Experimental and micromechanical study of size effects in the constrained deformation of metallic foams

Previous investigations have unveiled size effects in the strength of metallic foams under simple shear - the shear strength increases with diminishing specimen size, a phenomena similar to that shown by Fleck et al. (Acta Mat., 1994, Vol. 42, p. 475.) on the torsion tests of copper wires of various radii. In this study, experimental study of the constrained deformation of a foam layer sandwiched between two steel plates has been conducted. The sandwiched plates are subjected to combined shear and normal loading. It is found that measured yield loci of metallic foams in the normal and shear stress space corresponding to various foam layer thicknesses are self-similar in shape but their size increases as the foam layer thickness decreases. Moreover, the strains profiles across the foam layer thickness are parabolic instead of uniform; their values increase from the interfaces between the foam layer and the steel plates and reach their maximum in the middle of the foam layer, yielding boundary layers adjacent to the steel plates. In order to further explore the origin of observed size effects, micromechanics models have been developed, with the foam layer represented by regular and irregular honeycombs. Though the regular honeycomb model is seen to underestimate the size effects, the irregular honeycomb model faithfully captures the observed features of the constrained deformation of metallic foams.

Size effects in the constrained deformation of metallic foams

The constrained deformation of an aluminium alloy foam sandwiched between steel substrates has been investigated. The sandwich plates are subjected to through-thickness shear and normal loading, and it is found that the face sheets constrain the foam against plastic deformation and result in a size effect: the yield strength increases with diminishing thickness of foam layer. The strain distribution across the foam core has been measured by a visual strain mapping technique, and a boundary layer of reduced straining was observed adjacent to the face sheets. The deformation response of the aluminium foam layer was modelled by the elastic-plastic finite element analysis of regular and irregular two dimensional honeycombs, bonded to rigid face sheets; in the simulations, the rotation of the boundary nodes of the cell-wall beam elements was set to zero to simulate full constraint from the rigid face sheets. It is found that the regular honeycomb under-estimates the size effect whereas the irregular honeycomb provides a faithful representation of both the observed size effect and the observed strain profile through the foam layer. Additionally, a compressible version of the Fleck-Hutchinson strain gradient theory was used to predict the size effect; by identifying the cell edge length as the relevant microstructural length scale the strain gradient model is able to reproduce the observed strain profiles across the layer and the thickness dependence of strength. © 2002 Elsevier Science Ltd. All rights reserved.

In vivo regulation of the Vi antigen in Salmonella and induction of immune responses with an in vivo-inducible promoter.

Salmonella enterica serovar Typhi, the agent of typhoid fever in humans, expresses the surface Vi polysaccharide antigen that contributes to virulence. However, Vi expression can also be detrimental to some key steps of S. Typhi infectivity, for example, invasion, and Vi is the target of protective immune responses. We used a strain of S. Typhimurium carrying the whole Salmonella pathogenicity island 7 (SPI-7) to monitor in vivo Vi expression within phagocytic cells of mice at different times after systemic infection. We also tested whether it is possible to modulate Vi expression via the use of in vivo-inducible promoters and whether this would trigger anti-Vi antibodies through the use of Vi-expressing live bacteria. Our results show that Vi expression in the liver and spleen is downregulated with the progression of infection and that the Vi-negative population of bacteria becomes prevalent by day 4 postinfection. Furthermore, we showed that replacing the natural tviA promoter with the promoter of the SPI-2 gene ssaG resulted in sustained Vi expression in the tissues. Intravenous or oral infection of mice with a strain of S. Typhimurium expressing Vi under the control of the ssaG promoter triggered detectable levels of all IgG subclasses specific for Vi. Our work highlights that Vi is downregulated in vivo and provides proof of principle that it is possible to generate a live attenuated vaccine that induces Vi-specific antibodies after single oral administration.

A Salmonella Typhimurium-Typhi genomic chimera: a model to study Vi polysaccharide capsule function in vivo.

The Vi capsular polysaccharide is a virulence-associated factor expressed by Salmonella enterica serotype Typhi but absent from virtually all other Salmonella serotypes. In order to study this determinant in vivo, we characterised a Vi-positive S. Typhimurium (C5.507 Vi(+)), harbouring the Salmonella pathogenicity island (SPI)-7, which encodes the Vi locus. S. Typhimurium C5.507 Vi(+) colonised and persisted in mice at similar levels compared to the parent strain, S. Typhimurium C5. However, the innate immune response to infection with C5.507 Vi(+) and SGB1, an isogenic derivative not expressing Vi, differed markedly. Infection with C5.507 Vi(+) resulted in a significant reduction in cellular trafficking of innate immune cells, including PMN and NK cells, compared to SGB1 Vi(-) infected animals. C5.507 Vi(+) infection stimulated reduced numbers of TNF-α, MIP-2 and perforin producing cells compared to SGB1 Vi(-). The modulating effect associated with Vi was not observed in MyD88(-/-) and was reduced in TLR4(-/-) mice. The presence of the Vi capsule also correlated with induction of the anti-inflammatory cytokine IL-10 in vivo, a factor that impacted on chemotaxis and the activation of immune cells in vitro.