Preparation and Antiscaling Performance of Superhydrophobic Poly(phenylene sulfide)/Polytetrafluoroethylene Composite Coating

In this paper, the superhydrophobic poly­(phenylene sulfide) (PPS)/polytetrafluoroethylene (PTFE) composite coating was fabricated and applied to evaluate the antiscaling performance. Compared with the commercial hydrophobic epoxy–silicone resin coating, the superhydrophobic PPS/PTFE composite coating exhibited unique antiscaling performance. The deposition rate of CaCO₃ scaling on the superhydrophobic PPS/PTFE coating was only 38.6% of that on the epoxy–silicone resin coating. The surface morphology, size, and crystal type of the scaling were analyzed. The results indicated that the formation and growth of CaCO₃ scaling were significantly influenced by the cooperative effect of topography and low surface energy of the superhydrophobic PPS/PTFE composite coating. There were few nucleation sites at the surface of superhydrophobic coating owing to the relatively low surface energy and absorbed bubbles. Together with the space constraint of the topography, the nucleation and growth of CaCO₃ scaling were inhibited on the surface of superhydrophobic PPS/PTFE coating

Highly Active Ni₂P Catalyst Supported on Core–Shell Structured Al₂O₃@TiO₂ and Its Performance for Benzofuran Hydrodeoxygenation

Highly active Ni₂P catalyst supported on Al₂O₃@TiO₂ (core@shell) for hydrodeoxygenation (HDO) of benzofuran (BF) was described. The effect of the TiO₂ shell thickness on the structure and HDO properties of Ni₂P/Al₂O₃@TiO₂ was studied. The results showed that an appropriate TiO₂ shell thickness can effectively suppress the formation of AlPO₄ and change the transmission mechanism of Ni₂P particles, which is beneficial to the formation of highly dispersed Ni₂P particles on the Al₂O₃ core. The Ni₂P/A@T-25 showed the best HDO activity of 95% with oxygen-free products yield of 87% among the as-prepared Ni₂P/Al₂O₃@TiO₂ catalysts. As compared with Ni₂P/Al₂O₃ (BF conversion of 78% with oxygen-free products yield of 47%), the BF conversion and yields of oxygen-free products over Ni₂P/A@T-25 catalyst were increased by 22% and 85%, respectively

Methane Upgrading of Acetic Acid as a Model Compound for a Biomass-Derived Liquid over a Modified Zeolite Catalyst

The technical feasibility of coaromatization of acetic acid derived from biomass and methane was investigated under mild reaction conditions (400 °C and 30 bar) over silver-, zinc-, and/or gallium-modified zeolite catalysts. On the basis of GC-MS, Micro-GC, and TGA analysis, more light aromatic hydrocarbons, less phenol formation, lower coke production, and higher methane conversion are observed over 5%Zn-1%Ga/ZSM-5 catalyst in comparison with catalytic performance over the other catalysts. Direct evidence of methane incorporation into aromatics over 5%Zn-1%Ga/ZSM-5 catalyst is witnessed in ¹H, ²H, and ¹³C NMR spectra, revealing that the carbon from methane prefers to occupy the phenyl carbon sites and the benzylic carbon sites, and the hydrogen of methane favors the aromatic and benzylic substitutions of product molecules. In combination with the ¹³C NMR results for isotopically labeled acetic acid (¹³CH₃COOH and CH₃¹³COOH), it can be seen that the methyl and carbonyl carbons of acetic acid are equally involved in the formation of ortho, meta and para carbons of the aromatics, whereas the phenyl carbons directly bonded with alkyl substituent groups and benzylic carbons are derived mainly from the carboxyl carbon of acetic acid. After various catalyst characterizations by using TEM, XRD, DRIFT, NH₃-TPD, and XPS, the excellent catalytic performance might be closely related to the highly dispersed zinc and gallium species on the zeolite support, moderate surface acidity, and an appropriate ratio of weak acidic sites to strong acidic sites as well as the fairly stable oxidation state during acetic acid conversion under a methane environment. Two mechanisms of the coaromatization of acetic acid and methane have also been proposed after consulting all the collected data in this study. The results reported in this paper could potentially lead to more cost-effective utilization of abundant natural gas and biomass

Additional file 1: of Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy

Figure S1. T cell stimulated with αCD3/αCD28 microbeads proliferate in the presence of dexamethasone.Healthy donor T cells were cultured for four days with the indicated ratio of αCD3/αCD28 microbeads:total T cells in the presence of vehicle or dexamethasone. A, Representative flow cytometry plots of CellTrace violet dilution. Plots were derived from gated CD4 (top row) or CD8 (bottom row) T cells. B-D, Proliferation analyses of CD4 T cells (top) and CD8 T cells (bottom) performed on the samples shown in (A). Precursor Frequency (B), Expansion Index (C), and Proliferation Index (D) are shown. Samples were plated in duplicate and analyzed with an unpaired students T test. Data are representative of three independent experiments. (PDF 3563 kb

