High-Flux Positively Charged Nanocomposite Nanofiltration Membranes Filled with Poly(dopamine) Modified Multiwall Carbon Nanotubes.

The poor dispensability of pristine carbon nanotubes in water impedes their implications in thin-film nanocomposite membranes for crucial utilities such as water purification. In this work, high-flux positively charged nanocomposite nanofiltration membranes were exploited by uniformly embedding poly(dopamine) modified multiwall carbon nanotubes (PDA-MWCNTs) in polyamide thin-film composite membranes. With poly(dopamine) modification, fine dispersion of MWCNTs in polyethyleneimine (PEI) aqueous solutions was achieved, which was interracially polymerized with trimesoyl chloride (TMC) n-hexane solutions to prepare nanocomposite membranes. The compatibility and interactions between modified MWCNTs and polyamide matrix were enhanced, attributed to the poly(dopamine) coatings on MWCNT surfaces, leading to significantly improved water permeability. At optimized conditions, pure water permeability of the PEI/PDA-MWCNTs/TMC nanofiltration membrane (M-4) was 15.32 L m(-2) h(-1) bar(-1), which was ∼1.6 times increased compared with that of pristine PEI/TMC membranes. Salt rejection of M-4 to different multivalent cations decreased in the sequence ZnCl2 (93.0%) > MgCl2 (91.5%) > CuCl2 (90.5%) ≈ CaCl2, which is well-suited for water softening and heavy metal ion removal.

Upregulation of peroxisome proliferator-activated receptor-gamma and NADPH oxidases are involved in restenosis after balloon injury.

Restenosis is a major complication of percutaneous transluminal coronary angioplasty (PTCA) and is characterized by increased superoxide formation and accumulation of smooth muscle cells (SMCs). The mechanisms through which peroxisome proliferator-activated receptor-gamma (PPAR-gamma) modulates the pathological process are incompletely defined. In this study, balloon injury of porcine coronary arteries in vivo and cell scraping model in vitro were used to elucidate the pathway via this molecule. PPAR-gamma and NADPH oxidase expression significantly increased both in neointimal hyperplasia after balloon injury or in the cultured SMCs after scraping injury. In vitro, PPAR-gamma agonist 15-deoxy-Delta(12,14)-prostagladlin J(2) (15d-PGJ2) decreased cell-scraping-induced superoxide generation through suppression of NADPH oxidase activity via down-regulation of p22(phox) and gp91(phox). Furthermore, 15d-PGJ2 could suppress scraping-stimulated proliferation of SMCs. These data demonstrate that upregulation of PPAR-gamma and NADPH oxidases are involved in restenosis and activation of PPAR-gamma can inhibit the NADPH oxidase-dependent superoxide generation in SMCs after injury. These findings will provide a new potential drug target for restenosis after balloon injury.