RESUMO
Metal chalcogenide nanoparticles offer vast control over their optoelectronic properties via size, shape, composition, and morphology which has led to their use across fields including optoelectronics, energy storage, and catalysis. While cadmium and lead-based nanocrystals are prevalent in applications, concerns over their toxicity have motivated researchers to explore alternate classes of nanomaterials based on environmentally benign metals such as zinc and tin. The goal of this research is to identify material systems that offer comparable performance to existing metal chalcogenide systems from abundant, recyclable, and environmentally benign materials. With band gaps that span the visible through the infrared, II-V direct band gap semiconductors such as tetragonal zinc phosphide (α-Zn3P2) are promising candidates for optoelectronics. To date, syntheses of α-Zn3P2 nanoparticles have been hindered because of the toxicity of zinc and phosphorus precursors, surface oxidation, and defect states leading to carrier trapping and low photoluminescence quantum yield. This work reports a colloidal synthesis of quantum confined α-Zn3P2 nanoparticles from common phosphorus precursor tris(trimethylsilyl)phosphine and environmentally benign zinc carboxylates. Shelling of the nanoparticles with zinc sulfide is shown as a method of preventing oxidation and improving the optical properties of the nanoparticles. These results show a route to stabilizing α-Zn3P2 nanoparticles for optoelectronic device applications.
RESUMO
The small heat shock protein ΗspΒ5 (αB-crystallin) exhibits generally cytoprotective functions and possesses powerful neuroprotective capacity in the brain. However, little is known about the mode of action of ΗspΒ5 or other members of the HspB family particularly in neurons. To get clues of the neuronal function of HspBs, we overexpressed several HspBs in cultured rat hippocampal neurons and investigated their effect on neuronal morphology and stress resistance. Whereas axon length and synapse density were not affected by any HspB, dendritic complexity was enhanced by HspB5 and, to a lesser extent, by HspB6. Furthermore, we could show that this process was dependent on phosphorylation, since a non-phosphorylatable mutant of HspB5 did not show this effect. Rarefaction of the dendritic arbor is one hallmark of several neurodegenerative diseases. To investigate if HspB5, which is upregulated at pathophysiological conditions, might be able to protect dendrites during such situations, we exposed HspB5 overexpressing neuronal cultures to heat shock. HspB5 prevented heat shock-induced rarefaction of dendrites. In conclusion, we identified regulation of dendritic complexity as a new function of HspB5 in hippocampal neurons.
