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Institution

National Archives and Records Administration

ArchiveWashington D.C., District of Columbia, United States
About: National Archives and Records Administration is a archive organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: National archives & Population. The organization has 8414 authors who have published 7993 publications receiving 117195 citations. The organization is also known as: NARA & National Archives.


Papers
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Journal ArticleDOI
01 Jun 2009
TL;DR: In this article, a novel reflective LCD without polarizers, which is sure to provide excellent visibility (reflectance = 50%, CR = 10:1), achieved extremely low power consumption of 10 microwatts to introduce low frequency driving without flicker and image sticking.
Abstract: We have developed a novel reflective LCD without polarizers, which is sure to provide excellent visibility (reflectance = 50%, CR = 10:1). Moreover, we have also achieved extremely low power consumption of 10 microwatts to introduce low frequency driving (less than 1Hz) without flicker and image sticking. These characteristics were realized to combine pixel memory circuit and new PNLC material.

992 citations

Journal ArticleDOI
TL;DR: It is demonstrated for the first time that one of the major bactericidal functions of the silver ion is its interaction with the ribosome and the ensuing inhibition in expression of the enzymes and proteins essential to ATP production.
Abstract: Bactericidal actions of the silver ion on Escherichia coli as a model microorganism were studied using energy-filtering transmission electron microscopy (EFTEM), two-dimensional electrophoresis (2-DE), and matrix-assisted laser desorption ionization-time-of-flight mass spectrometry (MALDI-TOF MS). EFTEM observations demonstrated that the silver ion readily infiltrates the interior of E. coli, contrary to the early hypothesis that it resides initially in the cell membrane area. Furthermore, 2-DE and MALDI-TOF MS indicated that the expression of a ribosomal subunit protein as well as that of some other enzymes and proteins is affected by the silver ion. The present results demonstrate for the first time that one of the major bactericidal functions of the silver ion is its interaction with the ribosome and the ensuing inhibition in expression of the enzymes and proteins essential to ATP production.

819 citations

Journal ArticleDOI
TL;DR: Immunoelectron microscopic analysis revealed that TLR3, when stably expressed in the murine B cell line Ba/F3, was specifically accumulated in multivesicular bodies, a subcellular compartment situated in endocytic trafficking pathways, which may reflect participation of cell type-specific multiple pathways in antiviral IFN induction viaTLR3.
Abstract: Toll-like receptor (TLR)3 recognizes dsRNA and transduces signals to activate NF-kappaB and IFN-beta promoter. Type I IFNs (IFN-alpha/beta) function as key cytokines in anti-viral host defense. Human fibroblasts express TLR3 on the cell surface, and anti-TLR3 mAb inhibits dsRNA-induced IFN-beta secretion by fibroblasts, suggesting that TLR3 acts on the cell surface to sense viral infection. In this study, we examined the expression and localization of human TLR3 in various DC subsets using anti-TLR3 mAb. In monocyte-derived immature dendritic cells (iDCs), TLR3 predominantly resided inside the cells but not on the cell surface. iDCs produced IL-12p70 and IFN-alpha and -beta in response to poly(I:C). Similar response was observed in iDCs treated with rotavirus-derived dsRNA. These responses could not be blocked by pretreatment of the cells with anti-TLR3 mAb. In CD11c(+) blood DCs, cytoplasmic retention of TLR3 was also observed as in monocyte-derived iDCs, again endorsing a different TLR3 distribution profile from fibroblasts. In precursor DC2, however, TLR3 could not be detected inside or outside the cells. Of note, there was a putative centrosomal protein that shared an epitope with TLR3 in myeloid DCs and precursor DC2, but not peripheral blood monocytes. Immunoelectron microscopic analysis revealed that TLR3, when stably expressed in the murine B cell line Ba/F3, was specifically accumulated in multivesicular bodies, a subcellular compartment situated in endocytic trafficking pathways. Thus, regulation and localization of TLR3 are different in each cell type, which may reflect participation of cell type-specific multiple pathways in antiviral IFN induction via TLR3.

737 citations

Journal ArticleDOI
TL;DR: In this article, the authors investigated the change in the pseudoelasticity characteristics of Ti-Ni alloys during tension cycling and concluded that the cause for the effect of cyclic deformation is the generation of dislocations in the martensitic phase.
Abstract: Change in the pseudoelasticity characteristics of Ti-Ni alloys during tension cycling was investigated. The critical stress for inducing martensites and the hysteresis of a stress-strain curve decreased with increasing number of cyclic loading, while the permanent elongation increased. The degree of the change in these values showed a strong dependence on the maximum applied stress during stress-induced martensitic transformation. However, no change was induced by cyclic elastic deformation even though high stress was applied. It was also found that the stabilization of the pseudoelasticity characteristics during cyclic loading was established using special thermomechanical treatments which are effective to raise the critical stress for slip. Based on these results it is concluded that the cause for the effect of cyclic deformation is the generation of dislocations in the martensitic phase.

602 citations


Authors

Showing all 8415 results

NameH-indexPapersCitations
Kenji Kangawa1531117110059
Kozo Kaibuchi12949360461
Patrice Nordmann12779067031
Laurent Poirel11762153680
Liyuan Han11476665277
Katsuhiko Ariga11286445242
Shinya Yamanaka11139498438
Naoto Chatani8759726370
H. Hayashii8782733235
Mitsuo Kawato8642235640
Yoshihiko Saito8471130595
Taro Kawai8314166916
Tsukasa Seya7739622248
Nobuhiro Yuki7744220320
Katsuhiko Shirahige7424018587
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20231
20228
2021350
2020312
2019304
2018296