55 research outputs found

    Composite Index Construction with Expert Opinion

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    Composite index is a powerful and popularly used tool in providing an overall measure of a subject by summarizing a group of measurements (component indices) of different aspects of the subject. It is widely used in economics, finance, policy evaluation, performance ranking, and many other fields. Effective construction of a composite index has been studied extensively. The most widely used approach is to use a linear combination of the component indices, where the combination weights are determined by optimizing an objective function. To maximize the overall variation of the resulting composite index, the combination weights can be obtained through principal component analysis. In this article, we propose to incorporate expert opinions into the construction of the composite index. It is noted that expert opinion often provides useful information in assessing which of the component indices are more important for the overall measure of the subject. We consider the case that a group of experts have been consulted, each providing a set of importance scores for the component indices, along with a set of confidence scores which reflects the expert’s own confidence in his/her assessment. In addition, the constructor of the composite index can also provide an assessment of the expertise level of each expert. We use linear combinations to construct the composite index, where the combination weights are determined by maximizing the sum of resulting composite index variation and the negative weighted sum of squares of deviation between the combination weights used and the experts’ scores. A data-driven approach is used to find the optimal balance between the two sources of information. Theoretical properties of the procedure are investigated. Simulation examples and an economic application on constructing science and technology development index is carried out to illustrate the proposed method.</p

    Prognostic Value of Cancer Stem Cell Marker Aldehyde Dehydrogenase in Ovarian Cancer: A Meta-Analysis

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    <div><p>Objective</p><p>Aldehyde dehydrogenase (ALDH) has recently been reported as a marker of cancer stem-like cells in ovarian cancer. However, the prognostic role of ALDH in ovarian cancer still remains controversial. In this study, we aimed to evaluate the association between the expression of ALDH and the outcome of ovarian cancer patients by performing a meta-analysis.</p> <p>Methods</p><p>We systematically searched for studies investigating the relationships between ALDH expression and outcome of ovarian cancer patients. Only articles in which ALDH expression was detected by immunohistochemical staining were included. A meta-analysis was performed to generate combined hazard ratios (HRs) with 95% confidence intervals (CIs) for overall survival (OS) and disease-free survival (DFS).</p> <p>Results</p><p>A total of 1,258 patients from 7 studies (6 articles) were included in the analysis. Our results showed that high ALDH expression in patients with ovarian cancer was associated with poor prognosis in terms of Os (HR, 1.25; 95% CI, 1.07-1.47; P = 0.005) and DFS (HR, 1.58; 95% CI, 1.00-2.49; P = 0.052), though the difference for DFS was not statistically significant. In addition, there was no evidence of publication bias as suggested by Begg’s and Egger’s tests (Begg’s test, P = 0.707; Egger’s test, P = 0.355).</p> <p>Conclusion</p><p>The present meta-analysis indicated that elevated ALDH expression was associated with poor prognosis in patients with ovarian cancer.</p> </div

    DataSheet1_Accelerated catalytic ozonation for aqueous nitrobenzene degradation over Ce-loaded silicas: Active sites and pathways.docx

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    Cerium oxides loaded silica catalysts were synthesized by an impregnation method by simply mixing Ce precursor with silica spherule (Ce/SS) and ordered MCM-41 zeolites (Ce/MCM-41), followed by a mild calcination. Compared with pure SS and MCM-41, Ce modified Ce/SS and Ce/MCM-41 demonstrate much improved catalytic ozonation activities for mineralization of recalcitrant nitrobenzene (NB). At solution pH of 6, 86 and 97% TOC mineralization rates were achieved within 60 min for Ce/MCM-41 and Ce/SS, respectively. Characterization results suggest that Ce loading significantly increases the surface Lewis acidic sites, which would synergize with Ce3+/Ce4+ redox cycle for the activity improvement. With the aid of in situ electron paramagnetic resonance (EPR) spectra and quenching tests, hydroxyl radical (·OH), superoxide radical (O2•–), and singlet oxygen (1O2) are identified as the O3 catalytic decomposition products, while ·OH mainly accounts for NB mineralization. The detailed degradation route of NB was further investigated by the multi-chromatography analysis. NB is firstly oxidized into polyhydroxy compounds, followed by small molecular organic acids, and finally being mineralized into CO2 and H2O. This study established a facile strategy to synthesize highly active and stable Ce/SiO2 catalysts for catalytic ozonation, and elucidated the in-depth mechanisms for the activity origins of the Ce loaded silica-based materials in catalytic ozonation processes (COP).</p

    Loss of dendritic arbor complexity subsequent to ischemic stroke in ipsilateral layer II/III and layer V neurons of the motor cortex.

