Floating gated silicon-on-insulator nonvolatile memory devices with Au nanoparticles embedded in SiO1.3N insulators were fabricated. The tunneling SiO1.3N insulator, Au nanoparticles, and control SiO1.3N insulator were sequentially deposited by digital sputtering method at 300°C. The size of Au nanoparticles was controlled in the range of 1–5nm by adjusting the deposition thickness of Au layer and the density of Au nanoparticles was approximately 1.5×1012cm−2. A significant threshold voltage shift of fabricated floating gate memory devices was obtained due to the charging effects of Au particles and the memory window was larger than 2.5V.

The analysis of modulation-broadened experimental magnetic resonance spectra by the fitting of theoretical lineshape functions is described together with tests on zero field NMR lineshapes from 69Co in cubic cobalt. It is shown that for small modulation amplitudes values for the resonance width, intensity and mode admixture may be obtained. For large modulation amplitudes considerable errors may occur in the deduced values of intensity and width but their ratio, the resonance amplitude, is still accurately determinable. The application of correction curves to spectral parameters of resolved lines is summarized.

Proteasome inhibitors, such as bortezomib (BZ) and carfilzomib (CFZ), have been suggested as treatments for various cancers. To utilize BZ and/or CFZ as effective therapeutics for treating melanoma, we studied their molecular mechanisms using B16-F1 melanoma cells. Flow cytometry of Annexin V-fluorescein isothiocyanate-labeled cells indicated apoptosis induction by treatment with BZ and CFZ. Apoptosis was evidenced by the activation of various caspases, including caspase 3, 8, 9, and 12. Treatment with BZ and CFZ induced endoplasmic reticulum (ER) stress, as indicated by an increase in eIF2α phosphorylation and the expression of ER stress-associated proteins, including GRP78, ATF6α, ATF4, XBP1, and CCAAT/enhancer-binding protein homologous protein. The effects of CFZ on ER stress and apoptosis were lower than that of BZ. Nevertheless, CFZ and BZ synergistically induced ER stress and apoptosis in B16-F1 cells. Furthermore, the combinational pharmacological interactions of BZ and CFZ against the growth of B16-F1 melanoma cells were assessed by calculating the combination index and dose-reduction index with the CompuSyn software. We found that the combination of CFZ and BZ at submaximal concentrations could obtain dose reduction by exerting synergistic inhibitory effects on cell growth. Moreover, this drug combination reduced tumor growth in C57BL/6 syngeneic mice. Taken together, these results suggest that CFZ in combination with BZ may be a beneficial and potential strategy for melanoma treatment.

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