Collapse mechanism maps for the hollow pyramidal core of a sandwich panel under transverse shear

The finite element method has been used to develop collapse mechanism maps for the shear response of sandwich panels with a stainless steel core comprising hollow struts. The core topology comprises either vertical tubes or inclined tubes in a pyramidal arrangement. The dependence of the elastic and plastic buckling modes upon core geometry is determined, and optimal geometric designs are obtained as a function of core density. For the hollow pyramidal core, strength depends primarily upon the relative density ρ̄ of the core with a weak dependence upon tube slenderness. At ρ̄ below about 3%, the tubes of the pyramidal core buckle plastically and the peak shear strength scales linearly with ρ̄. In contrast, at ρ̄ above 3%, the tubes do not buckle and a stable shear response is observed. The predictions of the current study are in excellent agreement with previous measurements on the shear strength of the hollow pyramidal core, and suggest that this core topology is attractive from the perspectives of both core strength and energy absorption. © 2011 Elsevier Ltd. All rights reserved.

Attenuated Salmonella Typhimurium lacking the pathogenicity island-2 type 3 secretion system grow to high bacterial numbers inside phagocytes in mice.

Intracellular replication within specialized vacuoles and cell-to-cell spread in the tissue are essential for the virulence of Salmonella enterica. By observing infection dynamics at the single-cell level in vivo, we have discovered that the Salmonella pathogenicity island 2 (SPI-2) type 3 secretory system (T3SS) is dispensable for growth to high intracellular densities. This challenges the concept that intracellular replication absolutely requires proteins delivered by SPI-2 T3SS, which has been derived largely by inference from in vitro cell experiments and from unrefined measurement of net growth in mouse organs. Furthermore, we infer from our data that the SPI-2 T3SS mediates exit from infected cells, with consequent formation of new infection foci resulting in bacterial spread in the tissues. This suggests a new role for SPI-2 in vivo as a mediator of bacterial spread in the body. In addition, we demonstrate that very similar net growth rates of attenuated salmonellae in organs can be derived from very different underlying intracellular growth dynamics.