536 research outputs found

    Categorical colormap optimization with visualization case studies

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    Mapping a set of categorical values to different colors is an elementary technique in data visualization. Users of visualization software routinely rely on the default colormaps provided by a system, or colormaps suggested by software such as ColorBrewer. In practice, users often have to select a set of colors in a semantically meaningful way (e.g., based on conventions, color metaphors, and logological associations), and consequently would like to ensure their perceptual differentiation is optimized. In this paper, we present an algorithmic approach for maximizing the perceptual distances among a set of given colors. We address two technical problems in optimization, i.e., (i) the phenomena of local maxima that halt the optimization too soon, and (ii) the arbitrary reassignment of colors that leads to the loss of the original semantic association. We paid particular attention to different types of constraints that users may wish to impose during the optimization process. To demonstrate the effectiveness of this work, we tested this technique in two case studies. To reach out to a wider range of users, we also developed a web application called Colourmap Hospital

    Facial expression recognition in dynamic sequences: An integrated approach

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    Automatic facial expression analysis aims to analyse human facial expressions and classify them into discrete categories. Methods based on existing work are reliant on extracting information from video sequences and employ either some form of subjective thresholding of dynamic information or attempt to identify the particular individual frames in which the expected behaviour occurs. These methods are inefficient as they require either additional subjective information, tedious manual work or fail to take advantage of the information contained in the dynamic signature from facial movements for the task of expression recognition. In this paper, a novel framework is proposed for automatic facial expression analysis which extracts salient information from video sequences but does not rely on any subjective preprocessing or additional user-supplied information to select frames with peak expressions. The experimental framework demonstrates that the proposed method outperforms static expression recognition systems in terms of recognition rate. The approach does not rely on action units (AUs) and therefore, eliminates errors which are otherwise propagated to the final result due to incorrect initial identification of AUs. The proposed framework explores a parametric space of over 300 dimensions and is tested with six state-of-the-art machine learning techniques. Such robust and extensive experimentation provides an important foundation for the assessment of the performance for future work. A further contribution of the paper is offered in the form of a user study. This was conducted in order to investigate the correlation between human cognitive systems and the proposed framework for the understanding of human emotion classification and the reliability of public databases

    Rational Design of High-Performance Phosphine Sulfonate Nickel Catalysts for Ethylene Polymerization and Copolymerization with Polar Monomers

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    Use of palladium catalysts in olefin polymerization and copolymerization has evolved rapidly. In contrast, earth-abundant and low-cost nickel catalysts generally suffer from drawbacks that include low thermal stability and generation of low-molecular-weight polymers in the presence of polar monomers. By taking advantage of several design strategies, high-performance phosphine-sulfonate-based nickel catalysts were developed. These nickel catalysts demonstrated high activities and thermal stabilities to afford high-molecular-weight polyethylene. Most importantly, high-molecular-weight copolymers could be generated through the copolymerization of ethylene with a variety of polar monomers

    Additional file 3: Figure S1. of Genome-wide expression profiling of microRNAs in poplar upon infection with the foliar rust fungus Melampsora larici-populina

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    Precursor sequences and the predicted secondary structures of the 20 novel miRNAs from P. szechuanica (“(”represent base matches, “.” represent base mismatches). (PDF 387 kb

    ROS-dependent G2/M cell cycle arrest by DHA and IR respectively.

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    <p>(A) Dynamical fluorescence images of ROS generation in living cells after DHA treatment. Cells were incubated with 20 µM DCFH-DA, an oxidation-sensitive fluorescent probe, for 30 min in the dark and then treated with DHA. The levels of intracellular ROS were monitored by a confocal microscope. Scale bar: 20 µm. (B) Dynamics of DHA-induced ROS generation corresponding to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0059827#pone-0059827-g002" target="_blank">Figure 2</a> (A). (C and D) FCM assay of ROS generation at 30 min (C) and 120 min (D) after IR, DHA and combination treatment, respectively. (E and F) ROS-dependent G<sub>2</sub>/M arrest induced by IR (E) and DHA (F) respectively analyzed by FCM. Cells were irradiated with IR or DHA in the presence or absence of NAC, and then stained with 5 µg/ml of PI before being analyzed by FCM. *<i>*P</i><0.01, compared with control; <sup>##</sup><i>P</i><0.01, compared with DHA treatment alone (E) and <sup>##</sup><i>P<0.01</i> and <sup>&&</sup><i>P<0.01</i>, compared with IR treatment alone (F).</p

    IR potentiates DHA-induced extrinsic apoptosis pathway.

