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Development of new materials for tissue engineering can be facilitated by the capacity to efficiently monitor in vivo the survival, proliferation and differentiation behaviour of cells implanted in different target tissues. We present here the application of a previously developed platform that allows to monitor in real time the survival and proliferative behaviour of implanted cells in two anatomical sites: subcutaneous and intramuscular. Basically, the system is based on the use of a non-invasive bioluminescence imaging (BLI) technique to detect luciferase expressing C57BL/6 cells, mouse embryonic fibroblasts, seeded in two sets of scaffolds: 1, a RAD16-I self-assembling peptide nanofiber matrix and 2, a composite consisted of the same RAD16-I nanofibers contained into a microporous biorubber scaffold. Interestingly, our results indicated considerable differences in the behaviour of implanted cells in each scaffold type. We observed that the self-assembling peptide scaffold alone foster cell survival and promotes cell proliferation where the composite scaffold not. Since self-assembling peptide scaffolds presents value stiffness proximal to the implanted tissues it is suggestive to think that harder materials will provide a physical constriction for cells to proliferate as well as mechanical discontinuity. We therefore propose that it is important to close match the implantation environment with the cell/material constructs in order to obtain the best response of the cells, illustrating the convenience of this strategy for the development of new tissue engineering platforms. (C) 2008 Elsevier Ltd. All rights reserved.

The role of somatostatin analogs in the management of immunoproliferative disease.

Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1β. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1β production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation.