The production of Fresnel lenses in sol-gel derived Ormocers by holography

Micro Fresnel lenses were prepared from photosensitive organic-inorganic nanocomposites of the Ormocer-type by irradiation of films of 10 µm in thickness with an interference pattern of two laser beams, mixing a planar reference wavefront and a spherical object wavefront. To monitor the polymerization behavior of the organic groups during irradiation under real time conditions, a characterization method was developed to study changes in optical thickness n d by measuring changes of index of refraction and shrinkage during polymerization. Three-dimensional Fresnel structures were obtained by removing the unpolymerized areas by a solvent. Variation of index of refraction can also be obtained by diffusion of monomers in regions of higher light intensity. A model, similar to the Colburn-Haines model is presented

Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2

Dysregulated apoptotic cell death contributes to many pathological conditions, including sepsis, prompting the suggestion that caspase inhibition to block apoptosis could have useful therapeutic applications. Because the cytokine tumor necrosis factor (TNF, also known as TNF-alpha) is both proapoptotic and pro-inflammatory and is involved in septic shock, we tested whether caspase inhibition would alleviate TNF-induced toxicity in vivo. General caspase inhibition by the protease inhibitor zVAD-fmk exacerbated TNF toxicity by enhancing oxidative stress and mitochondrial damage, resulting in hyperacute hemodynamic collapse, kidney failure and death. Thus, survival of TNF toxicity depends on caspase-dependent processes. Our results demonstrated the pathophysiological relevance of caspase-independent, ROS-mediated pathways in response to lethal TNF-induced shock in mice. In addition, survival of TNF toxicity seemed to require a caspase-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation