11 research outputs found

    Faradaic Rectification in Electrochemical Deionization and Its Influence on Cyclic Stability

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    Capacitive deionization (CDI) is a typical configuration of electrochemical deionization, which suffers from severe desalination capacity degradation derived from uncontrolled parasitic reactions. In this work, Faradaic rectification, the phenomenon by which electrode potentials and side reactions are dynamically regulated due to the asymmetrical anode/cathode Faradaic reactions, was studied under various CDI operation conditions. It was found that the Faradaic rectification in CDI would lead to capacity degradation indirectly by accelerating carbon anode oxidation and would be influenced by the cell voltage, flow rate, and asymmetric electrode construction. We also found an unconventional degradation mechanism in Faradaic cathode hybrid-CDI (HCDI) caused by the dramatic electrode-potential redistribution, which is derived from Faradaic rectification rather than the electrode structure decay. By adding a cation-exchange membrane to block the dissolved oxygen from cathode, the Faradaic rectification was suppressed successfully, and thus, the cyclic performance of CDI and HCDI was significantly increased by 59 and 46%, respectively (in 100 h cycling). This study provides an insight into understanding the Faradaic rectification in electrochemical deionization and its influence on CDI/HCDI cyclic stability, which should be of value to future explore cost-competitive membrane-less electrochemical deionization construction

    Selective Catalytic Hydrodechlorination of 1,2-Dichloroethane to Ethylene over Ni–Rh Nanoparticle Catalysts Supported on γ‑Al<sub>2</sub>O<sub>3</sub>

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    Ni catalysts decorated with trace Rh supported on γ-Al2O3 were prepared by the co-impregnation method. To obtain the Ni–Rh nanoparticles with different nanostructures and chemical compositions, bimetallic catalysts with varied Ni/Rh molar ratios were prepared. For comparison, monometallic Ni/γ-Al2O3 and Rh/γ-Al2O3 catalysts were also prepared by the impregnation method. The selective gas phase catalytic hydrodechlorination of 1,2-dichloroethane to ethylene was used to evaluate catalytic performances of the catalysts. The catalysts were characterized by X-ray diffraction, N2 adsorption, X-ray photoelectron spectroscopy, H2 temperature-programmed reduction, transmission electron microscopy–energy-dispersive X-ray, and CO chemisorption. It was found that the introduction of Rh to Ni catalyst facilitated the generation of spillover hydrogen which could enhance the ability of the Ni catalyst for H2 activation. In bimetallic catalysts, there was an intimate interaction between Ni and Rh, and isolated Rh sites were formed due to the dilution effect of Ni. Accordingly, compared with the monometallic Ni catalyst for gas phase catalytic hydrodechlorination of 1,2-dichloroethane, the bimetallic Ni–Rh(800)/γ-Al2O3 catalyst exhibited markedly higher 1,2-dichloroethane conversion (37%) and comparable selectivity to ethylene (95%). The findings in this study indicate that Ni–Rh/γ-Al2O3 with trace Rh can be used as a promising catalyst for highly effective and selective catalytic hydrodechlorination of chlorinated hydrocarbons

    MiR-140 increased the sensitivity of AECs to PTX.

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    <p>A: Morphological characteristics. Scale bars: 150 µm. TGF-β1 was added into miR-140- or ASO-140-transfected A549 cells for 24 h prior to PTX (50 nM) treatment. A549 cells treated with TGF-β1 or ASO-140 presented a fibroblast-like morphology, and the fibroblast-like morphology was reversed to epithelial-like characteristics in PTX- or PTX+miR-140-treated cultures. B: Western blot analysis. The levels of vimentin, Smad3 and p-Smad3 levels were increased and E-cadherin was downregulated in TGF-β1-treated A549 cells, which were reversed in PTX-, or PTX+miR-140-treated cells, especially in both PTX and miR-140-treated cultures. n = 3 replicates.</p

    Lung-to-body weight ratio, the pulmonary inflammation and fibrosis scores.

