et en conséquence contrôlées par l'interface Pt/a-Si : H. Ceci ouvre de nouvelles perspectives pour les MESFET sur GaxIn1-xAs.The I(V,T) curves of such structures for 1000 Å of a-Si : H and x = 0.2 and 0.47 are both similar to those of Pt/a-Si : H diodes, so controlled by the Pt/a-Si : H interface. This opens new perspectives for MESFET on GaxIn1-xAs

Dynamic and Adaptive Replication for Large-Scale Reliable Multi-Agent Systems

Abstract. In order to make large-scale multi-agent systems reliable, we propose an adaptive application of replication strategies. Critical agents are replicated to avoid failures. As criticality of agents may evolve during the course of computation and problem solving, we need to dynamically and automatically adapt the number of replicas of agents, in order to maximize their reliability and availability based on available resources. We are studying an approach and mechanisms for evaluating the criticality of a given agent (based on application-level semantic information, e.g. messages intention, and also system-level statistical information, e.g., communication load) and for deciding what strategy to apply (e.g., active or passive replication) and how to parameterize it (e.g., number of replicas).

Cooperative expression of junctional adhesion molecule-C and -B supports growth and invasion of glioma.

Brain invasion is a biological hallmark of glioma that contributes to its aggressiveness and limits the potential of surgery and irradiation. Deregulated expression of adhesion molecules on glioma cells is thought to contribute to this process. Junctional adhesion molecules (JAMs) include several IgSF members involved in leukocyte trafficking, angiogenesis, and cell polarity. They are expressed mainly by endothelial cells, white blood cells, and platelets. Here, we report JAM-C expression by human gliomas, but not by their normal cellular counterpart. This expression correlates with the expression of genes involved in cytoskeleton remodeling and cell migration. These genes, identified by a transcriptomic approach, include poliovirus receptor and cystein-rich 61, both known to promote glioma invasion, as well as actin filament associated protein, a c-Src binding partner. Gliomas also aberrantly express JAM-B, a high affinity JAM-C ligand. Their interaction activates the c-Src proto-oncogene, a central upstream molecule in the pathways regulating cell migration and invasion. In the tumor microenvironment, this co-expression may thus promote glioma invasion through paracrine stimuli from both tumor cells and endothelial cells. Accordingly, JAM-C/B blocking antibodies impair in vivo glioma growth and invasion, highlighting the potential of JAM-C and JAM-B as new targets for the treatment of human gliomas