378 research outputs found

    A New Possibility of Dynamical Study on Solid State Ionic Materials by Inelastic Neutron Scattering

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    A new technique of inelastic neutron scattering measurement utilizing the multiple incident energies is applied to the dynamical study of vitreous silica. A wide variety of extracted information from a series of two-dimensional maps of dynamical structure factor with multiple different incident energies are greatly valuable. The applicability and its expected contribution of new experimental technique into the further progress of scientific activities in solid state ionic materials are discussed.Received: 30 September 2010; Revised: 25 October 2010; Accepted: 26 October 201

    3Rd-Order Nonlinearity Of 4-Dialkylamino-4\u27Nitro-Stilbene Wave-Guides At 1319 Nm

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    The intensity dependent optical properties of 4-dialkylamino-4\u27nitro-stilbene polymer channel waveguides were measured at 1319 nm with a pulse modulated Mach-Zehnder interferometer to be n2 = 0.8 x 10(-13) cm2/W and beta2 \u3c 0.08 cm/GW. This material is promising for all-optical switching at 1319 nm because it satisfies both the W and T figures of merit

    Crystal Structure of the Formin mDia1 in Autoinhibited Conformation

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    Formin proteins utilize a conserved formin homology 2 (FH2) domain to nucleate new actin filaments. In mammalian diaphanous-related formins (DRFs) the FH2 domain is inhibited through an unknown mechanism by intramolecular binding of the diaphanous autoinhibitory domain (DAD) and the diaphanous inhibitory domain (DID).Here we report the crystal structure of a complex between DID and FH2-DAD fragments of the mammalian DRF, mDia1 (mammalian diaphanous 1 also called Drf1 or p140mDia). The structure shows a tetrameric configuration (4 FH2 + 4 DID) in which the actin-binding sites on the FH2 domain are sterically occluded. However biochemical data suggest the full-length mDia1 is a dimer in solution (2 FH2 + 2 DID). Based on the crystal structure, we have generated possible dimer models and found that architectures of all of these models are incompatible with binding to actin filament but not to actin monomer. Furthermore, we show that the minimal functional monomeric unit in the FH2 domain, termed the bridge element, can be inhibited by isolated monomeric DID. NMR data on the bridge-DID system revealed that at least one of the two actin-binding sites on the bridge element is accessible to actin monomer in the inhibited state.Our findings suggest that autoinhibition in the native DRF dimer involves steric hindrance with the actin filament. Although the structure of a full-length DRF would be required for clarification of the presented models, our work here provides the first structural insights into the mechanism of the DRF autoinhibition

    Wave-Guiding In Substrate Supported And Freestanding Films Of Insoluble Conjugated Polymers

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    We demonstrate that waveguiding is possible in substrate supported and freestanding films of insoluble conjugated polymers. Photoresist gratings were used to couple 1.06-1.53 mum radiation into the waveguides allowing the refractive indices, the birefringence, and the linear losses to be measured

    Different Human Copper-Zinc Superoxide Dismutase Mutants, SOD1G93A and SOD1H46R, Exert Distinct Harmful Effects on Gross Phenotype in Mice

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    Amyotrophic lateral sclerosis (ALS) is a heterogeneous group of fatal neurodegenerative diseases characterized by a selective loss of motor neurons in the brain and spinal cord. Creation of transgenic mice expressing mutant Cu/Zn superoxide dismutase (SOD1), as ALS models, has made an enormous impact on progress of the ALS studies. Recently, it has been recognized that genetic background and gender affect many physiological and pathological phenotypes. However, no systematic studies focusing on such effects using ALS models other than SOD1G93A mice have been conducted. To clarify the effects of genetic background and gender on gross phenotypes among different ALS models, we here conducted a comparative analysis of growth curves and lifespans using congenic lines of SOD1G93A and SOD1H46R mice on two different genetic backgrounds; C57BL/6N (B6) and FVB/N (FVB). Copy number of the transgene and their expression between SOD1G93A and SOD1H46R lines were comparable. B6 congenic mutant SOD1 transgenic lines irrespective of their mutation and gender differences lived longer than corresponding FVB lines. Notably, the G93A mutation caused severer disease phenotypes than did the H46R mutation, where SOD1G93A mice, particularly on a FVB background, showed more extensive body weight loss and earlier death. Gender effect on survival also solely emerged in FVB congenic SOD1G93A mice. Conversely, consistent with our previous study using B6 lines, lack of Als2, a murine homolog for the recessive juvenile ALS causative gene, in FVB congenic SOD1H46R, but not SOD1G93A, mice resulted in an earlier death, implying a genetic background-independent but mutation-dependent phenotypic modification. These results indicate that SOD1G93A- and SOD1H46R-mediated toxicity and their associated pathogenic pathways are not identical. Further, distinctive injurious effects resulted from different SOD1 mutations, which are associated with genetic background and/or gender, suggests the presence of several genetic modifiers of disease expression in the mouse genome
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