601 research outputs found

    Modulated contrast and associated diffracted intensity of GaPySb1-y layers grown using organometallic vapor phase epitaxy

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    Journal ArticleWe have investigated the modulated structures and its associated diffracted diff_x000B_use intensity, of organometallic vapor phase epitaxially grown GaPSb (001) layers by using transmission electron microscopy (TEM) and transmission electron diff_x000B_raction (TED). The TEM results reveal the co-existence of a _x000C_fine-scale modulated contrast and a _x000C_fine-scale speckled contrast. In addition, a _x000C_fine needle-like contrast is observed. The [001] TED results show lines of [110]-oriented diff_x000B_use intensity diffuse streaks passing through the fundamental reflections, satellite spots at 1/4g[220] positions, and a [010]-oriented diff_x000B_use intensity with spacing of 1/6g[040]. Simulations using the Valence Force Field model were performed to understand the origin of the di_x000B_ffracted features. The observed distributions of di_x000B_ffuse intensity are shown to be partially consistent with random disorder. Furthermore, the [110]-oriented diff_x000B_use lines are attributed to a static displacement of the sites of the mixed sublattices

    Effects of V/III ratio on ordering and antiphase boundaries in GaInP layers

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    Journal ArticleTransmission electron microscope (TEM) and transmission electron diffraction (TED) studies have been performed to investigate the effects of V/III ratio on ordering and antiphase boundaries (APBs) in organometallic vapor phase epitaxial Ga0.5In0.5P layers grown onto (001) GaAs vicinal substrates at 670 °C. TED and TEM examination showed that the degree of order is higher in the layer grown using a V/III ratio of 160 than in the layer grown using a V/III ratio of 40. TEM results showed that the higher V/III ratio could be used to suppress APBs. In addition, the growth of order-induced heterostructures, where the V/III ratio is increased abruptly during growth, could be used to block the propagation of APBs. Mechanisms are proposed to explain these phenomena

    Enhancement of phase separation in the InGaN layer for self-assembled In-rich quantum dots

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    The enhancement of phase separation in the InGaN layer grown on a GaN layer with a rough surface was investigated for the formation of self-assembled In-rich quantum dots(QDs) in the InGaN layer. Transmission electron microscopy images showed that In-rich QDs with a size of 2–5 nm were formed even in an InGaN layer with a low indium content, and a layer thickness less than the critical thickness. The room-temperature photoluminescence(PL) spectrum of this layer showed emission peaks corresponding to In-rich QDs. The temperature-dependent PL spectra showed dominant peak shifts to the lower energy side, indicating that the self-assembled In-rich QDs are formed in the InGaN layer grown on a rough GaNsurface and that the carriers are localized in In-rich QDs

    Inhibitory Effect of Inflexinol on Nitric Oxide Generation and iNOS Expression via Inhibition of NF-κB Activation

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    Inflexinol, an ent-kaurane diterpenoid, was isolated from the leaves of Isodon excisus. Many diterpenoids isolated from the genus Isodon (Labiatae) have antitumor and antiinflammatory activities. We investigated the antiinflammatory effect of inflexinol in RAW 264.7 cells and astrocytes. As a result, we found that inflexinol (1, 5, 10 μM) suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and astrocytes. Consistent with the inhibitory effect on iNOS and COX-2 expression, inflexinol also inhibited transcriptional and DNA binding activity of NF-κB via inhibition of IκB degradation as well as p50 and p65 translocation into nucleus. These results suggest that inflexinol inhibits iNOS and COX-2 expression through inhibition of NF-κB activation, thereby inhibits generation of inflammatory mediators in RAW 264.7 cells and astrocytes, and may be useful for treatment of inflammatory diseases
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