2,723 research outputs found

    Quantitative evaluation of movement using the timed up-and-go test

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    Study of Liquefaction Damages of Quay-Walls and Breakwaters During Kobe Earthquake

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    During Kobe Earthquake, very extensive damages of harbor facilities such as quay-wall and breakwater occurred in Kobe Port and also along the coastal areas between Kobe and Osaka cities. Major causes of the damages were the liquefaction of sands underlying and behind the concrete caisson and also strong earthquake shaking force on the caisson. The degree of damage varied considerably depending on location and also on the size of structure. In order to understand the mechanism of damage as well as the factors that controlled the degree of damage, it was necessary to examine and analyze the case records of damages of these structures. This paper describes the result of such study on liquefaction damage of quay-walls and breakwaters. Through the study, it was found that the movement of sand at shallow depth below the caisson base is mainly responsible for a large settlement of caisson, but the mode of deformation is different between quay wall and breakwater. Also an effective stress liquefaction analysis was performed on the damaged quay-walls and breakwaters in order to check the applicability of effective stress liquefaction analysis on damage assessment. It was found that the effective stress analysis may be used to establish the overall trend of damage variation with the intensity of seismic motion, but problems exist in setting the dynamic parameters for the analysis, such as damping parameters, in order to obtain a reliable result

    Lack of antigen-specific tissue remodeling in mice deficient in the macrophage galactose-type calcium-type lectin 1/CD301a.

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    Macrophage galactose-type C-type lectins (MGLs), which were recently named CD301, have 2 homologues in mice: MGL1 and MGL2. MGLs are expressed on macrophages and immature dendritic cells. The persistent presence of granulation tissue induced by a protein antigen was observed in wild-type mice but not in mice lacking an endogenous, macrophage-specific, galactose-type calcium-type lectin 1 (MGL1) in an air pouch model. The anti-MGL1 antibody suppressed the granulation tissue formation in wild-type mice. A large number of cells, present only in the pouch of MGL1-deficient mice, were not myeloid or lymphoid lineage cells and the number significantly declined after administration of interleukin 1 alpha (IL-1alpha) into the pouch of MGL1-deficient mice. Furthermore, granulation tissue was restored by this treatment and the cells obtained from the pouch of MGL1-deficient mice were incorporated into the granulation tissue when injected with IL-1alpha. Taken together, MGL1 expressed on a specific subpopulation of macrophages that secrete IL-1alpha was proposed to regulate specific cellular interactions crucial to granulation tissue formation
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