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    *<p><i>P</i><0.05 versus saline-treated control,</p>**<p><i>P</i><0.05 versus BLM-treated 28 d rats, n = 12.</p

    MiR-140 suppresses the TGF-β1/Smad3 pathway in A549 cells.

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    <p>A: Fluorescence microscope detection. Scale bars: 150 µm. B: Flow cytometry analysis. n = 3 replicates. Control, cells untreated with miRNA or plasmid; GFP-Smad3, cells treated with pcDNA-GFP-UTR; D-NC, cells treated with both D-NC (miR-140 mutation control) and pcDNA-GFP-UTR plasmid; S-NC, cells treated with both S-NC (the single-stranded RNA control) and pcDNA-GFP-UTR; miR-140, cells treated with both miRNA-140 and pcDNA-GFP-UTR; ASO-140, cells treated with both ASO-140 and pcDNA-GFP-UTR. In <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070725#pone-0070725-g004" target="_blank">Fig. 4 A, B</a>, GFP expression and the number of GFP-positive cells in miR-140-treated cultures were much lower than those in D-NC- or ASO-140-treated controls. C: Western blot analysis. The gene expression/α-tubulin ratios were shown on the right of gel. The miR-140 treatment led to an obvious reduction in the expression of TGF-β1, vimentin, Smad3 and p-Smad3 compared to the D-NC control groups. α-tubulin was used as loading controls. *<i>P</i><0.05 versus miR-140 treatment, **<i>P</i><0.05 versus ASO-140 treatment, n = 3 replicates.</p

    The sequences of chemically synthesized oligos.

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    a<p>The selected miRNAs were chemically synthesized in the form of small interfering RNA (siRNA) duplexes.</p>*<p>the bold and underlined letters were the mutation sites of miRNA.</p

    PTX ameliorates pulmonary fibrosis andu pregulates miR-140 in fibrotic lungs.

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    <p>A: Upper, Haematoxylin and eosin (HE). The lungs initiated alveolar disruption on 7 d, and more severe on 28 d, while pulmonary fibrosis was ameliorated by PTX (0.6 mg/kg) treatment. Lower, Masson's trichrome for collagen and elastin evaluation. The lungs underwent a slight fibrotic invasion on 7 d, and more aggressive on 28 d, which was alleviated by PTX. Scale bars: 150 µm. B: Type-I collagen ELISA analysis. The type-I collagen level showed basally low in lung tissues of rats instilled with saline (sham control rats), similar to those in the untreated lungs (0 d). The collagen I levels in BLM-treated lung tissues on 28 d were increased seven folds than those in untreated or sham control lung tissues. Collagen I levels were reduced obviously in PTX-treated lungs compared to BLM-treated 28 d lung tissues. *<i>P</i><0.05 versus 28 d. C: Hydroxyproline analysis. BLM-treated lungs had much higher levels of hydroxyproline, but PTX treatment significantly decreased hydroxyproline levels compared to BLM-treated 28 d lungs. *<i>P</i><0.05 versus 28 d. D: Quantitative RT-PCR analysis of miR-140 expression. U6 was used as a control. n = 3 replicates. The miR-140 level in BLM-instilled rat lungs reached its nadir on 7 d, approximately two folds lower than that in untreated or sham control lung tissues, while it was dramatically upregulated in PTX-treated lung tissues. *<i>P</i><0.05 versus 0 d. **<i>P</i><0.05 versus PTX. E: miR-140 expression in human pulmonary fibrotic lungs. a–e: healthy control lungs, f–j: human pulmonary fibrosis lungs. The miR-140 levels are obvious lower in humanulmonary fibrotic lung tissues compared with those in healthy control lungs.</p

    MiR-140 affected EMT and Smad3/p-Smad3 expression.

