Fabrication of Stretchable Nanocomposites with High Energy Density and Low Loss from Cross-Linked PVDF Filled with Poly(dopamine) Encapsulated BaTiO₃

In this report, a simple solution-cast method was employed to prepare poly­(dopamine) (PDA) encapsulated BaTiO₃ (BT) nanoparticle (PDA@BT) filled composites using PVDF matrix cross-linked by the free radical initiator. The effects of both the particle encapsulation and matrix cross-linking on the mechanical and dielectric properties of the composites were carefully investigated. The results suggested that the introduction of BT particles improved permittivity of the composites to ∼30 at 100 Hz when particle contents of only 7 wt % were utilized. This was attributed to the enhanced polarization, which was induced by high permittivity ceramic particles. Compared to bare BT, PDA@BT particles could be dispersed more homogeneously in the matrix, and the catechol groups of PDA layer might form chelation with free ions present in the matrix. The latter might depress the ion conduction loss in the composites. Other results revealed that the formation of hydrogen-bonding between the PDA layer and the polymer, especially the chemical cross-linking across the matrix, resulted in increased Young’ modulus by ∼25%, improved breakdown strength by ∼40%, and declined conductivity by nearly 1 order of magnitude when compared to BT filled composites. The composite films filled with PDA@BTs indicated greater energy storage capacities by nearly 190% when compared to the pristine matrix. More importantly, the excellent mechanical performance allowed the composite films to adopt uni- or biaxially stretching, a crucial feature required for the realization of high breakdown strength. This work provided a facile strategy for fabrication of flexible and stretchable dielectric composites with depressed dielectric loss and enhanced energy storage capacity at low filler loadings (<10 wt %)

Suppression of TiO₂ Photocatalytic Activity by Low-Temperature Pulsed CVD-Grown SnO₂ Protective Layer

TiO₂ pigments are widely used in paint industries. Inert coating layers were usually deposited on the TiO₂ pigments to suppress the photocatalytic activity of TiO₂, which can prevent the degradation of surrounding polymer molecules. However, the traditional wet chemical methods normally form thick films, which would impair the pigment properties of TiO₂. In this work, SnO₂ and SiO₂ protective layers were grown on the TiO₂ particle surface by low<b>-</b>temperature pulsed chemical vapor deposition. At temperatures <60 °C, thin and uniform amorphous SnO₂ films were obtained. The photocatalytic activities of both TiO₂/SnO₂ and TiO₂/SiO₂ core–shell particles were suppressed, and TiO₂/SnO₂ core–shell particles showed higher lightening power than TiO₂/SiO₂. According to transient fluorescence, photocurrent, and electrochemical impedance spectroscopy measurements, the low electron mobility of amorphous SnO₂ and SiO₂ films led to fast recombination of photogenerated electrons and holes, thus preventing their migration to the surface and suppressing the photocatalytic activity of TiO₂

Image_3_Anti-inflammatory Effects of Curcumin in Microglial Cells.JPEG

<p>Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin’s anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-α [TNF-α, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt and translocation of NF-κB. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators release in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.</p

Effects of inhibitors of calcineurin, NF-κB and PI3K on TLR2 ligands and anti-IgE induced IL-8 release from LAD2 cells.

<p>(A) ciclosporin (2 µg/ml), (B) Bay 11-7821 (10 µM) or (C) wortmannin (0.5 µM) was incubated with LAD2 cells for 30 min before the addition of anti-IgE (2 µg/ml), PGN (50 µg/ml), Pam3CSK4 (20 µg/ml), anti-IgE with PGN or Pam3CSK4 for 24 h to induce the release of IL-8. The amounts of IL-8 release from activated LAD2 cells pre-incubated with an inhibitor and the corresponding control pre-incubated in culture medium were compared with student <i>t</i>-test. *p<0.05, **p<0.01, ***p<0.001 (n = 4–5).</p

Effects of TLR2 ligands on anti-IgE induced calcium mobilization in LAD2 cells.

<p>(A, B) LAD2 cells were incubated with anti-IgE (○), PGN/Pam3CSK4 (◊), anti-IgE with PGN/Pam3CSK4 (▪), and calcium mobilization was measured at the same time. (C, D) Cells were incubated with PGN or Pam3CSK4 for 24 h prior to being challenged with anti-IgE (▪). Changes in [Ca²⁺]_i were compared in the presence or absent of PGN or Pam3CSK4. Error bars were omitted for the clarity of the graph. The peak levels of calcium influx were compared with area under the curves analysis (E, F, G, H). Significant differences following student <i>t</i>-test were indicated by asterisks: *p<0.05, **p<0.01 (n = 4–6).</p

Effect of TLR2 ligands on anti-IgE induced degranulation and IL-8 release from LAD2 cells.

<p>(A, B) LAD2 cells were incubated with only PGN or Pam3CSK4 for 30 min (○). LAD2 cells were incubated with anti-IgE (2 µg/ml) at the same time (▴) or after 24 h pre-incubation (•) with PGN or Pam3CSK4. The levels of β-hex release induced by anti-IgE alone and in the present of TLR2 ligands were compared with one-way ANOVA and Dunnett’s multiple comparison tests. *p<0.05, **p<0.01, ***p<0.001 (n = 3–5). (C, D) LAD2 cells were incubated alone with anti-IgE (2 µg/ml, •), PGN/Pam3CSK4 (▪) or combination of anti-IgE with PGN/Pam3CSK4 (▴) for 24 h. Two-way ANOVA and Bonferroni posttests were applied to compare the actual amount of IL-8 released with the predicted value obtained by adding the individual amounts released by anti-IgE and PGN or Pam3CSK4 (○). **p<0.01 (n = 5).</p

Effects of PGN and Pam3CSK4 on the expression of FcεRI on LAD2 cells.

<p>LAD2 cells (without IgE sensitization) were incubated with PGN (50 µg/ml) (A) and Pam3CSK4 (20 µg/ml) (B) for 24 h and FcεRI surface expression was analyzed by flow cytometry after cells were incubated with FITC-conjugated anti-human FcεRI antibody, FITC-conjugated mouse IgG2b isotype control or FACS buffer for specific labelling of FcεRI, isotype and blank control respectively. The FcεRI expression of cells that were not treated (grey curve) or treated (blank curve) with the TLR2 ligands was not different as shown. Results were representative of four independent experiments.</p

Effects of inhibitors of MAPKs on TLR2 ligands and anti-IgE induced IL-8 release from LAD2 cells.

<p>(A) ERK inhibitor, PD98059 (10 µM), (B) JNK inhibitor, SP600125 (20 µM) or (C) p38 inhibitor, SB2023580 (10 µM) was incubated with LAD2 cells for 30 min before the addition of anti-IgE (2 µg/ml), PGN (50 µg/ml), Pam3CSK4 (20 µg/ml), anti-IgE with PGN or Pam3CSK4 for 24 h to induce the release of IL-8. The amounts of IL-8 release from activated LAD2 cells pre-incubated with an inhibitor and the corresponding control pre-incubated in culture medium were compared with student <i>t</i>-test. *p<0.05, **p<0.01, ***p<0.01 (n = 4–6).</p