Characterization and deformation response of orthotropic fibre networks with auxetic out-of-plane behaviour

In the present paper, highly porous fibre networks made of 316L fibres, with different fibre volume fractions, are characterized in terms of network architecture, elastic constants and fracture energies. Elastic constants are measured using quasi-static mechanical and modal vibration testing, yielding local and globally averaged properties, respectively. Differences between quasi-static and dynamic elastic constants are attributed to through-thickness shear effects. Regardless of the method employed, networks show signs of material inhomogeneity at high fibre densities, in agreement with X-ray nanotomography results. Strong auxetic (or negative Poisson's ratio) behaviour is observed in the through-thickness direction, which is attributed to fibre kinking induced during processing. Measured fracture energies are compared with model predictions incorporating information about in-plane fibre orientation distribution, fibre volume fraction and single fibre work of fracture. Experimental values are broadly consistent with model predictions, based on the assumption that this energy is primarily associated with plastic deformation of individual fibres within a process zone of the same order as the inter-joint spacing. © 2013 Published by Elsevier Ltd. on behalf of Acta Materialia Inc. All rights reserved.

A dynamic view of the spread and intracellular distribution of Salmonella enterica.

The events that determine the dynamics of proliferation, spread and distribution of microbial pathogens within their hosts are surprisingly heterogeneous and poorly understood. We contend that understanding these phenomena at a sophisticated level with the help of mathematical models is a prerequisite for the development of truly novel, targeted preventative measures and drug regimes. We describe here recent studies of Salmonella enterica infections in mice which suggest that bacteria resist the antimicrobial environment inside host cells and spread to new sites, where infection foci develop, and thus avoid local escalation of the adaptive immune response. We further describe implications for our understanding of the pathogenic mechanism inside the host.