Dynamic pore collapse in viscoplastic materials

Dynamic pore collapse in porous materials is studied by analyzing the finite deformation of an elastic/viscoplastic spherical shell under impulsive pressure loading. Effects of dynamic loading rate, pore size, initial porosity, strain-i-ate sensitivity, strain hardening, thermal softening, and mass density of the matrix material on the pore collapse process are examined and results are compared with those from quasistatic analyses of both rate-independent and rate-dependent matrix materials. Dynamic (inertia) effects are found to be significant or even dominant in certain shock wave consolidation conditions. An approximate method is proposed to incorporate dynamic effects into quasistatic pore-collapse relations of viscoplastic matrix materials. Implications of results of current study are discussed in terms of understanding the processes of shock wave consolidation of powders

A Parameterized Centrality Metric for Network Analysis

A variety of metrics have been proposed to measure the relative importance of nodes in a network. One of these, alpha-centrality [Bonacich, 2001], measures the number of attenuated paths that exist between nodes. We introduce a normalized version of this metric and use it to study network structure, specifically, to rank nodes and find community structure of the network. Specifically, we extend the modularity-maximization method [Newman and Girvan, 2004] for community detection to use this metric as the measure of node connectivity. Normalized alpha-centrality is a powerful tool for network analysis, since it contains a tunable parameter that sets the length scale of interactions. By studying how rankings and discovered communities change when this parameter is varied allows us to identify locally and globally important nodes and structures. We apply the proposed method to several benchmark networks and show that it leads to better insight into network structure than alternative methods.Comment: 11 pages, submitted to Physical Review

Effective Elastic Moduli and Characterization of a Particulate-Reinforced Metal Matrix Composite with Damaged Particles

A brief derivation of the expression is given for the effective bulk modulus of discontinuously reinforced metal matrix composites (DMMCs) with damaged particles (either complete voids as shattered particles or debonded particles). The analytical results are then compared with elastic moduli determined from nondestructive ultrasonic wave speed measurements of SiC particle-reinforced titanium matrix composites produced via shock wave consolidation. For the shock consolidated Ti-SiC metal matrix composites compacts, the overall particle damage mode is found to be similar to debonded particles and the effective volume fraction of damaged particles is determined to be 39% based on the data of both Young's and bulk moduli. Ultrasonic wave speed measurements combining with analytical and/or numerical results on overall elastic properties (Young's, bulk, and shear moduli, and Poisson's ratio) could be a useful tool in assessing the damage of particles in DMMCs

VCP-dependent muscle degeneration is linked to defects in a dynamic tubular lysosomal network in vivo.

Lysosomes are classically viewed as vesicular structures to which cargos are delivered for degradation. Here, we identify a network of dynamic, tubular lysosomes that extends throughout Drosophila muscle, in vivo. Live imaging reveals that autophagosomes merge with tubular lysosomes and that lysosomal membranes undergo extension, retraction, fusion and fission. The dynamics and integrity of this tubular lysosomal network requires VCP, an AAA-ATPase that, when mutated, causes degenerative diseases of muscle, bone and neurons. We show that human VCP rescues the defects caused by loss of Drosophila VCP and overexpression of disease relevant VCP transgenes dismantles tubular lysosomes, linking tubular lysosome dysfunction to human VCP-related diseases. Finally, disruption of tubular lysosomes correlates with impaired autophagosome-lysosome fusion, increased cytoplasmic poly-ubiquitin aggregates, lipofuscin material, damaged mitochondria and impaired muscle function. We propose that VCP sustains sarcoplasmic proteostasis, in part, by controlling the integrity of a dynamic tubular lysosomal network

A postsynaptic PI3K-cII dependent signaling controller for presynaptic homeostatic plasticity.

Presynaptic homeostatic plasticity stabilizes information transfer at synaptic connections in organisms ranging from insect to human. By analogy with principles of engineering and control theory, the molecular implementation of PHP is thought to require postsynaptic signaling modules that encode homeostatic sensors, a set point, and a controller that regulates transsynaptic negative feedback. The molecular basis for these postsynaptic, homeostatic signaling elements remains unknown. Here, an electrophysiology-based screen of the Drosophila kinome and phosphatome defines a postsynaptic signaling platform that includes a required function for PI3K-cII, PI3K-cIII and the small GTPase Rab11 during the rapid and sustained expression of PHP. We present evidence that PI3K-cII localizes to Golgi-derived, clathrin-positive vesicles and is necessary to generate an endosomal pool of PI(3)P that recruits Rab11 to recycling endosomal membranes. A morphologically distinct subdivision of this platform concentrates postsynaptically where we propose it functions as a homeostatic controller for retrograde, trans-synaptic signaling