3,482 research outputs found

    Evaluating topology quality through random walks

    Get PDF
    A distributed system or network can be modeled as a graph representing the "who knows who" relationship. The conductance of a graph expresses the quality of the connectivity. In a network composed of large dense clusters, connected through only a few links, the risk of partitioning is high; this is typically reflected by a low conductance of the graph. Computing the conductance of a graph is a complex and cumbersome task. Basically, it requires the full knowledge of the graph and is prohibitively expensive computation-wise. Beyond the information carried by the conductance of a graph, what really matters is to identify critical nodes from the topology point of view. In this paper we propose a fully decentralized algorithm to provide each node with a value reflecting its connectivity quality. Comparing these values between nodes, enables to have a local approximation of a global characteristic of the graph. Our algorithm relies on an anonymous probe visiting the network in a unbiased random fashion. Each node records the time elapsed between visits of the probe (called return time in the sequel). Computing the standard deviation of such return times enables to give an information to all system nodes, information that may be used by those nodes to assess their relative position, and therefore the fact that they are critical, in a graph exhibiting low conductance. Based on this information, graph improvement algorithms may be triggered. Moments of order 1 and 2 of the return times are evaluated analytically using a Markov chain model, showing that standard deviation of return time is related to the position of nodes in the graph. We evaluated our algorithm through simulations. Results show that our algorithm is able give informations that are correlated to the conductance of the graph. For example we were able to precisely detect bridges in a network composed of two dense clusters connected through a single link

    Abnormal proactive and reactive cognitive control during conflict processing in major depression

    Get PDF
    According to the Dual Mechanisms of Control framework, cognitive control consists of two complementary components: proactive control refers to anticipatory maintenance of goal-relevant information, whereas reactive control acts as a correction mechanism that is activated when a conflict occurs. Possibly, the well-known diminished inhibitory control in response to negative stimuli in Major Depressive Disorder (MDD) patients stems from a breakdown in proactive control, and/or anomalies in reactive cognitive control. In our study, MDD patients specifically showed increased response latencies when actively inhibiting a dominant response to a sad compared with a happy face. This condition was associated with a longer duration of a dominant ERP topography (800-900 ms poststimulus onset) and a stronger activity in the bilateral dorsal anterior cingulate cortex, reflecting abnormal reactive control when inhibiting attention to a negative stimulus. Moreover, MDD patients showed abnormalities in proactive cognitive control when preparing for the upcoming imperative stimulus (abnormal modulation of the contingent negative variation component), accompanied by more activity in brain regions belonging to the default mode network. All together, deficits to inhibit attention to negative information in MDD might originate from an abnormal use of both proactive resources and reactive control processes. This document is copyrighted by the American Psychological Association or one of its allied publishers. This article is intended solely for the personal use of the individual user and is not to be disseminated broadly

    Electrical brain imaging reveals the expression and timing of altered error monitoring functions in major depression

    Get PDF
    Major depressive disorder (MDD) is characterized by disturbances in affect, motivation, and cognitive control processes, including error detection. However, the expression and timing of the impairments during error monitoring remain unclear in MDD. The behavior and event-related brain responses (ERPs) of 20 patients with MDD were compared with those of 20 healthy controls (HCs), while they performed a Go/noGo task. Errors during this task were associated with 2 ERP components, the error-related negativity (ERN/Ne) and the error positivity (Pe). Results show that the ERN/Ne-correct-related negativity (CRN) amplitude difference was significantly larger in MDD patients (after controlling for speed), compared with HCs, although MDD patients exhibited overactive medial frontal cortex (MFC) activation. By comparison, the subsequent Pe component was smaller in MDD patients compared with HCs and this effect was accompanied by a reduced activation of ventral anterior cingulate cortex (ACC) regions. These results suggest that MDD has multiple cascade effects on early error monitoring brain mechanisms

    Valeur des collégiens et réussite scolaire filles et garçons au collÚge : des univers parallÚles ? : étude sur la problématique des genres et la réussite scolaire en milieu collégial /

    Get PDF
    "Recherche subventionnĂ©e par le ministĂšre de l'Éducation, du Loisir et du Sport dans le cadre du Programme d'aide Ă  la recherche sur l'enseignement et l'apprentissage (PAREA)"Titre de l'Ă©cran-titre (visionnĂ© le 20 sept. 2010)Également disponible en version papier.Bibliogr

    Reversible inactivation of the transcriptional function of P53 protein by farnesylation

    Get PDF
    BACKGROUND: The use of integrating viral vectors in Gene therapy clinical trials has pointed out the problem of the deleterous effect of the integration of the ectopic gene to the cellular genome and the safety of this strategy. We proposed here a way to induce the death of gene modified cells upon request by acting on a pro-apoptotic protein cellular localization and on the activation of its apoptotic function. RESULTS: We constructed an adenoviral vector coding a chimeric p53 protein by fusing p53 sequence with the 21 COOH term amino acids sequence of H-Ras. Indeed, the translation products of Ras genes are cytosolic proteins that become secondarily associated with membranes through a series of post-translational modifications initiated by a CAAX motif present at the C terminus of Ras proteins. The chimeric p53HRCaax protein was farnesylated efficiently in transduced human osteosarcoma p53-/- cell line. The farnesylated form of p53 resided mainly in the cytosol, where it is non-functional. Farnesyl transferase inhibitors (FTIs) specifically inhibited farnesyl isoprenoid lipid modification of proteins. Following treatment of the cells with an FTI, p53HRCaax underwent translocation into the nucleus where it retained transcription factor activity. Shifting p53 into the nucleus resulted in the induction of p21(waf1/CIP1 )and Bax transcription, cell growth arrest, caspase activation and apoptosis. CONCLUSION: Artificial protein farnesylation impaired the transcriptional activity of p53. This could be prevented by Farnesyl transferase inhibition. These data highlight the fact that the artificial prenylation of proteins provides a novel system for controlling the function of a transactivating factor