Additional file 4: of Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy

Figure S4. Increased co-stimulation ameliorates the inhibitory effects of dexamethasone. Negatively-selected healthy donor T cells were cultured with 5 μg/mL αCD3 and increasing concentrations of CD80 in the presence of vehicle or dexamethasone. A-B. CD8 T cells cultured with vehicle (A) or dexamethasone (B). Flow cytometry plots showing proliferation of cells cultured with the indicated concentration of CD80 (left) and total numbers of naïve (TN), central memory (TCM), effector memory (TEM), and terminal effector (TTE) T cells following four days of culture (right) are shown. Differentiation subsets were assessed by CD45RO and CCR7 staining. Each condition was plated in duplicate, and data are representative of three independent experiments. Data were analyzed with an unpaired, two-tailed T Test. (PDF 2573 kb

Additional file 5: of Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy

Figure S5 PD-1 blockade does not rescue dexamethasone-mediated proliferation defects. A, Flow cytometry analysis of PD-1 surface expression on CD4 (left) or CD8 (right) T cells stimulated with αCD3/αCD28 microbeads. Unstimulated (dashed line), stimulated in presence of vehicle (solid line), and stimulated in presence of dexamethasone (filled red line) are shown. B, Geometric median fluorescence intensity (gMFI) of PD-1 staining on CD4 or CD8 T cells. Cells cultured with vehicle (black bars) and dexamethasone (red bars) are shown. Data are an average of duplicate samples. C, Expression of PD-1 by qPCR of T cells stimulated in the presence of vehicle or dexamethasone. Data are representative of four independent experiments. D-E. Healthy donor T cells were stimulated for four days in the presence of vehicle or dexamethasone and nivolumab or ipilimumab F(ab’)2 antibody as indicated. Precursor frequency of CD4 and CD8 T cells was quantified by FlowJo. The ratio of dexamethasone to vehicle for CD4 (C) and CD8 (D) T cells is shown. All samples were plated in duplicate and the ratios were analyzed with a one-way ANOVA. Data are representative of n = 4 healthy donors. (PDF 2522 kb

Additional file 3: of Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy

Figure S3. T cell differentiation subsets formed during in vitro stimulation with ιCD3/CD80 stimulation. Negatively-selected healthy donor T cells were cultured with 5 Οg/mL ιCD3 and the indicated concentration of CD80. T cell differentiation subsets were quantified following four days of culture. A, Flow plot of gating strategy to identify the indicated T cell differentiation subsets. B, Flow plots of CD4 (top) and CD8 (bottom) T cells cultured under the indicated conditions. (PDF 3995 kb

Additional file 7: of Dexamethasone-induced immunosuppression: mechanisms and implications for immunotherapy

Figure S7. Quantification of Treg and checkpoint molecules in tumor-bearing mice. GL261 ffluc-mCherry tumor-bearing mice were randomized into the indicated cohorts based on bioluminescence values from tumor. Vehicle or dexamethasone treatment was initiated on day 7, and isotype or CTLA-4 blocking antibody were administered on days 13, 16, and 19 following tumor implantation. Mice were euthanized on day 23 and tissues were harvested for flow cytometry analysis. A, Treg cell number from tumor-bearing brain hemisphere (left; n = 8) or the cervical tumor-draining lymph nodes (right; n = 10). B, The percentage of CD4 (top two plots) or CD8 (bottom two plots) T cells expressing the indicated checkpoint molecules. Co-expression of molecules was quantified using a Boolean gating strategy. Data were analyzed using a unpaired students T test. (PDF 1891 kb

DNA methylation profiles of patient tumors and <i>in vitro</i>, <i>in vivo</i>, <i>ex vivo</i> GSCs for two cell lines.

<p>(A,B) HC and PCA for PT, <i>in vitro</i>, <i>in vivo</i> and <i>ex vivo</i> samples for early and late passages (ep, lp). 6825 sites with standard deviation greater than 0.15 are presented. These sites are not differentially methylated between 827 and 923 (Mann-Whitney p-value more than 0.5). (C) Median methylation values for each sample based on selected 6825 sites.</p

Fold changes (x-axis) and mean methylation differences (y-axis) between paired <i>in vitro</i>-PT pairs for both differentially expressed and differentially methylated genes.

<p>Differentially expressed genes determined with paired t-test. Genes with false discovery rate less than 0.05 (Benjamini-Hochberg) and absolute fold change greater than three are used. Differentially methylated sites determined with paired non-parametric Quade test and sites with false discovery rate less than 0.05 (Benjamini-Hochberg) and absolute methylation difference greater than 0.3 are used.</p