Fuel cells based on polymer electrolyte membranes (PEM) show promise as a means of energy conversion for a wide range of applications both in the transportation sector and for stationary power production due to their high charge density and low operating temperatures. While the structure and transport of bulk PEMs for fuel cell applications have been studied extensively, much less is known about these materials at interfaces and under confinement, conditions that are highly relevant in the membrane electrode assembly of a working PEM fuel cell. Using X-ray reflectivity, neutron reflectivity, grazing-incidence small-angle X-ray scattering, quartz crystal microbalance, and polarization-modulation infrared reflection–absorption spectroscopy, we have studied the structure, swelling, water solubility, and water transport kinetics as a function of relative humidity for confined polyelectrolyte films thinner than 222 nm. While the humidity-dependent equilibrium swelling ratio, volumetric water fraction, and effective diffusivity are relatively constant for films thicker than ca. 60 nm, we observe measurable suppressions of these properties in films less than ca. 60 nm. These effects occur at length scales that are relevant to transport (ion and water) in the polyelectrolyte binders found in the catalyst layer of the membrane–electrode assembly (MEA) of a functional fuel cell. The thin film methodology and findings presented here provide a platform to quantify and validate models of interfacial impedance used within the fuel cell community and have the potential to lead to improvements in MEA materials, design, and optimization.

Ion-conductive polymers, or ionomers, are critical materials for a wide range of electrochemical technologies. For optimizing the complex heterogeneous structures in which they occur, there is a need to elucidate the governing structure-property relationships, especially at nanoscale dimensions where interfacial interactions dominate the overall materials response due to confinement effects. It is widely acknowledged that polymer physical behavior can be drastically altered from the bulk when under confinement and the literature is replete with examples thereof. However, there is a deficit in the understanding of ionomers when confined to the nanoscale, although it is apparent from literature that confinement can influence ionomer properties. Herein we show that as one particular ionomer, Nafion, is confined to thin films, there is a drastic increase in the modulus over the bulk value, and we demonstrate that this stiffening can explain previously observed deviations in materials properties such as water transport and uptake upon confinement. Moreover, we provide insight into the underlying confinement-induced stiffening through the application of a simple theoretical framework based on self-consistent micromechanics. This framework can be applied to other polymer systems and assumes that as the polymer is confined the mechanical response becomes dominated by the modulus of individual polymer chains.

We investigate the effect of the ordering temperature (T) and film thickness (h(f)) on the surface morphology of flow-coated block copolymer (BCP) films of asymmetric poly(styrene-block-methyl methacrylate). Morphology transitions observed on the ordered film surface by atomic force microscopy (AFM) are associated with a perpendicular to a parallel cylinder BCP microphase orientation transition with respect to the substrate with increasing h(f). "Hybrid" surface patterns for intermediate h(f) between these limiting morphologies are correspondingly interpreted by a coexistence of these two BCP microphase orientations so that two "transitional" h(f) exist for each T. This explanation of our surface patterns is supported by both neutron reflectivity and rotational SANS measurements. The transitional h(f) values as a function of T define upper and lower surface morphology transition lines, h(fu) (T) and h(fl) (T), respectively, and a surface morphology diagram that should be useful in materials fabrication. Surprisingly, the BCP film surface morphology depends on the method of film formation (flow-coated versus spun-cast films) so that nonequilibrium effects are evidently operative. This morphological variability is attributed primarily to the trapping of residual solvent (toluene) within the film (quantified by neutron reflectivity) due to film vitrification while drying. This effect has significant implications for controlling film structure in nanomanufacturing applications based on BCP templates.