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    <p>(A–B): IR did not accelerate the DHA-induced loss of Δψ<sub>m</sub> at 24 h (A) and 36 h (B) after treatment assessed by FCM. <i>**P</i><0.01, compared with control. (C) IR did not accelerate DHA-induced caspase-9 activation. <i>**P</i><0.01, compared with control. (D and E) IR accelerated DHA-induced activation of caspase-8 (D) and -3 (E). Cells treated with IR were then cultured with DHA for 36 h. Caspase-8, -9 and -3 activities were measured by the fluorescence substrate Ac-IETD-AFC, Ac-LEHD-AFC and Ac-DEVD-AFC, respectively. <i>**P</i><0.01, compared with control, <i><sup>##</sup>P</i><0.01, compared with treatment with DHA alone.</p

    DHA induces apoptosis via both extrinsic and intrinsic apoptosis pathways.

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    <p>(A) DHA induced activation of caspase-8 and -9 assessed by fluorometric assay. Cells were treated with DHA for 36 h. **<i>P</i><0.01, compared with control. (B) DHA induced caspase-8- and -9-dependent caspase-3 activation by fluorometric assay. Cells were treated with DHA for 48 h in the presence or absence of zIETD-fmk and zLEHD-fmk, respectively. <i>**P</i><0.01, compared with control; <i><sup>##</sup>P</i><0.01, compared with DHA treatment alone. (C) DHA induced caspase-8- and -9-dependent cytotoxicity assessed by CCK-8 assay. Cells were treated with DHA for 24 and 48 h in the presence or absence of zIETD-fmk and zLEHD-fmk, respectively. *8<i>P<0.01</i>, compared with control; <sup></sup><i>P<0.05</i>,<sup></sup><i>P<0.05</i>, <sup>$</sup><i>P<0.01</i> and <sup>&</sup><i>P</i><0.05, compared with DHA treatment alone. (D) DHA ROS-mediated apoptosis assessed by FCM. **<i>P<0.01,</i> compared with control; <sup>##</sup><i>P<0.01</i>compared with DHA alone. (E) DHA induced ROS-dependent caspase-8 activation. **<i>P<0.01</i>, compared with control; <sup>##</sup><i>P<0.01</i>, compared with DHA treatment alone. (F) DHA induced ROS- and caspase-8-dependnent loss of Δψ<sub>m</sub> determined by FCM analysis. <i>**P</i><0.01, compared with control; <sup>##</sup><i>P<0.01</i>, compared with DHA treatment alone. (G) DHA induced caspase-8-dependent caspase-9 activation. *<i>P<0.05</i> and **<i>P<0.01</i>, compared with control; <sup>#</sup><i>P<0.05</i>, compared with DHA treatment alone. (H) Typical fluorescence images of Bid translocation to mitochondria inside single living cell after DHA treatment for 36 h. Control cells show the uniform distribution of Bid, while DHA-treated cells show the co-localization between Bid and mitochondria. Scale Bar: 5 µm.</p

    IR synergistically enhances DHA-induced G<sub>2</sub>/M arrest and apoptosis.

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    <p>(A) FCM analysis of cells cycle after low-dose IR treatment for 24 h and 36 h in the presence or absence of DHA. (B and C): IR potentiated the DHA-induced G<sub>2</sub>/M arrest at 24 h (B) and apoptosis at 36 h (C) analyzed by FCM. <i>**P</i><0.01, compared with treatment with control; <i><sup>##</sup>P</i><0.01, compared with DHA treatment alone, <i><sup></sup>P</i><0.01 compared with 2 Gy IR treatment; <i><sup>&&</sup>P</i><0.01, compared with 4 Gy IR treatment. Cells treated with different doses of IR were cultured with 20 µg/ml of DHA for indicated time and then stained with 5 µg/ml of PI before being analyzed by FCM.</p
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