Asymptotic function for multi-growth surfaces using power-law noise

Numerical simulations are used to investigate the multiaffine exponent $\alpha_q$ and multi-growth exponent $\beta_q$ of ballistic deposition growth for noise obeying a power-law distribution. The simulated values of $\beta_q$ are compared with the asymptotic function $\beta_q = \frac{1}{q}$ that is approximated from the power-law behavior of the distribution of height differences over time. They are in good agreement for large $q$. The simulated $\alpha_q$ is found in the range $\frac{1}{q} \leq \alpha_q \leq \frac{2}{q+1}$. This implies that large rare events tend to break the KPZ universality scaling-law at higher order $q$.Comment: 5 pages, 4 figures, to be published in Phys. Rev.

Scaling of impact fragmentation near the critical point

We investigated two-dimensional brittle fragmentation with a flat impact experimentally, focusing on the low impact energy region near the fragmentation-critical point. We found that the universality class of fragmentation transition disagreed with that of percolation. However, the weighted mean mass of the fragments could be scaled using the pseudo-control parameter multiplicity. The data for highly fragmented samples included a cumulative fragment mass distribution that clearly obeyed a power-law. The exponent of this power-law was 0.5 and it was independent of sample size. The fragment mass distributions in this regime seemed to collapse into a unified scaling function using weighted mean fragment mass scaling. We also examined the behavior of higher order moments of the fragment mass distributions, and obtained multi-scaling exponents that agreed with those of the simple biased cascade model.Comment: 6 pages, 6 figure

Classification of KPZQ and BDP models by multiaffine analysis

We argue differences between the Kardar-Parisi-Zhang with Quenched disorder (KPZQ) and the Ballistic Deposition with Power-law noise (BDP) models, using the multiaffine analysis method. The KPZQ and the BDP models show mono-affinity and multiaffinity, respectively. This difference results from the different distribution types of neighbor-height differences in growth paths. Exponential and power-law distributions are observed in the KPZQ and the BDP, respectively. In addition, we point out the difference of profiles directly, i.e., although the surface profiles of both models and the growth path of the BDP model are rough, the growth path of the KPZQ model is smooth.Comment: 11 pages, 6 figure

Surface Scaling Analysis of a Frustrated Spring-network Model for Surfactant-templated Hydrogels

We propose and study a simplified model for the surface and bulk structures of crosslinked polymer gels, into which voids are introduced through templating by surfactant micelles. Such systems were recently studied by Atomic Force Microscopy [M. Chakrapani et al., e-print cond-mat/0112255]. The gel is represented by a frustrated, triangular network of nodes connected by springs of random equilibrium lengths. The nodes represent crosslinkers, and the springs correspond to polymer chains. The boundaries are fixed at the bottom, free at the top, and periodic in the lateral direction. Voids are introduced by deleting a proportion of the nodes and their associated springs. The model is numerically relaxed to a representative local energy minimum, resulting in an inhomogeneous, ``clumpy'' bulk structure. The free top surface is defined at evenly spaced points in the lateral (x) direction by the height of the topmost spring, measured from the bottom layer, h(x). Its scaling properties are studied by calculating the root-mean-square surface width and the generalized increment correlation functions C_q(x)= . The surface is found to have a nontrivial scaling behavior on small length scales, with a crossover to scale-independent behavior on large scales. As the vacancy concentration approaches the site-percolation limit, both the crossover length and the saturation value of the surface width diverge in a manner that appears to be proportional to the bulk connectivity length. This suggests that a percolation transition in the bulk also drives a similar divergence observed in surfactant templated polyacrylamide gels at high surfactant concentrations.Comment: 17 pages RevTex4, 10 imbedded eps figures. Expanded discussion of multi-affinit

Experimental and numerical investigation of the compression and expansion of a granular bed of repelling magnetic disks

peer reviewe

Reversible Keap1 inhibitors are preferential pharmacological tools to modulate cellular mitophagy