Fucoidan is a sulfated polysaccharide found in edible brown algae, such as Undaria pinnatifida, Fucus vesiculosus and Ecklonia cava. Fucoidan usually contains a large proportion of L-fucose and sulfate. Fucoidan has been reported to show various biological activities such as anti-tumor, [1][2][3][4] anti-coagulant, 5,6) anti-viral, 7) and anti-inflammatory. 8) Furthermore, its anti-tumor activity may be due to the inhibition of tumor angiogenesis in Ehrlich ascites carcinoma 1) and lung carcinoma, 9) as well as the direct induction of apoptosis in U9373) and HS-sultan cells. 4) Several marine algal polysaccharides, fucoidan in particular, have been found to induce apoptosis in cancer cells. [10][11][12] Nevertheless, there is no report on the effect of fucoidan in colon cancer, one of the most malignant neoplasias and a frequently occurring tumor in the world.Recently, it has been demonstrated that the phosphorylation/de-phosphorylation states of some regulatory proteins are crucial events along the pathways controlling cell growth and apoptosis. A well-established apoptotic signaling cascade is regulated by mitogen activated protein (MAP) kinases.13) The MAPK pathway consists of a three-tiered kinase core where MAP3K activates an MAP2K which in turn activates an MAPK (ERK, JNK; c-Jun N-terminal kinase, and p38), resulting in the activation of nuclear factor-kB (NF-kB) and cell survival.14,15) Akt signaling is another important transduction pathway that plays a critical role in controlling the balance between cell survival and apoptosis. 16) In this study, we investigated the effect of fucoidan on the induction of apoptosis in HCT-15 cells, human colon adenocarcinoma cells. Because MAPK and PI3K/Akt pathways are involved in cellular proliferation, differentiation, and apoptosis, [17][18][19][20] the phosphorylation and activities of two MAPKs, ERK and p38 MAPK as well as Akt were investigated. Understanding of the underlying mechanism of the induction of apoptosis by fucoidan will benefit the development of chemopreventive and/or chemotherapeutics for colon cancer. MATERIALS AND METHODS Fucoidan and Diallyl DisulfideFucoidan (from Fucus vesiculosus) and diallyl disulfide (DADS) were purchased from Sigma (St. Louis, MO, U.S.A.). The fucoidan was dissolved in phosphate-buffered saline (PBS; Sigma, St. Louis, MO, U.S.A.) to 50 mg/ml and the DADS was dissolved in dimethylsulfoxide (DMSO; Sigma, St. Louis, MO, U.S.A.) to 50 mM at Ϫ20°C until further use.Cell Culture The HCT-15 human colon cancer cells were purchased from the Korea Cell Line Bank (KCLB) and cultured in RPMI1640 (Gibco BRL, Grand Island, NY, U.S.A.) medium supplemented with 10% fetal bovine serum (FBS) (Gibco BRL, Grand Island, NY, U.S.A.) at 37°C in a 5% CO 2 atmosphere. The exponentially growing cells were used throughout the experiments.MTT Assay The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Saint Louis, MO, U.S.A.) assay was performed as previously described. 21) In brief, HCT-15 cells were cultured in a 96-well pla...

Fucoidan, a sulfated polysaccharide, has a variety of biological activities, such as anti-cancer, anti-angiogenic and anti-inflammatory. However, the mechanisms of action of fucoidan as an anti-cancer agent have not been fully elucidated. The present study examined the anti-cancer effect of fucoidan obtained from Undaria pinnatifida in PC-3 cells, human prostate cancer cells. Fucoidan induced the apoptosis of PC-3 cells by activating both intrinsic and extrinsic pathways. The induction of apoptosis was accompanied by the activation of extracellular signal-regulated kinase mitogen-activated protein kinase (ERK1/2 MAPK) and the inactivation of p38 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt. In addition, fucoidan also induced the up-regulation of p21Cip1/Waf and down-regulation of E2F-1 cell-cycle-related proteins. Furthermore, in the Wnt/β-catenin pathway, fucoidan activated GSK-3β that resulted in the decrease of β-catenin level, followed by the decrease of c-myc and cyclin D1 expressions, target genes of β-catenin in PC-3 cells. These results suggested that fucoidan treatment could induce intrinsic and extrinsic apoptosis pathways via the activation of ERK1/2 MAPK, the inactivation of p38 MAPK and PI3K/Akt signaling pathway, and the down-regulation of Wnt/β-catenin signaling pathway in PC-3 prostate cancer cells. These data support that fucoidan might have potential for the treatment of prostate cancer.