Controllable Interfacial Polymerization for Nanofiltration Membrane Performance Improvement by the Polyphenol Interlayer

It is a huge challenge to have a controllable interfacial polymerization in the fabrication process of nanofiltration (NF) membranes. In this work, a polyphenol interlayer consisting of polyethyleneimine (PEI)/tannic acid (TA) was simply assembled on the polysulfone (PSf) substrate to fine-tune the interfacial polymerization process, without additional changes to the typical NF membrane fabrication procedures. In addition, three decisive factors in the interfacial polymerization process were examined, including the diffusion kinetics of fluorescence-labeled piperazine (FITC-PIP), the spreading behavior of the hexane solution containing acyl chloride, and the polyamide layer formation on the porous substrate by in situ Fourier transform infrared (FT-IR) spectroscopy. The experimental results demonstrate that the diffusion kinetics of FITC-PIP is greatly reduced, and the spreading behavior of the hexane solution is also impeded to some extent. Furthermore, in situ FT-IR spectroscopy demonstrates that by the mitigation of this PEI/TA interlayer, the interfacial polymerization process is greatly controlled. Moreover, the as-prepared NF membrane exhibits an increased water permeation flux of 65 L m–2 h–1 (at the operation pressure of 0.6 MPa), high Na2SO4 rejection of >99%, and excellent long-term structural stability

Air quality benefit of China’s mitigation target to peak its emission by 2030

<p>In 2015, China committed to reducing its emission intensity per unit of gross domestic product by 60–65% from its 2005 rate and to peak its carbon emission by 2030. Problems related to local pollutants and haze are simultaneously worsening in China. This article focuses on the critical topic of co-controlling carbon emission and local air pollutants and evaluates the co-benefit of carbon mitigation in local pollutant reduction by using a partial equilibrium model that links carbon emission and local air pollutants at the technological level. Three conclusions can be drawn from the scenario analysis. First, in the reference scenario, energy consumption and carbon emission continue to increase and air quality is expected to deteriorate in the future. Therefore, current pollutant control measures should be improved. Second, local pollutants will be significantly reduced in the end-of-pipe control scenario, but the reduction will still be inadequate to fulfil the air quality target. Third, emissions of SO₂, NO<i>_x</i>, and PM_2.5 in 2030 will be reduced by 78.85%, 77.56%, and 83.32%, respectively, compared with the 2010 levels in the co-control scenario involving the peaking effort in China. Therefore, the air quality targets can also be achieved when the peaking target is fulfilled. The Nationally Determined Contribution (INDC) of China to peak its emission by 2030 is consistent with its domestic interest to improve local air quality.</p> <p><b>POLICY RELEVANCE</b></p> <p>China submitted its INDC to the United Nations Framework Convention on Climate Change in 2015 and has promised to peak its carbon emission by 2030. In recent years, China has also faced severe pressure to address its air pollution problem. Air quality is an important driving force to incentivize more ambitious mitigation measures that can contribute to the simultaneous reduction of carbon emission and air pollutants. Air quality benefit provides a strong justification for the INDC of China and the possibility of early peaking. Moreover, the co-benefit in China can be a reference for other developing countries that are facing the same challenge and can reinforce the initiative of these countries to promote ambitious mitigation actions.</p

T cell specific cytokine pattern in the lungs of pDC depleted mice following <i>Cpn</i> infection.

<p>Following <i>Cpn</i> infection (day 9), the cytokine pattern of CD8 and CD4 T cells in the lungs of pDC depleted and control mice was analysed by intracellular cytokine staining. Graphs show the summary data for TNFα <i>(</i><b><i>A</i></b><i>),</i> and IFNγ <i>(</i><b><i>B</i></b><i>)</i> production by CD8 and CD4 T cells and IL-4 <i>(</i><b><i>C</i></b><i>)</i> and IL-10 <i>(</i><b><i>D</i></b><i>)</i> production by CD4 T cells. Data are expressed as mean ± SD. Three independent experiments with three mice in each group were performed and one representative experiment is shown. *, p<0.05, **, p<0.01.</p

<i>Cpn</i> infection activated pDCs induce Treg IL-10 production <i>in vitro</i>.

<p>pDC isolated from the lungs of <i>Cpn</i> infected (day 9 p.i.) and uninfected mice were co-cultured with CD4 T cells purified from <i>Cpn</i> immunized mice in the presence of SK-EB as described in the <i>Materials & Methods.</i> Following three days of co-culture, the cells were washed and analysed by flow cytometry. <b><i>A&B</i></b>, The cells were stained for intracellular Foxp3 expression. The analysis was performed on gated CD4+ cells. Representative histograms <i>(</i><b><i>A</i></b><i>)</i> are shown and the summary graph <i>(</i><b><i>B</i></b><i>)</i> provided. <b><i>C&D,</i></b> IL-10 production by Tregs; analysis was performed on CD4+Foxp3+ gated cells. Shown are representative dot plots <i>(</i><b><i>C</i></b><i>)</i> and a graphical summary <i>(</i><b><i>D</i></b><i>)</i> of the percentages of IL-10 producing Tregs. Data are shown as mean ± SD. Results of one representative (of three) experiment with five mice in each group are shown. *, p<0.05, **, p<0.01.</p

Reduced Treg numbers and lower IL-10 production by Tregs in pDC depleted mice.

