183 research outputs found

    Distribution of funding countries.

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    <p>Distribution of funding countries.</p

    Distribution of funding sources.

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    <p>Distribution of funding sources.</p

    Supplemental Material - Exploring shared identity theory as an expanded conceptualization of Alzheimer’s caregiving

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    Supplemental Material for Exploring shared identity theory as an expanded conceptualization of Alzheimer’s caregiving by Samantha F. Lang, Blaine J. Fowers and Jue Wang in Journal of Social and Personal Relationships</p

    Studies toward the Total Synthesis of Nagelamide K

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    A stereocontrolled strategy toward the synthesis of nagelamide K has been developed. The dimeric imidazole acrylate, diimidazolidenesuccinate, was constructed as a synthetic precursor by a Ni-catalyzed coupling reaction; the microwave-promoted intramolecular aza-Michael addition afforded the imidazo[1,5-<i>a</i>]pyridine core structure of nagelamide K in high stereoselectivity. A detaurine–dediamino analogue of nagelamide K has been prepared

    Results of the Morris water maze test.

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    <p><b>A</b>, comparisons of average latency in the oriented navigation trial (A1) and average time spent in the target quadrant in the probe trial (A2) after Aβ<sub>1–42</sub> injection. <b>B</b>, comparisons of average latency (B1) and average time spent in the target quadrant (B2) after Rg1 treatment. Control group, intrahippocampal injection of normal saline and intraperitoneal injection of normal saline; Untreated group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of normal saline; Rg1+GW9662 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1 and GW9662; Rg1 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1. Bars represent mean±SEM. <i>n</i> = 10. +,vs. control group, <i>P</i><0.05. *, vs. untreated group, <i>P</i><0.05. #, vs. Rg1+GW9662 group, <i>P</i><0.05.</p

    Extreme Learning Machine-Based Classification of ADHD Using Brain Structural MRI Data

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    <div><p>Background</p><p>Effective and accurate diagnosis of attention-deficit/hyperactivity disorder (ADHD) is currently of significant interest. ADHD has been associated with multiple cortical features from structural MRI data. However, most existing learning algorithms for ADHD identification contain obvious defects, such as time-consuming training, parameters selection, etc. The aims of this study were as follows: (1) Propose an ADHD classification model using the extreme learning machine (ELM) algorithm for automatic, efficient and objective clinical ADHD diagnosis. (2) Assess the computational efficiency and the effect of sample size on both ELM and support vector machine (SVM) methods and analyze which brain segments are involved in ADHD.</p><p>Methods</p><p>High-resolution three-dimensional MR images were acquired from 55 ADHD subjects and 55 healthy controls. Multiple brain measures (cortical thickness, etc.) were calculated using a fully automated procedure in the FreeSurfer software package. In total, 340 cortical features were automatically extracted from 68 brain segments with 5 basic cortical features. F-score and SFS methods were adopted to select the optimal features for ADHD classification. Both ELM and SVM were evaluated for classification accuracy using leave-one-out cross-validation.</p><p>Results</p><p>We achieved ADHD prediction accuracies of 90.18% for ELM using eleven combined features, 84.73% for SVM-Linear and 86.55% for SVM-RBF. Our results show that ELM has better computational efficiency and is more robust as sample size changes than is SVM for ADHD classification. The most pronounced differences between ADHD and healthy subjects were observed in the frontal lobe, temporal lobe, occipital lobe and insular.</p><p>Conclusion</p><p>Our ELM-based algorithm for ADHD diagnosis performs considerably better than the traditional SVM algorithm. This result suggests that ELM may be used for the clinical diagnosis of ADHD and the investigation of different brain diseases.</p></div

    Chemical structure of ginsenoside Rg1.

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    <p>Chemical structure of ginsenoside Rg1.</p

    Real-time PCR results.

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    <p><b>A</b>, <b>B</b>, comparisons of mRNA levels of PPARγ and IDE among control, untreated, Rg1+GW9662, and Rg1 groups. Control group, intrahippocampal injection of normal saline and intraperitoneal injection of normal saline; Untreated group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of normal saline; Rg1+GW9662 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1 and GW9662; Rg1 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1. Bars represent mean±SEM. <i>n</i> = 7. *, vs. untreated group, <i>P</i><0.05. #, vs. Rg1+GW9662 group, <i>P</i><0.05.</p

    HE staining (×400).

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    <p><b>A</b>, control group; <b>B</b>, untreated group; <b>C</b>, Rg1+GW9662 group; <b>D</b>, Rg1 group. Control group, intrahippocampal injection of normal saline and intraperitoneal injection of normal saline; Untreated group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of normal saline; Rg1+GW9662 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1 and GW9662; Rg1 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1. Rats in the control group did not show histopathological abnormalities. In the untreated and Rg1+GW9662 groups, the number of cells in the hippocampal CA1 region appeared decreased. Furthermore, the remnants of the pyramidal cells were arranged irregularly and some exhibited shrunken and irregular shape. The cells in the Rg1 group had better cell morphology and were more numerous than those in the untreated and Rg1+GW9662 groups.</p

    Western blot results.

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    <p><b>A</b>, <b>B</b>, and <b>C</b>, comparisons of protein levels of Aβ<sub>1–42</sub>, PPARγ, and IDE among control, untreated, Rg1+GW9662, and Rg1 groups, respectively. <b>D</b>, detection of Aβ<sub>1–42</sub>, PPARγ, and IDE proteins by western blot. Control group, intrahippocampal injection of normal saline and intraperitoneal injection of normal saline; Untreated group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of normal saline; Rg1+GW9662 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1 and GW9662; Rg1 group, intrahippocampal injection of Aβ<sub>1–42</sub> and intraperitoneal injection of Rg1. Bars represent mean±SEM. <i>n</i> = 7. *, vs. untreated group, <i>P</i><0.05. #, vs. Rg1+GW9662 group, <i>P</i><0.05.</p
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