Microstructure and mechanical properties of a polyethylene/polydimethylsiloxane composite prepared using supercritical carbon dioxide

A polymer composite of polyethylene (PE) and polydimethylsiloxane (PDMS) was prepared using supercritical carbon dioxide despite the two polymers usually being immiscible and possessing a phase‐separated morphology. This article reports in detail the preparation, microstructure, crystallinity, and mechanical properties of the resulting PE/PDMS composite. The formation mechanism of the PE/PDMS composite consisted of supercritical impregnation of an octamethylcyclotetrasiloxane (D4) monomer and an initiator into a PE substrate followed by in situ polymerization within the substrate. Differential scanning calorimetry, wide‐angle X‐ray diffraction, and small‐angle X‐ray scattering measurements showed that PE and PDMS were blended at the nanometer level. The PDMS generated in the amorphous region of PE did not affect its crystallinity. Dynamic viscoelastic analyses and tensile tests were used to measure the mechanical properties of the composites including storage and Young's modulus, fracture stress, and strain. These properties were found to depend on the composition of the composite. © 2012 Wiley Periodicals, Inc. J. Appl. Polym. Sci., 2013     

Surface graphitization of Furan-resin-derived carbon

Furan-resin-derived carbon generally produces a glass-like carbon having entangled graphene layers (graphite structure) after high temperature heat-treatments. However, Raman spectroscopy reveals that it produces well-graphitized thin skins on surfaces. The graphitization is promoted on the faces that are formed at lower heat-treatment temperatures. Fractured faces of specimens pre-heat-treated at 1000°C result in well-developed structures in graphitization after re-heat-treatment at 3000°C. It is considered that the surfaces, i.e. free faces, play an important role in the graphitization.     

Molybdenum (IV) pyrophosphate isostructural with ZrP2O7

A new molybdenum pyrophosphate, MoP₂O₇, isomorphic with ZrP₂O₇, was prepared at the reductive atmosphere and its magnetic property was measured. The lattice constant of this compound was determined to be $\text{a}\text{=7.952(4)}\text{A}\text{?}$ in the cubic system. A paramgnetic behavior was observed from the liquid N₂ temperature to 500K. The effective magnetic moment for this compound was calculated to be 2.6μ_B in agreement with the calculated spin-only value of 2.83μ_B for Mo⁴⁺.     

AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke

A-kinase anchor protein 12 (AKAP12) is a scaffolding protein that associates with intracellular molecules to regulate multiple signal transductions. Although the roles of AKAP12 in the central nervous system are still relatively understudied, it was previously shown that AKAP12 regulates blood-retinal barrier formation. In this study, we asked whether AKAP12 also supports the function and integrity of the blood-brain barrier (BBB). In a mouse model of focal ischemia, the expression level of AKAP12 in cerebral endothelial cells was upregulated during the acute phase of stroke. Also, in cultured cerebral endothelial cells, oxygen-glucose deprivation induced the upregulation of AKAP12. When AKAP12 expression was suppressed by an siRNA approach in cultured endothelial cells, endothelial permeability was increased along with the dysregulation of ZO-1/Claudin 5 expression. In addition, the loss of AKAP12 expression caused an upregulation/activation of the Rho kinase pathway, and treatment of Rho kinase inhibitor Y-27632 mitigated the increase of endothelial permeability in AKAP12-deficient endothelial cell cultures. These in vitro findings were confirmed by our in vivo experiments using Akap12 knockout mice. Compared to wild-type mice, Akap12 knockout mice showed a larger extent of BBB damage after stroke. However, the inhibition of rho kinase by Y-27632 tightened the BBB in Akap12 knockout mice. These data may suggest that endogenous AKAP12 works to alleviate the damage and dysfunction of the BBB caused by ischemic stress. Therefore, the AKAP12-rho-kinase signaling pathway represents a novel therapeutic target for stroke.