Mitophagy orchestrates the autophagic degradation of dysfunctional mitochondria preventing their pathological accumulation and contributing to cellular homeostasis. We previously identified a novel chemical tool (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their membrane potential (ΔΨm). PMI is an inhibitor of the protein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Keap1 and is able to up-regulate the expression of autophagy-associated proteins, including p62/SQSTM1. Here we show that PMI promotes mitochondrial respiration, leading to a superoxide-dependent activation of mitophagy. Structurally distinct Keap1-Nrf2 PPI inhibitors promote mitochondrial turnover, while covalent Keap1 modifiers, including sulforaphane (SFN) and dimethyl fumarate (DMF), are unable to induce a similar response. Additionally, we demonstrate that SFN reverses the effects of PMI in co-treated cells by reducing the accumulation of p62 in mitochondria and subsequently limiting their autophagic degradation. This study highlights the unique features of Keap1-Nrf2 PPI inhibitors as inducers of mitophagy and their potential as pharmacological agents for the treatment of pathological conditions characterized by impaired mitochondrial quality control

Transgenic expression of the dicotyledonous pattern recognition receptor EFR in rice leads to ligand-dependent activation of defense responses

Plant plasma membrane localized pattern recognition receptors (PRRs) detect extracellular pathogen-associated molecules. PRRs such as Arabidopsis EFR and rice XA21 are taxonomically restricted and are absent from most plant genomes. Here we show that rice plants expressing EFR or the chimeric receptor EFR::XA21, containing the EFR ectodomain and the XA21 intracellular domain, sense both Escherichia coli- and Xanthomonas oryzae pv. oryzae (Xoo)-derived elf18 peptides at sub-nanomolar concentrations. Treatment of EFR and EFR::XA21 rice leaf tissue with elf18 leads to MAP kinase activation, reactive oxygen production and defense gene expression. Although expression of EFR does not lead to robust enhanced resistance to fully virulent Xoo isolates, it does lead to quantitatively enhanced resistance to weakly virulent Xoo isolates. EFR interacts with OsSERK2 and the XA21 binding protein 24 (XB24), two key components of the rice XA21-mediated immune response. Rice-EFR plants silenced for OsSERK2, or overexpressing rice XB24 are compromised in elf18-induced reactive oxygen production and defense gene expression indicating that these proteins are also important for EFR-mediated signaling in transgenic rice. Taken together, our results demonstrate the potential feasibility of enhancing disease resistance in rice and possibly other monocotyledonous crop species by expression of dicotyledonous PRRs. Our results also suggest that Arabidopsis EFR utilizes at least a subset of the known endogenous rice XA21 signaling components

Importance of a C-Terminal Conserved Region of Chk1 for Checkpoint Function

BACKGROUND: The protein kinase Chk1 is an essential component of the DNA damage checkpoint pathway. Chk1 is phosphorylated and activated in the fission yeast Schizosaccharomyces pombe when cells are exposed to agents that damage DNA. Phosphorylation, kinase activation, and nuclear accumulation are events critical to the ability of Chk1 to induce a transient delay in cell cycle progression. The catalytic domain of Chk1 is well-conserved amongst all species, while there are only a few regions of homology within the C-terminus. A potential pseudosubstrate domain exists in the C-terminus of S. pombe Chk1, raising the possibility that the C-terminus acts to inhibit the catalytic domain through interaction of this domain with the substrate binding site. METHODOLOGY/PRINCIPAL FINDINGS: To evaluate this hypothesis, we characterized mutations in the pseudosubstrate region. Mutation of a conserved aspartic acid at position 469 to alanine or glycine compromises Chk1 function when the mutants are integrated as single copies, demonstrating that this domain of Chk1 is critical for function. Our data does not support, however, the hypothesis that the domain acts to inhibit Chk1 function as other mutations in the amino acids predicted to comprise the pseudosubstrate do not result in constitutive activation of the protein. When expressed in multi-copy, Chk1D469A remains non-functional. In contrast, multi-copy Chk1D469G confers cell survival and imposes a checkpoint delay in response to some, though not all forms of DNA damage. CONCLUSIONS/SIGNIFICANCE: Thus, we conclude that this C-terminal region of Chk1 is important for checkpoint function and predict that a limiting factor capable of associating with Chk1D469G, but not Chk1D469A, interacts with Chk1 to elicit checkpoint activation in response to a subset of DNA lesions