18 research outputs found

    Strain balancing of MOVPE InAs/GaAs quantum dots using GaAs0.8P0.2

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    MOVPE growth of stacked InAs/ GaAs QDs with and without GaAs 0.8 P 0.2 strain balancing layers has been studied. The GaAsP layers reduce the accumulated strain whilst maintaining the electrical characteristics. This should enable closer stacking of QD layers leading to higher gain and improved laser performance

    Strain Balancing of Metal-Organic Vapour Phase Epitaxy InAs/GaAs Quantum Dot Lasers

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    Incorporation of a GaAs0.8P0.2 layer allows strain balancing to be achieved in self-assembled InAs/GaAs quantum dots (QDs) grown by metal organic vapor phase epitaxy. Tuneable wavelength and high density are obtained through growth parameter optimization, with emission at 1.27 μm and QD layer density 3 × 10 10 cm-2. Strain balancing allows close vertical stacking (30 nm) of the QD layers, giving the potential for increased optical gain. Modeling and device characterization indicates minimal degradation in the optical and electrical characteristics unless the phosphorus percentage is increased above 20%. Laser structures are fabricated with a layer separation of 30 nm, demonstrating low temperature lasing with a threshold current density of 100 A/cm2 at 130 K without any facet coating

    Adherence to a MIND-Like Dietary Pattern, Long-Term Exposure to Fine Particulate Matter Air Pollution, and MRI-Based Measures of Brain Volume: The Women’s Health Initiative Memory Study-MRI

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    BACKGROUND: Previous studies suggest that certain dietary patterns and constituents may be beneficial to brain health. Airborne exposures to fine particulate matter [particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5)] are neurotoxic, but the combined effects of dietary patterns and PM2.5 have not been investigated. OBJECTIVES: We examined whether previously reported association between PM2.5 exposure and lower white matter volume (WMV) differed between women whose usual diet during the last 3 months before baseline was more or less consistent with a Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND)-like diet, a dietary pattern that may slow neurodegenerative changes. METHODS: This study included 1,302 U.S. women who were 65-79 y old and free of dementia in the period 1996-1998 (baseline). In the period 2005-2006, structural brain magnetic resonance imaging (MRI) scans were performed to estimate normal-appearing brain volumes (excluding areas with evidence of small vessel ischemic disease). Baseline MIND diet scores were derived from a food frequency questionnaire. Three-year average PM2.5 exposure prior to MRI was estimated using geocoded participant addresses and a spatiotemporal model. RESULTS: Average total and temporal lobe WMVs were 0:74 cm3 [95% confidence interval (CI): 0.001, 1.48) and 0:19 cm3 (95% CI: 0.002, 0.37) higher, respectively, with each 0.5-point increase in the MIND score and were 4:16 cm3 (95% CI: -6:99, -1:33) and 1:46 cm3 (95% CI: -2:16, -0:76) lower, respectively, with each interquartile range (IQR) (IQR = 3:22 μg/m3) increase in PM2.5. The inverse association between PM2.5 per IQR and WMV was stronger (p-interaction <0:001) among women with MIND scores below the median (for total WMV, -12:47 cm3; 95% CI: −17:17, −7:78), but absent in women with scores above the median (0:16 cm3; 95% CI: −3:41, 3.72), with similar patterns for WMV in the frontal, parietal, and temporal lobes. For total cerebral and hippocampus brain volumes or WMV in the corpus callosum, the associations with PM2.5 were not significantly different for women with high MIND scores and women with low MIND scores

    Lipolysis drives expression of the constitutively active receptor GPR3 to induce adipose thermogenesis

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    Thermogenic adipocytes possess a therapeutically appealing, energy-expending capacity, which is canonically cold-induced by ligand-dependent activation of beta-adrenergic G protein-coupled receptors (GPCRs). Here, we uncover an alternate paradigm of GPCR-mediated adipose thermogenesis through the constitutively active receptor, GPR3. We show that the N terminus of GPR3 confers intrinsic signaling activity, resulting in continuous Gscoupling and cAMP production without an exogenous ligand. Thus, transcriptional induction of Gpr3 represents the regulatory parallel to ligand-binding of conventional GPCRs. Consequently, increasing Gpr3 expression in thermogenic adipocytes is alone sufficient to drive energy expenditure and counteract metabolic disease in mice. Gpr3 transcription is cold-stimulated by a lipolytic signal, and dietary fat potentiates GPR3-dependent thermogenesis to amplify the response to caloric excess. Moreover, we find GPR3 to be an essential, adrenergic-independent regulator of human brown adipocytes. Taken together, our findings reveal a noncanonical mechanism of GPCR control and thermogenic activation through the lipolysis-induced expression of constitutively active GPR3.Diabetes mellitus: pathophysiological changes and therap

    Automatic Foreground Extraction of Head Shoulder Images

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    Abstract. Most existing techniques of foreground extracting work only in interactive mode. This paper introduces a novel algorithm of auto-matic foreground extraction for special object, and verifies its effective-ness with head shoulder images. The main contribution of our idea is to make the most use of the prior knowledge to constrain the processing of foreground extraction. For human head shoulder images, we first detect face and a few facial features, which helps to estimate an approximate mask covering the interesting region. The algorithm then extracts the hard edge of foreground from the specified area using an iterative graph cut method incorporated with an improved Gaussian Mixture Model. To generate accurate soft edges, a Bayes matting is applied. The whole process is fully automatic. Experimental results demonstrate that our algorithm is both robust and efficient.

    Magnesium intake, bone mineral density, and fractures: Results from the Women's Health Initiative Observational Study

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    10.3945/ajcn.113.067488American Journal of Clinical Nutrition994926-93
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