Films with high pore density and regularity that are easy to manufacture by conventional large-scale technology are key components aimed for fabrication of new generations of magnetic arrays for storage media, medical scaffolds, and artificial membranes. However, potential manufacture strategies like the self-assembly of block copolymers, which lead to amazing regular patterns, could be hardly reproduced up to now using commercially feasible methods. Here we report a unique production method of nanoporous films based on the self-assembly of copper(II) ion-polystyrene-b-poly(4-vinylpyridine) complexes and nonsolvent induced phase separation. Extremely high pore densities and uniformity were achieved. Water fluxes of 890 L m -2 h -1 bar -1 were obtained, which are at least 1 order of magnitude higher than those of commercially available membranes with comparable pore size. The pores are also stimuli (pH)-responsive.

A process is described to manufacture monodisperse asymmetric pH-responsive nanochannels with very high densities (pore density >2 × 10(14) pores per m(2)), reproducible in m(2) scale. Cylindric pores with diameters in the sub-10 nm range and lengths in the 400 nm range were formed by self-assembly of metal-block copolymer complexes and nonsolvent-induced phase separation. The film morphology was tailored by taking into account the stability constants for a series of metal-polymer complexes and confirmed by AFM. The distribution of metal-copolymer micelles was imaged by transmission electron microscopy tomography. The pH response of the polymer nanochannels is the strongest reported with synthetic pores in the nm range (reversible flux increase of more than 2 orders of magnitude when switching the pH from 2 to 8) and could be demonstrated by cryo-field emission scanning electron microscopy, SAXS, and ultra/nanofiltration experiments.

The supramolecular assembly of PS-b-P4VP copolymer micelles induced by selective solvent mixtures was used to manufacture isoporous membranes. Micelle order in solution was confirmed by cryo-scanning electron microscopy in casting solutions, leading to ordered pore morphology. When dioxane, a solvent that interacts poorly with the micelle corona, was added to the solution, polymer-polymer segment contact was preferential, increasing the intermicelle contact. Immersion in water gave rise to asymmetric porous membranes with exceptional pore uniformity and high porosity. The introduction of a small number of carbon nanotubes to the casting solution improved the membrane stability and the reversibility of the gate response in the presence of different pH values.

No abstract

We fabricated block copolymer hollow fiber membranes with self-assembled, shell-side, uniform pore structures. The fibers in these membranes combined pores able to respond to pH and acting as chemical gates that opened above pH 4, and catalytic activity, achieved by the incorporation of gold nanoparticles. We used a dry/wet spinning process to produce the asymmetric hollow fibers and determined the conditions under which the hollow fibers were optimized to create the desired pore morphology and the necessary mechanical stability. To induce ordered micelle assembly in the doped solution, we identified an ideal solvent mixture as confirmed by small-angle X-ray scattering. We then reduced p-nitrophenol with a gold-loaded fiber to confirm the catalytic performance of the membranes.

No abstract

demiologic studies have shown an association between exposure to ambient particulate air pollution Ͻ10 m in diameter (PM10) and increased cardiovascular morbidity and mortality. We previously showed that PM10 exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM10-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM10. Female Watanabe heritable hyperlipidemic rabbits, which naturally develop systemic atherosclerosis, were exposed to PM10 (EHC-93) or vehicle by intratracheal instillation twice a week for 4 wk. Monocytes, labeled with 5-bromo-2Ј-deoxyuridine (BrdU) in donors, were transfused to recipient rabbits as whole blood, and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients was measured by quantitative histological methodology. Exposure to PM10 caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31 (platelet endothelial cell adhesion molecule-1) and CD49d (very late antigen-4 ␣-chain), and increased expression of CD54 (ICAM-1) and CD106 (VCAM-1) in plaques. Exposure to PM10 increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increased the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM10-induced progression of atherosclerosis. atherosclerosis; adhesion molecules EPIDEMIOLOGIC STUDIES have associated exposure to ambient particulate air pollution Ͻ10 m in diameter (PM 10

The parvovirus Minute virus of mice (MVM) is a small DNA virus that replicates in the nucleus of its host cells. However, very little is known about the mechanisms underlying parvovirus' nuclear import. Recently, it was found that microinjection of MVM into the cytoplasm of Xenopus oocytes causes damage to the nuclear envelope (NE), suggesting that the nuclear-import mechanism of MVM involves disruption of the NE and import through the resulting breaks. Here, fluorescence microscopy and electron microscopy were used to examine the effect of MVM on host-cell nuclear structure during infection of mouse fibroblast cells. It was found that MVM caused dramatic changes in nuclear shape and morphology, alterations of nuclear lamin immunostaining and breaks in the NE of infected cells. Thus, it seems that the unusual nuclear-import mechanism observed in Xenopus oocytes is in fact used by MVM during infection of host cells.Parvoviruses are small, non-enveloped DNA viruses with properties that make them attractive as potential vectors for gene therapy. As part of their replication cycle, parvoviruses must enter the nucleus of their host cells. How this is accomplished remains unclear. Most viruses that enter the nucleus do so by hijacking the host nuclear-transport machinery. Many viruses bind soluble cytoplasmic-import receptors by using specific nuclear-localization signals (NLSs) on viral proteins; the receptor-cargo complex is then transported through the nuclear pore complex (NPC) to the nucleus (reviewed by Izaurralde et al., 1999;Smith & Helenius, 2004;Whittaker et al., 2000). Thus, it has been largely assumed that parvoviruses also enter the nucleus through the NPC.We have recently shown that, after microinjection into Xenopus oocytes, the parvovirus Minute virus of mice (MVM) induces breaks in the nuclear envelope (NE) that support nuclear import of proteins in a manner that is independent of the NPC (Cohen & Panté, 2005). We have also shown that MVM damages the nuclear membranes of purified rat liver nuclei (Cohen & Panté, 2005). Based on these results, we proposed that MVM enters the nucleus by using a unique mechanism that is independent of the host nuclear-import machinery: instead of crossing the NPC, MVM disrupts the NE and enters the nucleus through the resulting breaks. Consistent with this mechanism, Hansen et al. (2001) previously found that another parvovirus, adeno-associated virus (AAV), can enter purified intact nuclei in the absence of nuclear-import receptors and other cytoplasmic factors required for NPC-mediated import. In addition, blocking the NPCs with the lectin wheatgerm agglutinin had no effect on the uptake of AAV into purified nuclei. These two studies suggest strongly that parvoviruses can bypass the host nuclear-transport machinery during entry to the nucleus. However, both studies used experimental systems that are ideal for studying nuclear import (Beck et al., 2004;Panté, 2006;Panté & Aebi, 1996;Panté & Kann, 2002), but are far removed from the situation during infection of host cel...