Bioactivity of Polycrystalline Silicon Layers

Abstract

After oxygen, silicon is the second most abundant element in the environment and is present as an impurity in most materials. The widespread occurrence of siliceous biominerals as structural elements in lower plants and animals suggests that Si plays a role in the production and maintenance of connective tissue in higher organisms. It has been shown that the presence of Si is necessary in bones, cartilage and in the formation of connective tissue, as well as in some important metabolic processes. In this work, polycrystalline silicon layers are tested in terms of bioactivity, i.e., their ability to induce hydroxyapatite formation from simulated body fluid. Hydroxyapatite is a biologically compatible material with chemical similarity to the inorganic part of bones and teeth. Polycrystalline silicon layers are obtained by aluminum induced crystallization of Al and amorphous Si thin films deposited sequentially on glass substrates by radio-frequency magnetron sputtering and subsequently annealed in different atmospheres. The hydroxyapatite formation is induced by applying a method of laser-liquid-solid interaction. The method consists of irradiating the samples with laser light while immersed in a solution that is supersaturated with respect to Ca and P. As a result, heterogeneous porous sponge-like carbonate-containing hydroxyapatite is grown on the polysilicon surfaces. Crystals that are spherical in shape, containing Ca, P and O, Na, Cl, Mg, Al, Si and S, as well as well-faceted NaCl crystals are embedded in the hydroxyapatite layer. Enhancement of the hydroxyapatite growth and increased crystallinity is observed due to the applied laser-liquid-solid interaction.

Enhanced β-secretase processing of amyloid precursor protein in the skeletal muscle of ALS animal models

“…A study showed skeletal muscle-restricted expression of human SOD1 is sufficient to cause MN degeneration in mice [10]. In contrast, specific neuronal or astrocytic expression of mutant SOD1 in transgenic animals did not result in MN degeneration, clearly negating neurons or astrocytes as the sole mediators of ALS pathology [13][14][15]. These results demonstrate a causal role of skeletal muscle in ALS and suggest the possibility that skeletal muscle is a key factor for the study of ALS pathogenesis and potential therapy.…”