The direct preparation of amphiphilic graft copolymers from commercial poly(vinylidene fluoride) (PVDF) using atom transfer radical polymerization (ATRP) is demonstrated. Here, direct initiation of the secondary fluorinated site of PVDF facilitates grafting of the hydrophilic comonomer. Amphiphilic comb copolymer derivatives of PVDF having poly(methacrylic acid) side chains (PVDF-g-PMAA) and poly(oxyethylene methacrylate) side chains (PVDF-g-POEM) are prepared using this method. Surface segregation of PVDF-g-POEM additives in PVDF is examined as a route to wettable, foul-resistant surfaces on PVDF filtration membranes. Because of surface segregation during the standard immersion precipitation process for membrane fabrication, a PVDF/5 wt % PVDF-g-POEM membrane, having a bulk POEM concentration of 3.4 wt %, exhibits a near-surface POEM concentration of 42 wt % as measured by X-ray photoelectron spectroscopy (XPS). This membrane displays substantial resistance to BSA fouling compared with pure PVDF and wets spontaneously when placed in contact with water.

Background-Although 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are known to modulate endothelial function, the transcriptional mechanisms underlying these effects are incompletely understood. We hypothesized that Lung-Kruppel-like factor (LKLF/KLF2), a novel and potent regulator of endothelial gene expression, may mediate the downstream effects of statins. Here we report that statin-induced expression of endothelial NO synthase (eNOS) and thrombomodulin is KLF2 dependent. Methods and Results-KLF2 mRNA was induced by treatment with multiple statins in a concentration-dependent manner.Multiple lines of evidence suggest that this induction is dependent on inhibition of the Rho pathway and requires de novo transcription. Furthermore, promoter deletion and mutational analyses suggest that mevastatin induced KLF2 promoter activity through a single myocyte enhancer factor binding site. Finally, small-interfering RNA-mediated knockdown of KLF2 strongly attenuated the ability of mevastatin to increase eNOS and thrombomodulin accumulation in endothelial cells. Conclusions-Taken

An analysis of the morphological behavior of substrate-supported diblock copolymer films for thicknesses t below the equilibrium period L 0 of the copolymer is presented. Substrate-supported films generally exhibit dissimilar interactions between the copolymer block components and the free and substrate surfaces. Accordingly, in this study, self-consistent-field calculations that incorporate asymmetric surface energetics were used to assess equilibrium film morphologies. Phase diagrams were constructed as a function of film thickness, surface interaction energies, the segmental interaction, and the chain length. In conjunction, experiments were conducted on a series of polystyrene-b-poly(n-alkyl methacrylate) copolymer films supported by silicon substrates. These employed a novel atomic force microscopy technique that allowed for the precise tracking of morphology as a function of film thickness. Comparison of the experimental results and calculations revealed several common trends. In particular, hybrid morphologies, incorporating both surface-parallel and surface-perpendicular elements, were observed both experimentally and through the calculations for the thickness regime, t ∼ 0.5L 0. The stability of such structures was found to be closely linked to the symmetry of the surface energetics.