The regulation of electro-optical properties and polymer morphology of polymer-dispersed liquid crystal films with silicon nanostructure

In this work, the thiol modified silica nanostructures (SiO2-SH) were doped into polymer-dispersed liquid crystal (PDLC) films. The SEM was used to observe the morphology of the polymer microstructure. The electro-optical (E-O) property test was determined by a liquid crystal parameter tester. The SEM images suggested that the SiO2-SH nanoparticles can react with acrylate groups to form the polymer matrix. The saturation voltage decreased by half in the sample when the dosage of the SiO2-SH nanoparticles was 7.5 wt%, which may be due to the reduced anchoring strength of the polymer matrix incorporated with silicon nanoparticles resulting from the lower surface energy and the enhanced steric repulsions of LC droplets and polymer matrix. In addition, the preparation conditions like polymerisation temperatures and UV light intensity also effectively regulated the E-O properties and polymer microstructure of the PDLC film with silica nanostructure. Thus, the results showed that the E-O properties and the polymer morphology of PDLC films with silicon nanostructures can be effectively regulated by doping SiO2-SH nanoparticles and regulating the preparation conditions such as the polymerisation temperature and UV light intensity. This work can provide practical guidance for modulating the properties of PDLC films.</p

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Data_Sheet_1_Lipid A Has Significance for Optimal Growth of Coxiella burnetii in Macrophage-Like THP-1 Cells and to a Lesser Extent in Axenic Media and Non-phagocytic Cells.DOCX

<p>Lipid A is an essential basal component of lipopolysaccharide of most Gram-negative bacteria. Inhibitors targeting LpxC, a conserved enzyme in lipid A biosynthesis, are antibiotic candidates against Gram-negative pathogens. Here we report the characterization of the role of lipid A in Coxiella burnetii growth in axenic media, monkey kidney cells (BGMK and Vero), and macrophage-like THP-1 cells by using a potent LpxC inhibitor -LPC-011. We first determined the susceptibility of C. burnetii LpxC to LPC-011 in a surrogate E. coli model. In E. coli, the minimum inhibitory concentration (MIC) of LPC-011 against C. burnetii LpxC is < 0.05 μg/mL, a value lower than the inhibitor's MIC against E. coli LpxC. Considering the inhibitor's problematic pharmacokinetic properties in vivo and Coxiella's culturing time up to 7 days, the stability of LPC-011 in cell cultures was assessed. We found that regularly changing inhibitor-containing media was required for sustained inhibition of C. burnetii LpxC in cells. Under inhibitor treatment, Coxiella has reduced growth yields in axenic media and during replication in non-phagocytic cells, and has a reduced number of productive vacuoles in such cells. Inhibiting lipid A biosynthesis in C. burnetii by the inhibitor was shown in a phase II strain transformed with chlamydial kdtA. This exogenous KdtA enzyme modifies Coxiella lipid A with an α-Kdo-(2 → 8)-α-Kdo epitope that can be detected by anti-chlamydia genus antibodies. In inhibitor-treated THP-1 cells, Coxiella shows severe growth defects characterized by poor vacuole formation and low growth yields. Coxiella progenies prepared from inhibitor-treated cells retain the capability of normally infecting all tested cells in the absence of the inhibitor, which suggests a dispensable role of lipid A for infection and early vacuole development. In conclusion, our data suggest that lipid A has significance for optimal development of Coxiella-containing vacuoles, and for robust multiplication of C. burnetii in macrophage-like THP-1 cells. Unlike many bacteria, C. burnetii replication in axenic media and non-phagocytic cells was less dependent on normal lipid A biosynthesis.</p