Non-linear Response of the trap model in the aging regime : Exact results in the strong disorder limit

We study the dynamics of the one dimensional disordered trap model presenting a broad distribution of trapping times $p(\tau) \sim 1/\tau^{1+\mu}$, when an external force is applied from the very beginning at $t=0$, or only after a waiting time $t_w$, in the linear as well as in the non-linear response regime. Using a real-space renormalization procedure that becomes exact in the limit of strong disorder $\mu \to 0$, we obtain explicit results for many observables, such as the diffusion front, the mean position, the thermal width, the localization parameters and the two-particle correlation function. In particular, the scaling functions for these observables give access to the complete interpolation between the unbiased case and the directed case. Finally, we discuss in details the various regimes that exist for the averaged position in terms of the two times and the external field.Comment: 27 pages, 1 eps figur

Thermal noise properties of two aging materials

In this lecture we review several aspects of the thermal noise properties in two aging materials: a polymer and a colloidal glass. The measurements have been performed after a quench for the polymer and during the transition from a fluid-like to a solid-like state for the gel. Two kind of noise has been measured: the electrical noise and the mechanical noise. For both materials we have observed that the electric noise is characterized by a strong intermittency, which induces a large violation of the Fluctuation Dissipation Theorem (FDT) during the aging time, and may persist for several hours at low frequency. The statistics of these intermittent signals and their dependance on the quench speed for the polymer or on sample concentration for the gel are studied. The results are in a qualitative agreement with recent models of aging, that predict an intermittent dynamics. For the mechanical noise the results are unclear. In the polymer the mechanical thermal noise is still intermittent whereas for the gel the violation of FDT, if it exists, is extremely small.Comment: to be published in the Proceedings of the XIX Sitges Conference on ''Jammming, Yielding and Irreversible Deformation in Condensed Matter'', M.-C.Miguel and M. Rubi eds.,Springer Verlag, Berli

Dictyostelium LvsB Mutants Model the Lysosomal Defects Associated with Chediak-Higashi Syndrome

Chediak-Higashi syndrome is a genetic disorder caused by mutations in a gene encoding a protein named LYST in humans (“lysosomal trafficking regulator”) or Beige in mice. A prominent feature of this disease is the accumulation of enlarged lysosome-related granules in a variety of cells. The genome of Dictyostelium discoideum contains six genes encoding proteins that are related to LYST/Beige in amino acid sequence, and disruption of one of these genes, lvsA (large volume sphere), results in profound defects in cytokinesis. To better understand the function of this family of proteins in membrane trafficking, we have analyzed mutants disrupted in lvsA, lvsB, lvsC, lvsD, lvsE, and lvsF. Of all these, only lvsA and lvsB mutants displayed interesting phenotypes in our assays. lvsA-null cells exhibited defects in phagocytosis and contained abnormal looking contractile vacuole membranes. Loss of LvsB, the Dictyostelium protein most similar to LYST/Beige, resulted in the formation of enlarged vesicles that by multiple criteria appeared to be acidic lysosomes. The rates of endocytosis, phagocytosis, and fluid phase exocytosis were normal in lvsB-null cells. Also, the rates of processing and the efficiency of targeting of lysosomal α-mannosidase were normal, although lvsB mutants inefficiently retained α-mannosidase, as well as two other lysosomal cysteine proteinases. Finally, results of pulse-chase experiments indicated that an increase in fusion rates accounted for the enlarged lysosomes in lvsB-null cells, suggesting that LvsB acts as a negative regulator of fusion. Our results support the notion that LvsB/LYST/Beige function in a similar manner to regulate lysosome biogenesis