2,105 research outputs found

    Multiple scaling regimes in simple aging models

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    We investigate aging in glassy systems based on a simple model, where a point in configuration space performs thermally activated jumps between the minima of a random energy landscape. The model allows us to show explicitly a subaging behavior and multiple scaling regimes for the correlation function. Both the exponents characterizing the scaling of the different relaxation times with the waiting time and those characterizing the asymptotic decay of the scaling functions are obtained analytically by invoking a `partial equilibrium' concept.Comment: 4 pages, 3 figure

    Fluctuation-dissipation relations in trap models

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    Trap models are intuitively appealing and often solvable models of glassy dynamics. In particular, they have been used to study aging and the resulting out-of-equilibrium fluctuation-dissipation relations between correlations and response functions. In this note I show briefly that one such relation, first given by Bouchaud and Dean, is valid for a general class of mean-field trap models: it relies only on the way a perturbation affects the transition rates, but is independent of the distribution of trap depths and the form of the unperturbed transition rates, and holds for all observables that are uncorrelated with the energy. The model with Glauber dynamics and an exponential distribution of trap depths, as considered by Barrat and Mezard, does not fall into this class if the perturbation is introduced in the standard way by shifting all trap energies. I show that a similar relation between response and correlation nevertheless holds for the out-of-equilibrium dynamics at low temperatures. The results point to intriguing parallels between trap models with energetic and entropic barriers.Comment: Extended introduction and discussion of relation to results of cond-mat/0303445. 13 pages, 2 figures, IOP styl

    Aging in the random energy model

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    In this letter we announce rigorous results on the phenomenon of aging in the Glauber dynamics of the random energy model and their relation to Bouchaud's 'REM-like' trap model. We show that, below the critical temperature, if we consider a time-scale that diverges with the system size in such a way that equilibrium is almost, but not quite reached on that scale, a suitably defined autocorrelation function has the same asymptotic behaviour than its analog in the trap model.Comment: 4pp, P

    Genomics in 2011: challenges and opportunities

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    As we come to the end of 2011, Genome Biology has asked some members of our Editorial Board for their views on the state of play in genomics. What was their favorite paper of 2011? What are the challenges in their particular research area? Who has had the biggest influence on their careers? What advice would they give to young researchers embarking on a career in research

    Anomalous diffusion, Localization, Aging and Sub-aging effects in trap models at very low temperature

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    We study in details the dynamics of the one dimensional symmetric trap model, via a real-space renormalization procedure which becomes exact in the limit of zero temperature. In this limit, the diffusion front in each sample consists in two delta peaks, which are completely out of equilibrium with each other. The statistics of the positions and weights of these delta peaks over the samples allows to obtain explicit results for all observables in the limit T0T \to 0. We first compute disorder averages of one-time observables, such as the diffusion front, the thermal width, the localization parameters, the two-particle correlation function, and the generating function of thermal cumulants of the position. We then study aging and sub-aging effects : our approach reproduces very simply the two different aging exponents and yields explicit forms for scaling functions of the various two-time correlations. We also extend the RSRG method to include systematic corrections to the previous zero temperature procedure via a series expansion in TT. We then consider the generalized trap model with parameter α[0,1]\alpha \in [0,1] and obtain that the large scale effective model at low temperature does not depend on α\alpha in any dimension, so that the only observables sensitive to α\alpha are those that measure the `local persistence', such as the probability to remain exactly in the same trap during a time interval. Finally, we extend our approach at a scaling level for the trap model in d=2d=2 and obtain the two relevant time scales for aging properties.Comment: 33 pages, 3 eps figure

    1D Aging

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    We derive exact expressions for a number of aging functions that are scaling limits of non-equilibrium correlations, R(tw,tw+t) as tw --> infinity with t/tw --> theta, in the 1D homogenous q-state Potts model for all q with T=0 dynamics following a quench from infinite temperature. One such quantity is (the two-point, two-time correlation function) when n/sqrt(tw) --> z. Exact, closed-form expressions are also obtained when one or more interludes of infinite temperature dynamics occur. Our derivations express the scaling limit via coalescing Brownian paths and a ``Brownian space-time spanning tree,'' which also yields other aging functions, such as the persistence probability of no spin flip at 0 between tw and tw+t.Comment: 4 pages (RevTeX); 2 figures; submitted to Physical Review Letter

