20 research outputs found

    Simplified ICA based denoising method

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    Hyvarinen et al have developed an ICA based method for image denoising. The major advantage of their method is that the transformation matrix can by adjusted to suit the available data. However, in their method, the transformation matrix and shrinkage parameters need to be learned from noise-free data. In this paper, we propose a simplified shrinkage scheme, which has only one heuristic control parameter. Experimental results show that the ICA based method with this new shrinkage scheme achieves comparable performance as that of Hyvarinen et al.</p

    Study on the Performance of a Surface with Coupled Wettability Difference and Convex-Stripe Array for Improved Air Layer Stability

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    The existence of an air layer reduces friction drag on superhydrophobic surfaces. Therefore, improving the air layer stability of superhydrophobic surfaces holds immense significance in reducing both energy consumption and environmental pollution caused by friction drag. Based on the properties of mathematical discretization and the contact angle hysteresis generated by the wettability difference, a surface coupled with a wettability difference treatment and a convex-stripe array is developed by laser engraving and fluorine modification, and its performance in improving the air layer stability is experimentally studied in a von Kármán swirling flow field. The results show that the destabilization of the air layer is mainly caused by the Kelvin–Helmholtz instability, which is triggered by the density difference between gas and liquid, as well as the tangential velocity difference between gas and liquid. When the air layer is relatively thin, tangential wave destabilization occurs, whereas for larger thicknesses, the destabilization mode is coupled wave destabilization. The maximum Reynolds number that keeps the air layer fully covering the surface of the rotating disk (with drag reduction performance) during the disk rotation process is defined as the critical Reynolds number (Rec), which is 1.62 × 105 for the uniform superhydrophobic surface and 3.24 × 105 for the superhydrophobic surface with a convex stripe on the outermost ring (SCSSP). Individual treatments of wettability difference and a convex-stripe array on the SCSSP further improve the air layer stability, but Rec remains at 3.24 × 105. Finally, the coupling of the wettability difference treatment with a convex-stripe array significantly improves the air layer stability, resulting in an increase of Rec to 4.05 × 105, and the drag reduction rate stably maintained around 30%

    A Water-Stable 3D Luminescent Metal−Organic Framework Based on Heterometallic [Eu<sup>III</sup><sub>6</sub>Zn<sup>II</sup>] Clusters Showing Highly Sensitive, Selective, and Reversible Detection of Ronidazole

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    A water-stable 3D luminescent metal–organic framework (MOF), [Eu<sub>6</sub>Zn­(ÎŒ<sub>3</sub>-OH)<sub>8</sub>(NDC)<sub>6</sub>(H<sub>2</sub>O)<sub>6</sub>]<sub><i>n</i></sub> (<b>1</b>), constructed from heterometallic [Eu<sup>III</sup><sub>6</sub>Zn<sup>II</sup>] clusters and electron-rich π-conjugated 1,4-naphthalenedicarboxylic acid (H<sub>2</sub>NDC) ligands exhibits highly sensitive, selective, and reversible detection of ronidazole, which represents the first example of luminescent MOFs based on Ln-TM heterometallic clusters for the detection of antibiotics in aqueous solution

    SOCS3 inhibiting migration of A549 cells correlates with PYK2 signaling in vitro-4

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    YK2 expression. A549 cells were vector- or the SOCS-box mutant-transfected for 48 h, and cell lysates were analysed by western blot using the indicated antibodies. (b) PYK2 mRNA levels were unaffected regardless of transfection or not. The amplified PYK2 products were 629 bp in length. ÎČ-actin amplification demonstrated the consistency of PT-PCR. (c) Cell migration suppressed by the SOCS-box mutant was not statistically significant. The values are means of three replicates.<p><b>Copyright information:</b></p><p>Taken from "SOCS3 inhibiting migration of A549 cells correlates with PYK2 signaling in vitro"</p><p>http://www.biomedcentral.com/1471-2407/8/150</p><p>BMC Cancer 2008;8():150-150.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2429913.</p><p></p

    (a) Methylation status of SOCS3 in HBE and A549 cells, using the primer set designed in the exon 2, and detection of SOCS3 expression by western blot

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    The observed bands in lane M are methylated 159 bp products with methylation-specific primers and that in lane U are unmethylated 159 bp products with unmethylation-specific primers. Methylation was found in A549 cells but not in HBE cells and HBE cells expressed higher level of SOCS3. (b) The visible band in lane U appeared in A549 cells and SOCS3 was reactivated by the treatment of 5-aza-2'-deoxycytidine. The results are representative of three independent experiments.<p><b>Copyright information:</b></p><p>Taken from "SOCS3 inhibiting migration of A549 cells correlates with PYK2 signaling in vitro"</p><p>http://www.biomedcentral.com/1471-2407/8/150</p><p>BMC Cancer 2008;8():150-150.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2429913.</p><p></p

    (a) PYK2 expression, Tyr402 and ERK1/2 phosphorylations in HBE and A549 cells by western blot

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    (b) Comparisons of migratory abilities between HBE and A549 cells by Transwell assay. The data are representative of three individual experiments.<p><b>Copyright information:</b></p><p>Taken from "SOCS3 inhibiting migration of A549 cells correlates with PYK2 signaling in vitro"</p><p>http://www.biomedcentral.com/1471-2407/8/150</p><p>BMC Cancer 2008;8():150-150.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2429913.</p><p></p

    JAM-A knockdown impaired cell cycle progression.

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    <p>Effectiveness of JAM-A knockdown on cell cycle progression was analyzed by fluorescence-activated cell sorting. Data are shown as a representative experiment (Left panel), the percentage of cells in different cell cycle phase is shown as the mean ± SD of 3 independent experiments, *p<0.05; **p<0.01 (right panel).</p

    MicroRNA-449a Is Downregulated in Non-Small Cell Lung Cancer and Inhibits Migration and Invasion by Targeting c-Met

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    <div><p>MicroRNA-449a is expressed at a low level in several tumors and cancer cell lines, and induces G1 arrest, apoptosis, and senescence. To identify the function of miR-449a in non-small cell lung cancer (NSCLC), we discussed the potential relevance of miR-449a to clinicopathological characteristics and prognosis in NSCLC. We also investigated the impact of miR-449a on migration and invasion in NSCLC cells. The expression of miR-449a in NSCLC tissues and cell lines was detected using RT-qPCR. <i>In vitro</i>, gain-of-function, loss-of-function experiments, and fluorescence assays were performed to identify the potential target of miR-449a and the function of miR-449a in NSCLC cells. MiR-449a was downregulated in both NSCLC tissues and cell lines. Moreover, a low expression level of miR-449a appeared to be correlated with lymph node metastasis and poor survival. <i>In vitro</i>, miR-449 regulated cell migration and invasion in NSCLC cells as a potential tumor suppressor, at least in part by targeting c-Met. Furthermore, reciprocal expression of miR-449a and c-Met was shown in NSCLC tissue samples. This study indicates that miR-449a might be associated with NSCLC progression, and suggests a crucial role for miR-449a in NSCLC.</p></div

    Expression of miR-449a was downregulated in NSCLC cell lines.

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    <p>The relative quantity of miR-449a in 4 NSCLC cell lines were compared to the mean expression level of 10 normal lung specimens based on the equation RQ = 2<sup>–ΔΔCT</sup>.</p
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