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    A–F, Representative images of Golgi–Cox-stained (left panels) and individual Imaris-reconstructed (right panels) layer II/III (A–C) and layer V (D–F) pyramidal neurons of M1 from the ipsilateral side of sham-treated control mice (A, D) and of mice subjected to 30-minute MCAO analyzed after 6 hours (B, E) and 24 hours (C, F) reperfusion times. The position of the cell bodies are marked by a gray dot. Scale bars, 30 μm. G–N, Quantitative determinations of dendritic branching points, terminal points, total dendritic tree length, and Sholl intersections of dendritic trees in layer II/III (G–J) and layer V (K–N). Note that all parameters of dendritic complexity at the ipsilateral side decreased subsequent to MCAO and that layer II/III neurons responded faster, as they already show the decreased dendritic arborization at 6 hours after MCAO (for contralateral data, see S3 Fig). Layer II/III: nSham = 60; nMCAO+6h = 22; nMCAO+24h = 11 neurons. Layer V: nSham = 47; nMCAO+6h = 19; nMCAO+24h = 18 neurons from 3 mice for each MCAO group and 6 mice for the sham control (ipsi). Quantitative data represent mean ± SEM. Statistical significance calculations, 1-way ANOVA with Tukey posttest (G–I, K–M) and 2-way ANOVA with Sidak posttest for Sholl analysis (J, N), respectively. *P **P ***P S4 Data. MCAO, middle cerebral artery occlusion; WT, wild-type.</p

    Numerical data underlying the quantitative data panels of S6 Fig.

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    This Excel file contains all numerical information of all data panels in S6 Fig organized in form of subfolders. The data include mean, SEM, n number, and all individual data points. (XLSX)</p

    Numerical data underlying the quantitative data panels of Fig 4.

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    This Excel file contains all numerical information of all data panels in Fig 4 organized in form of subfolders. The data include mean, SEM, n number, and all individual data points. (XLSX)</p

    (Related to Fig 5).

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    The dendritic arborization of neurons at the contralateral side is not affected by the MCAO-induced dendritic regrowth processes occurring simultaneously at the ipsilateral side. A–L, Quantitative determinations of dendritic arborization parameters of layer II/III neurons (A–F) and layer V neurons (G–L) in the contralateral M1. Note that, at the contralateral side, dendritic branching points (A, G), dendritic terminal points (B, H), total dendritic tree length (C, I) and Sholl intersections (D–F, J–L) at different reperfusion times all remained similar to their respective sham controls and at the same level for all 3 time points (24 hours, 4 days, and 7 days). Layer II/III: nSham+24h = 29; nMCAO+24h = 53; nSham+4d = 38; nMCAO+4d = 29; nSham+7d = 46; nMCAO+7d = 49 neurons from 3 mice for the sham+24h, sham+4d and MCAO+4d groups, and from 6 mice for the sham+7d, MCAO+24h, and MCAO+7d groups (3 to 4 months of age). Layer V: nSham+24h = 17; nMCAO+24h = 57; nSham+4d = 30; nMCAO+4d = 30; nSham+7d = 57; nMCAO+7d = 50 neurons from 3 mice of each group. For corresponding ipsilateral data, see Fig 5. Data, mean ± SEM. Statistical significances were calculated using 2-way ANOVA with Sidak posttest (all n.s.). The numerical data underlying this figure can be found in S12 Data. MCAO, middle cerebral artery occlusion. (TIF)</p

    Numerical data underlying the quantitative data panels of S4 Fig.

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    This Excel file contains all numerical information of all data panels in S4 Fig organized in form of subfolders. The data include mean, SEM, n number, and all individual data points. (XLSX)</p
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