Growth studies of m-GaN layers on LiAlO2 by MOCVD

This paper reports that the m-plane GaN layer is grown on (200)-plane LiAlO2 substrate by metal-organic chemical vapour deposition (MOCVD) method. Tetragonal-shaped crystallites appear at the smooth surface. Raman measurement illuminates the compressive stress in the layer which is released with increasing the layer's thickness. The high transmittance (80%), sharp band edge and excitonic absorption peak show that the GaN layer has good optical quality. The donor acceptor pair emission peak located at similar to 3.41 eV with full-width at half maximum of 120 meV and no yellow peaks in the photoluminescence spectra partially show that no Li incorporated into GaN layer from the LiAlO2 substrate.

Fabrication of beta-BaB2O4 layers on (001) Sr2+-doped alpha-BaB2O4 by vapor transport equilibration (VTE)

Crystalline beta-BBO layers have been successfully prepared on (0 0 1)-oriented Sr2+-doped alpha-BBO substrates using vapor transport equilibration technique. The layers were characterized by X-ray diffraction, X-ray rocking curve and transmission spectra. The present results manifest that the VTE treatment time and powder ratio are important factors on the preparation of beta-BBO layers. beta-BBO layers with a highly (0 0 l) preferred orientation were obtained according to XRD profiles. The full width at half-maximum of the rocking curve for the layer is as low as about 1000 in., which shows the high crystallinity of the layer. These results reveal the possibility of fabricating beta-BBO (0 0 1) layers on (0 0 1)-oriented Sr2+-doped alpha-BBO substrates by VTE. (C) 2006 Elsevier Ltd. All rights reserved.

CGP37157, an inhibitor of the mitochondrial Na+/Ca2+ exchanger, protects neurons from excitotoxicity by blocking voltage-gated Ca2+ channels

Inhibition of the mitochondrial Na+/Ca2+ exchanger (NCLX) by CGP37157 is protective in models of neuronal injury that involve disruption of intracellular Ca2+ homeostasis. However, the Ca2+ signaling pathways and stores underlying neuroprotection by that inhibitor are not well defined. In the present study, we analyzed how intracellular Ca2+ levels are modulated by CGP37157 (10 mu M) during NMDA insults in primary cultures of rat cortical neurons. We initially assessed the presence of NCLX in mitochondria of cultured neurons by immunolabeling, and subsequently, we analyzed the effects of CGP37157 on neuronal Ca2+ homeostasis using cameleon-based mitochondrial Ca2+ and cytosolic Ca2+ ([Ca2+](i)) live imaging. We observed that NCLX-driven mitochondrial Ca2+ exchange occurs in cortical neurons under basal conditions as CGP37157 induced a decrease in [Ca-2](i) concomitant with a Ca2+ accumulation inside the mitochondria. In turn, CGP37157 also inhibited mitochondrial Ca2+ efflux after the stimulation of acetylcholine receptors. In contrast, CGP37157 strongly prevented depolarization-induced [Ca2+](i) increase by blocking voltage-gated Ca2+ channels (VGCCs), whereas it did not induce depletion of ER Ca2+ stores. Moreover, mitochondrial Ca2+ overload was reduced as a consequence of diminished Ca2+ entry through VGCCs. The decrease in cytosolic and mitochondrial Ca2+ overload by CGP37157 resulted in a reduction of excitotoxic mitochondrial damage, characterized here by a reduction in mitochondrial membrane depolarization, oxidative stress and calpain activation. In summary, our results provide evidence that during excitotoxicity CGP37157 modulates cytosolic and mitochondrial Ca2+ dynamics that leads to attenuation of NMDA-induced mitochondrial dysfunction and neuronal cell death by blocking VGCCs.