    Genome-Wide Analysis of KAP1 Binding Suggests Autoregulation of KRAB-ZNFs

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    We performed a genome-scale chromatin immunoprecipitation (ChIP)-chip comparison of two modifications (trimethylation of lysine 9 [H3me3K9] and trimethylation of lysine 27 [H3me3K27]) of histone H3 in Ntera2 testicular carcinoma cells and in three different anatomical sources of primary human fibroblasts. We found that in each of the cell types the two modifications were differentially enriched at the promoters of the two largest classes of transcription factors. Specifically, zinc finger (ZNF) genes were bound by H3me3K9 and homeobox genes were bound by H3me3K27. We have previously shown that the Polycomb repressive complex 2 is responsible for mediating trimethylation of lysine 27 of histone H3 in human cancer cells. In contrast, there is little overlap between H3me3K9 targets and components of the Polycomb repressive complex 2, suggesting that a different histone methyltransferase is responsible for the H3me3K9 modification. Previous studies have shown that SETDB1 can trimethylate H3 on lysine 9, using in vitro or artificial tethering assays. SETDB1 is thought to be recruited to chromatin by complexes containing the KAP1 corepressor. To determine if a KAP1-containing complex mediates trimethylation of the identified H3me3K9 targets, we performed ChIP-chip assays and identified KAP1 target genes using human 5-kb promoter arrays. We found that a large number of genes of ZNF transcription factors were bound by both KAP1 and H3me3K9 in normal and cancer cells. To expand our studies of KAP1, we next performed a complete genomic analysis of KAP1 binding using a 38-array tiling set, identifying ~7,000 KAP1 binding sites. The identified KAP1 targets were highly enriched for C2H2 ZNFs, especially those containing Krüppel-associated box (KRAB) domains. Interestingly, although most KAP1 binding sites were within core promoter regions, the binding sites near ZNF genes were greatly enriched within transcribed regions of the target genes. Because KAP1 is recruited to the DNA via interaction with KRAB-ZNF proteins, we suggest that expression of KRAB-ZNF genes may be controlled via an auto-regulatory mechanism involving KAP1

    Aging, rejuvenation and memory phenomena in spin glasses

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    In this paper, we review several important features of the out-of-equilibrium dynamics of spin glasses. Starting with the simplest experiments, we discuss the scaling laws used to describe the isothermal aging observed in spin glasses after a quench down to the low temperature phase. We report in particular new results on the sub-aging behaviour of spin glasses. We then discuss the rejuvenation and memory effects observed when a spin glass is submitted to temperature variations during aging, from the point of view of both energy landscape pictures and of real space pictures. We highlight the fact that both approaches point out the necessity of hierarchical processes involved in aging. Finally, we report an investigation of the effect of small temperature variations on aging in spin glass samples with various anisotropies which indicates that this hierarchy depends on the spin anisotropy.Comment: submitted for the Proceedings of Stat Phys 22, Bangalore (India

    HOXA3 Modulates Injury-Induced Mobilization and Recruitment of Bone Marrow-Derived Cells

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    The regulated recruitment and differentiation of multipotent bone marrow-derived cells (BMDCs) to sites of injury are critical for efficient wound healing. Previously we demonstrated that sustained expression of HOXA3 both accelerated wound healing and promoted angiogenesis in diabetic mice. In this study, we have used green fluorescent protein-positive bone marrow chimeras to investigate the effect of HOXA3 expression on recruitment of BMDCs to wounds. We hypothesized that the enhanced neovascularization induced by HOXA3 is due to enhanced mobilization, recruitment, and/or differentiation of BMDCs. Here we show that diabetic mice treated with HOXA3 displayed a significant increase in both mobilization and recruitment of endothelial progenitor cells compared with control mice. Importantly, we also found that HOXA3-treated mice had significantly fewer inflammatory cells recruited to the wound compared with control mice. Microarray analyses of HOXA3-treated wounds revealed that indeed HOXA3 locally increased expression of genes that selectively promote stem/progenitor cell mobilization and recruitment while also suppressing expression of numerous members of the proinflammatory nuclear factor κB pathway, including myeloid differentiation primary response gene 88 and toll-interacting protein. Thus HOXA3 accelerates wound repair by mobilizing endothelial progenitor cells and attenuating the excessive inflammatory response of chronic wounds
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