<p>The frequencies of Tregs in the lungs and dLNs in pDC depleted and the sham-treated mice were analyzed following <i>Cpn</i> infection (day 9 p.i.). <b><i>A,</i></b> representative flowcytometry images show the percentages of CD4+Foxp3+ Tregs in the lungs and dLN<b>.</b> The absolute numbers of Tregs were depicted in the respective graphs. <b><i>B</i></b><i>,</i> Intracellular staining for IL-10; The dLN cells were cultured with SK-EB for 3 days and restimulated with PMA and ionomycin. The cells were stained first for surface markers, fixed, permeabilized and stained intracellularly for IL-10 as described in <i>Materials and Methods.</i> Shown are representative flowcytometry plots and the summary graphs for IL-10 production by Tregs (gated on CD4+Foxp3+CD8− cells). Data expressed as mean ± SD. Results are representative of three independent experiments with three mice in each group. **, p<0.01, ***, p<0.001.</p

pDC deficiency leads to inflammatory type effector CD8 T and CD4 cell responses after <i>Cpn</i> infection.

<p>Lung T cells as described in the legends to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0083463#pone-0083463-g004" target="_blank">Figure 4</a> were analyzed by multi-color intracellular cytokine staining. Shown are representative flowcytometry dot plot images and summary graphs depicting the nature of cytokine responses by T cells. Analysis was performed on gated CD3+ CD8+ cells and CD3+CD4+ cells. Note increased inflammatory type-1 (IFNγ+TNFα+) CD8 <i>(</i><b><i>A</i></b><i>)</i> and CD4 T cells <i>(</i><b><i>B</i></b><i>)</i> and inflammatory Th2 type (IL-4+ TNFα+) CD4 T cells <i>(</i><b><i>C</i></b><i>)</i> in the lungs of pDC depleted mice compared to the control group mice. At least three independent experiments were performed and the data from one representative experiment is depicted. Data expressed as mean ± SD. *, p<0.05, and ***, p<0.001.</p

pDC deficiency <i>in vivo</i> leads to altered cytokine responses.

<p><b><i>A</i></b>, pDC depleted and the sham-treated mice (four mice/group), after <i>Cpn</i> infection were sacrificed 9 days postinfection and the lungs and draining (mediastinum) lymph nodes were collected. The draining lymph node (dLN) cells were cultured in the presence of SK-EB as described in <i>Materials and Methods</i>. Cytokine levels (IFN-γ, TNFα, IL-4 and IL-10) in 72-h dLN cell culture supernatants <i>(</i><b><i>A</i></b><i>)</i> and lung homogenates <i>(</i><b><i>B</i></b><i>)</i> were measured by ELISA. Data are presented as the mean ± SD of each group. Results of one of the three experiments with similar results are shown. *, <i>p</i><0.05, **, <i>p</i><0.01, and ***, <i>p</i><0.001; Student’s t test.</p

pDC depletion leads to increased bacterial loads and tissue inflammatory changes in the lungs.

<p>Mice were depleted of pDCs using anti-mPDCA Ab prior to and during the course of infection as described in the <i>Materials and Methods.</i> Control group mice received Rat IgG2b Ab. Following infection, the animals were monitored everyday for body weight changes (<b>A</b>). At day 9 p.i., the mice were sacrificed and the lungs were collected and quantitative assessment of bacterial loads was performed as described in <i>Materials and Methods</i>. <b><i>C,</i></b> Increased tissue pathological response in the lungs of pDC depleted mice compared to control mice as analysed by H&E staining. <b><i>D &E,</i></b> Shown are the graphs depicting differences in the percentage and absolute numbers of lung T cells (CD3+), Mφ, alveolar macrophages (F4/80+CD11c+ cells), cDCs, conventional DCs (F4/80−CD11c+ cells) and Gr, granulocytes (Gr-1+ F4/80−CD11c− cells). Results are shown as mean ± SD. Results of one representative (of three) experiment with four mice in each group are depicted. *, p<0.05, and ***, p<0.001.</p

Activation of pDCs following <i>Cpn</i> infection.

<p>C57BL/6 mice were intranasally infected with <i>Cpn</i> (3×10⁶ IFUs). Mice were killed at day 9 p.i., and lungs were aseptically collected. To analyse pDCs, lung cells were stained and analysed by flowcytometery as decribed in the <i>Materials and Methods</i>. pDCs were identified as mPDCA+ CD11c ^int/lo cells. <b><i>A,</i></b> pDC expansion after <i>Cpn</i> infection. Shown are representative dot plots with the percentages of pDCs in <i>Cpn</i> infected mice in comparison with uninfected mice (left) and the graphical summary for the absolute numbers of pDCs in the lungs. Total pDC number per mouse lung was calculated as % mPDCA+ CD11c ^int/lo cells x total number of cells per mouse lung/100. <b><i>B,</i></b> Expression of MHC II and costimulatory molecules CD40, CD80 and CD86 on gated pDCs (filled histograms) and isotype control (dotted line) are shown. The mean fluorescence intensity (<i>left</i>) and the percentages of positive cells (<i>right</i>) are indicated. <b><i>C,</i></b> pDCs purified (as described in <i>Materials and Methods</i>) from <i>Cpn</i> infected (PDC-Inf) and uninfected mice (PDC-N) were cultured in the presence or absence of <i>Cpn</i> (SK-EB). IL-12p40, IL-12p70 in the 72 hrs supernatants were measured by ELISA. IFNα production by pDCs was analysed by intracellular staining and the graph shows the percentages of IFNα producing cells. Results are shown as mean ± SD. At least three independent experiments with four mice in each group were performed and one representative experiment is shown. *, p<0.05, and ***, p<0.001, Student’s t test.</p