Electroactive alumina particles embedded in an acrylic elastomer

Composites of alumina particles embedded in a polar acrylic rubber polymer matrix are being investigated as potential electroactive polymer actuators. The measured FTIR spectra, XRD patterns, and SEM micrographs suggest that the alumina particles with an average diameter of 9.873 ± 0.034 μm having the rhombohedral form of the corundum phase are intercalated homogeneously within the acrylic rubber matrix. At an Al₂O₃ volume fraction of 0.144, the electrical conductivity increases from 10⁻⁹ to 10⁻⁸ (Ω m)⁻¹ at 500 Hz. The storage modulus without applied electrical field, G′_o, increases from 9,533 to 105,540 Pa, an order of—a single—magnitude increase, as the particle volume fraction is varied from 0 to 0.144. The increase in the matrix rigidity of the hybrid organic‐inorganic composites are because of the stress transfer from matrix to the reinforcement particles, the partial substitution of a soft matrix with a stiffer filler, and the segmental immobilization caused by the interaction between the matrix polymer chains and the filler surface. Under an applied electric field, induced dipole moments and particle‐particle interaction are generated, leading to an increase in the matrix rigidity. Under an applied electrical field, G′_{2 kV/mm} increases from 9,775 to 139,080 within the same volume fraction range, a difference of more than 30% is observed because of presence of an electrical field. POLYM. COMPOS., 2011. © 2010 Society of Plastics Engineers     

Uremia-Induced Gut Barrier Defect in 5/6 Nephrectomized Mice Is Worsened by Candida Administration through a Synergy of Uremic Toxin,Lipopolysaccharide, and (1➔3)-β-D-Glucan,but Is Attenuated by Lacticaseibacillus rhamnosus L34

A chronic kidney disease (CKD) causes uremic toxin accumulation and gut dysbiosis, which further induces gut leakage and worsening CKD. Lipopolysaccharide (LPS) of Gram-negative bacteria and (1➔3)-β-D-glucan (BG) of fungi are the two most abundant gut microbial molecules. Due to limited data on the impact of intestinal fungi in CKD mouse models, the influences of gut fungi and Lacticaseibacillus rhamnosus L34 (L34) on CKD were investigated using oral C. albicans-administered 5/6 nephrectomy (5/6Nx) mice. At 16 weeks post-5/6Nx, Candida-5/6Nx mice demonstrated an increase in proteinuria, serum BG, serum cytokines (tumor necrotic factor-α; TNF-α and interleukin-6), alanine transaminase (ALT), and level of fecal dysbiosis (Proteobacteria on fecal microbiome) when compared to non-Candida-5/6Nx. However, serum creatinine, renal fibrosis, or gut barrier defect (FITC-dextran assay and endotoxemia) remained comparable between Candida- versus non-Candida-5/6Nx. The probiotics L34 attenuated several parameters in Candida-5/6Nx mice, including fecal dysbiosis (Proteobacteria and Bacteroides), gut leakage (fluorescein isothiocyanate (FITC)-dextran), gut-derived uremic toxin (trimethylamine-N-oxide; TMAO) and indoxyl sulfate; IS), cytokines, and ALT. In vitro, IS combined with LPS with or without BG enhanced the injury on Caco-2 enterocytes (transepithelial electrical resistance and FITC-dextran permeability) and bone marrow-derived macrophages (supernatant cytokines (TNF-α and interleukin-1 β; IL-1β) and inflammatory genes (TNF-α, IL-1β, aryl hydrocarbon receptor, and nuclear factor-κB)), compared with non-IS activation. These injuries were attenuated by the probiotics condition media. In conclusion, Candida administration worsens kidney damage in 5/6Nx mice through systemic inflammation, partly from gut dysbiosis-induced uremic toxins, which were attenuated by the probiotics. The additive effects on cell injury from uremic toxin (IS) and microbial molecules (LPS and BG) on enterocytes and macrophages might be an important underlying mechanism.