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    <p>A: Morphological characteristics. Scale bars: 150 µm. A549 cells treated with TGF-β1 or TGF-β1+ D-NC underwent a fibroblast-like morphology, while their morphologies were reversed by miR-140 or miR-140 plus PTX treatment. B: Western blot analysis. α-tubulin was used as loading controls. The Smad3 and p-Smad3 levels were decreased obviously in miR-140- or PTX+miR-140-treated A549 cells, especially in PTX+miR-140-treated cells, compared to those in TGF-β1- or TGF-β1+D-NC-treated cultures. n = 3 replicates.</p

    PTX suppresses the TGF-β1/Smad3 signaling pathway.

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    <p>A: Smad3 and p-Smad3 expression in A549 cells by western blot analysis. α-tubulin was used as loading controls. B: Quantitative RT-PCR analysis of Smad3 expression in A549 cells. GAPDH was used a control gene. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070725#pone-0070725-g003" target="_blank">In Fig. 3A,B</a>, TGF-β1-treatment increased the expression of p-Smad3 and Smad3 in A549 cells, which could be reduced by PTX treatment. *<i>P</i><0.05 versus TGF-β1 treatment group, n = 3 replicates. C: Immunohistochemical staining of Smad3, p-Smad3 and α-SMA in rat lung tissues. Black arrows, Smad3, p-Smad3 or α-SMA positive staining AECs. Stars, vasculature. Scale bars: 150 µm. A majority of Smad3, p-Smad3 and α-SMA staining was found to be localized in the AECs of fibrotic lungs. The BLM-untreated (0 d) or sham control lung tissues showed almost a total absence of α-SMA and p-Smad3. TGF-β1-treatment increased the expression of p-Smad3 and α-SMA in fibrotic lungs (7 d, 28 d), which was restored by PTX treatment to some extent. D: Western blot analysis. E: The ratios of Smad3 (p-Smad3, or α-SMA)/α-tubulin of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070725#pone-0070725-g003" target="_blank">Fig. 3D</a>. α-tubulin was used as the internal standard. n = 3 replicates. F: Quantitative RT-PCR analysis of Smad3 and α-SMA expressions in rat lung tissues (n = 3 replicates). GAPDH was used as a control gene. In <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070725#pone-0070725-g003" target="_blank">Fig. 3D–F</a>: the quantity of p-Smad3 in lung tissues reached peaked on day 7 and the quantity of α-SMA in lung tissues reached peaked on day 28 after BLM treatment. PTX could reduce the expression of p-Smad3 and α-SMA obviously, but had no effect on Smad3. *<i>P</i><0.05 versus 0 d. **<i>P</i><0.05 versus PTX.</p

    Popcorn-Derived Porous Carbon Flakes with an Ultrahigh Specific Surface Area for Superior Performance Supercapacitors

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    Popcorn-derived porous carbon flakes have been successfully fabricated from the biomass of maize. Utilizing the “puffing effect”, the nubby maize grain turned into materials with an interconnected honeycomb-like porous structure composed of carbon flakes. The following chemical activation method enabled the as-prepared products to possess optimized porous structures for electrochemical energy-storage devices, such as multilayer flake-like structures, ultrahigh specific surface area (<i>S</i><sub>BET</sub>: 3301 m<sup>2</sup> g<sup>–1</sup>), and a high content of micropores (microporous surface area of 95%, especially the optimized sub-nanopores with the size of 0.69 nm) that can increase the specific capacitance. The as-obtained sample displayed excellent specific capacitance of 286 F g<sup>–1</sup> at 90 A g<sup>–1</sup> for supercapacitors. Moreover, the unique porous structure demonstrated an ideal way to improve the volumetric energy density performance. A high energy density of 103 Wh kg<sup>–1</sup> or 53 Wh L<sup>–1</sup> has been obtained in the case of ionic liquid electrolyte, which is the highest among reported biomass-derived carbon materials and will satisfy the urgent requirements of a primary power source for electric vehicles. This work may prove to be a fast, green, and large-scale synthesis route by using the large nubby granular materials to synthesize applicable porous carbons in energy-storage devices
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