    Repairing Multiple Failures with Coordinated and Adaptive Regenerating Codes

    Get PDF
    Accepted as a Regular Paper (6 pages) at NetCod 2011 : The 2011 International Symposium on Network Coding, Honk-Kong, July 2011. Also available on arXiv: http://arxiv.org/abs/1102.0204Erasure correcting codes are widely used to ensure data persistence in distributed storage systems. This paper addresses the repair of such codes in the presence of simultaneous failures. It is crucial to maintain the required redundancy over time to prevent permanent data losses. We go beyond existing work (i.e., regenerating codes by Dimakis et al.) and propose coordinated regenerating codes allowing devices to coordinate during simultaneous repairs thus reducing the costs further. We provide closed form expressions of the communication costs of our new codes depending on the number of live devices and the number of devices being repaired. We prove that deliberately delaying repairs does not bring additional gains in itself. This means that regenerating codes are optimal as long as each failure can be repaired before a second one occurs. Yet, when multiple failures are detected simultaneously, we prove that our coordinated regenerating codes are optimal and outperform uncoordinated repairs (with respect to communication and storage costs). Finally, we define adaptive regenerating codes that self-adapt to the system state and prove they are optimal.Les codes correcteurs d'effacements sont largement utilisĂ©s pour assurer la persistance des donnĂ©es dans les systĂšmes de stockage distribuĂ©s. Ce rapport s'intĂ©resse Ă  la rĂ©paration de tels codes dans le cas de dĂ©faillances simultanĂ©es. Cette maintenance est cruciale afin de prĂ©venir les pertes de donnĂ©es permanentes. Nous Ă©tendons les travaux existants (codes rĂ©gĂ©nĂ©rants par Dimakis et al.) et proposons des codes rĂ©gĂ©nĂ©rants coordonnĂ©s qui permettent aux Ă©lĂ©ments du systĂšmes de se coordonner durant les rĂ©parations de dĂ©faillances simultanĂ©es afin de rĂ©duire les coĂ»ts de rĂ©paration. Nous fournissons une forme close des coĂ»ts de communications de nos codes en fonction du nombre d'Ă©quipements vivants et du nombre d'Ă©quipements en cours de rĂ©paration. Nous prouvons, par ailleurs, que retarder les rĂ©parations de façon dĂ©libĂ©rĂ©e n'apporte pas de gains additionnels. Cela signifie que les codes rĂ©gĂ©nĂ©rants sont optimaux tant qu'une premiĂšre dĂ©faillance peut ĂȘtre rĂ©parĂ©e avant une seconde. Cependant, quand de multiples dĂ©faillances sont dĂ©tectĂ©s simultanĂ©ment, nous prouvons que nos codes rĂ©gĂ©nĂ©rants coordonnĂ©s sont optimaux et dĂ©passe les rĂ©parations non coordonnĂ©es (vis Ă  vis des coĂ»ts de stockage et de rĂ©paration). Enfin, nous dĂ©finissons des codes rĂ©gĂ©nĂ©rants adaptatifs qui s'auto-adapte Ă  l'Ă©tat du systĂšme et prouvons qu'ils sont optimaux

    The two authentic methionine aminopeptidase genes are differentially expressed in Bacillus subtilis

    Get PDF
    BACKGROUND: Two putative methionine aminopeptidase genes, map (essential) and yflG (non-essential), were identified in the genome sequence of Bacillus subtilis. We investigated whether they can function as methionine aminopeptidases and further explored possible reasons for their essentiality or dispensability in B. subtilis. RESULTS: In silico analysis of MAP evolution uncovered a coordinated pattern of MAP and deformylase that did not correlate with the pattern of 16S RNA evolution. Biochemical assays showed that both MAP (MAP_Bs) and YflG (YflG_Bs) from B. subtilis overproduced in Escherichia coli and obtained as pure proteins exhibited a methionine aminopeptidase activity in vitro. Compared with MAP_Bs, YflG_Bs was approximately two orders of magnitude more efficient when assayed on synthetic peptide substrates. Both map and yflG genes expressed in multi-copy plasmids could complement the function of a defective map gene in the chromosomes of both E. coli and B. subtilis. In contrast, lacZ gene transcriptional fusions showed that the promoter activity of map was 50 to 100-fold higher than that of yflG. Primer extension analysis detected the transcription start site of the yflG promoter. Further work identified that YvoA acted as a possible weak repressor of yflG expression in B. subtilis in vivo. CONCLUSION: Both MAP_Bs and YflG_Bs are functional methionine aminopeptidases in vitro and in vivo. The high expression level of map and low expression level of yflG may account for their essentiality and dispensality in B. subtilis, respectively, when cells are grown under laboratory conditions. Their difference in activity on synthetic substrates suggests that they have different protein targets in vivo
    • 

    corecore