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Institution

Osaka University

EducationOsaka, Japan
About: Osaka University is a education organization based out in Osaka, Japan. It is known for research contribution in the topics: Laser & Catalysis. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Catalysis, Population, Gene, Thin film


Papers
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Journal ArticleDOI
04 Aug 2000-Science
TL;DR: Preliminary radiation damage experiments substantiate the prediction that fluorites are inherently more radiation resistant than pyrochlores, and may permit the chemical durability and radiation tolerance of potential hosts for actinides and radioactive wastes to be tailored.
Abstract: The radiation performance of a variety of complex oxides is predicted on the basis of a material's propensity to accommodate lattice point defects. The calculations indicate that a particular class of oxides possessing the fluorite crystal structure should accept radiation-induced defects into their lattices far more readily than a structurally similar class of oxides based on the pyrochlore crystal structure. Preliminary radiation damage experiments substantiate the prediction that fluorites are inherently more radiation resistant than pyrochlores. These results may permit the chemical durability and radiation tolerance of potential hosts for actinides and radioactive wastes to be tailored.

847 citations

Journal ArticleDOI
TL;DR: It is suggested that inhibiting the IL-1R–Myd88 pathway in vivo could block the damage from acute inflammation that occurs in response to sterile cell death, and do so in a way that might not compromise tissue repair or host defense against pathogens.
Abstract: Dying cells stimulate inflammation, and this response is thought to contribute to the pathogenesis of many diseases. Very little has been known, however, about how cell death triggers inflammation. We found here that the acute neutrophilic inflammatory response to cell injury requires the signaling protein myeloid differentiation primary response gene 88 (Myd88). Analysis of the contribution of Myd88-dependent receptors to this response revealed only a minor reduction in mice doubly deficient in Toll-like receptor 2 (Tlr2) and Tlr4 and normal responses in mice lacking Tlr1, Tlr3, Tlr6, Tlr7, Tlr9, Tlr11 or the interleukin-18 receptor (IL-18R). However, mice lacking IL-1R showed a markedly reduced neutrophilic inflammatory response to dead cells and tissue injury in vivo as well as greatly decreased collateral damage from inflammation. This inflammatory response required IL-1alpha, and IL-1R function was required on non-bone-marrow-derived cells. Notably, the acute monocyte response to cell death, which is thought to be important for tissue repair, was much less dependent on the IL-1R-Myd88 pathway. Also, this pathway was not required for the neutrophil response to a microbial stimulus. These findings suggest that inhibiting the IL-1R-Myd88 pathway in vivo could block the damage from acute inflammation that occurs in response to sterile cell death, and do so in a way that might not compromise tissue repair or host defense against pathogens.

846 citations

Journal ArticleDOI
TL;DR: It is shown that neuronal macroautophagy is induced early in Alzheimer's disease (AD) and before β-amyloid (Aβ) deposits extracellularly in the presenilin (PS) 1/Aβ precursor protein (APP) mouse model of β- amyloidosis.
Abstract: Macroautophagy, which is a lysosomal pathway for the turnover of organelles and long-lived proteins, is a key determinant of cell survival and longevity. In this study, we show that neuronal macroautophagy is induced early in Alzheimer's disease (AD) and before β-amyloid (Aβ) deposits extracellularly in the presenilin (PS) 1/Aβ precursor protein (APP) mouse model of β-amyloidosis. Subsequently, autophagosomes and late autophagic vacuoles (AVs) accumulate markedly in dystrophic dendrites, implying an impaired maturation of AVs to lysosomes. Immunolabeling identifies AVs in the brain as a major reservoir of intracellular Aβ. Purified AVs contain APP and β-cleaved APP and are highly enriched in PS1, nicastrin, and PS-dependent γ-secretase activity. Inducing or inhibiting macroautophagy in neuronal and nonneuronal cells by modulating mammalian target of rapamycin kinase elicits parallel changes in AV proliferation and Aβ production. Our results, therefore, link β-amyloidogenic and cell survival pathways through macroautophagy, which is activated and is abnormal in AD.

845 citations

Journal ArticleDOI
30 Sep 2015
TL;DR: This position paper position that a new shift is necessary in computing, taking the control of computing applications, data, and services away from some central nodes to the other logical extreme of the Internet, and refers to this vision of human-centered edge-device based computing as Edge-centric Computing.
Abstract: In many aspects of human activity, there has been a continuous struggle between the forces of centralization and decentralization. Computing exhibits the same phenomenon; we have gone from mainframes to PCs and local networks in the past, and over the last decade we have seen a centralization and consolidation of services and applications in data centers and clouds. We position that a new shift is necessary. Technological advances such as powerful dedicated connection boxes deployed in most homes, high capacity mobile end-user devices and powerful wireless networks, along with growing user concerns about trust, privacy, and autonomy requires taking the control of computing applications, data, and services away from some central nodes (the "core") to the other logical extreme (the "edge") of the Internet. We also position that this development can help blurring the boundary between man and machine, and embrace social computing in which humans are part of the computation and decision making loop, resulting in a human-centered system design. We refer to this vision of human-centered edge-device based computing as Edge-centric Computing. We elaborate in this position paper on this vision and present the research challenges associated with its implementation.

844 citations

Journal ArticleDOI
TL;DR: The aged-rejuvenation-glue-liquid (ARGL) shear band model has been proposed for metallic glasses based on small-scale molecular dynamics simulations up to 20,000 atoms and thermomechanical analysis as mentioned in this paper.
Abstract: The aged-rejuvenation-glue-liquid (ARGL) shear band model has been proposed for metallic glasses (Acta Mater. 54 (2006) 4293), based on small-scale molecular dynamics simulations up to 20,000 atoms and thermomechanical analysis. The model predicts the existence of a critical lengthscale � 10 nm, above which melting could occur in shear-alienated glass. Large-scale molecular dynamics simulations with up to 5 million atoms have directly verified this prediction. When the applied stress exceeds the glue traction (computed separately before in a shear cohesive zone, or an amorphous-amorphous ‘‘generalized stacking fault energy’’ calculation), we indeed observe maturation of the shear band embryo into bona fide shear crack, accompanied by melting. In contrast, when the applied stress is below the glue traction, the shear band embryo does not propagate, becomes diffuse, and eventually dies. Thus this all-important quantity, the glue traction which is a property of shearalienated glass, controls the macroscopic yield point of well-aged glass. We further suggest that the disruption of chemical short-range order (‘‘chemical softening’’) governs the glue traction microscopically. Catastrophic thermal softening occurs only after chemical alienation and softening in our simulation, after the shear band embryo has already run a critical length. [doi:10.2320/matertrans.MJ200769]

843 citations


Authors

Showing all 84130 results

NameH-indexPapersCitations
Shizuo Akira2611308320561
Thomas C. Südhof191653118007
Tadamitsu Kishimoto1811067130860
Yusuke Nakamura1792076160313
H. S. Chen1792401178529
Hyun-Chul Kim1764076183227
Masayuki Yamamoto1711576123028
Kenji Kangawa1531117110059
Jongmin Lee1502257134772
Yoshio Bando147123480883
Takeo Kanade147799103237
Olaf Reimer14471674359
Yuji Matsuzawa143836116711
Kim Nasmyth14229459231
Tasuku Honjo14171288428
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023139
2022637
20216,915
20206,865
20196,462
20186,189