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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
TL;DR: The complete chromosome sequence of an O157:H7 strain isolated from the Sakai outbreak is reported, and the results of genomic comparison with a benign laboratory strain, K-12 MG1655, are identified, which may represent the fundamental backbone of the E. coli chromosome.
Abstract: Escherichia coli O157:H7 is a major food-borne infectious pathogen that causes diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Here we report the complete chromosome sequence of an O157:H7 strain isolated from the Sakai outbreak, and the results of genomic comparison with a benign laboratory strain, K-12 MG1655. The chromosome is 5.5 Mb in size, 859 Kb larger than that of K-12. We identified a 4.1-Mb sequence highly conserved between the two strains, which may represent the fundamental backbone of the E. coli chromosome. The remaining 1.4-Mb sequence comprises of O157:H7-specific sequences, most of which are horizontally transferred foreign DNAs. The predominant roles of bacteriophages in the emergence of O157:H7 is evident by the presence of 24 prophages and prophage-like elements that occupy more than half of the O157:H7-specific sequences. The O157:H7 chromosome encodes 1632 proteins and 20 tRNAs that are not present in K-12. Among these, at least 131 proteins are assumed to have virulence-related functions. Genome-wide codon usage analysis suggested that the O157:H7-specific tRNAs are involved in the efficient expression of the strain-specific genes. A complete set of the genes specific to O157:H7 presented here sheds new insight into the pathogenicity and the physiology of O157:H7, and will open a way to fully understand the molecular mechanisms underlying the O157:H7 infection.

1,265 citations

Journal Article
TL;DR: This study addressed the question of whether apoptosis depends on intracellular ATP levels, since longer incubation under ATP-depleting conditions results in necrotic cell death, and indicated that ATP levels are a determinant of manifestation of cell death.
Abstract: Although apoptosis and necrosis are morphologically distinct manifestations of cell death, apoptosis and some necroses share common features in the death signaling pathway involving functional steps of death-driving interleukin 1beta-converting enzyme family proteases and anti-cell death protein Bcl-2. One evident physiological difference in cells undergoing apoptosis versus necrosis is in intracellular levels of ATP. In this study, we specifically addressed the question of whether apoptosis depends on intracellular ATP levels, since longer incubation under ATP-depleting conditions results in necrotic cell death. Incubation of cells in glucose-free medium with an inhibitor of mitochondrial F0F1-ATPases reduces intracellular ATP levels and completely blocks Fas/Apo-1-stimulated apoptosis. ATP supplied through glycolysis or oxidative phosphorylation restores the apoptotic cell death pathway. ATP depletion also leads to a block in Fas-induced activation of CPP32/Yama(-like) proteases, and when ATP is depleted after the activation of the proteases, subsequent apoptosis is significantly blocked. Thus, ATP-dependent steps exist both upstream and downstream of CPP32/Yama(-like) protease activation in apoptotic signal transduction. Treatment with the calcium ionophore induces apoptosis under ATP-supplying conditions but induces necrotic cell death under ATP-depleting conditions, indicating that ATP levels are a determinant of manifestation of cell death.

1,264 citations

Journal ArticleDOI
23 Sep 1994-Science
TL;DR: The basal ganglia are neural structures within the motor and cognitive control circuits in the mammalian forebrain and are interconnected with the neocortex by multiple loops that have a distributed modular architecture resembling local expert architectures of computational learning models during sensorimotor learning.
Abstract: The basal ganglia are neural structures within the motor and cognitive control circuits in the mammalian forebrain and are interconnected with the neocortex by multiple loops. Dysfunction in these parallel loops caused by damage to the striatum results in major defects in voluntary movement, exemplified in Parkinson's disease and Huntington's disease. These parallel loops have a distributed modular architecture resembling local expert architectures of computational learning models. During sensorimotor learning, such distributed networks may be coordinated by widely spaced striatal interneurons that acquire response properties on the basis of experienced reward.

1,257 citations

Journal ArticleDOI
TL;DR: Assessment of the contribution of the pro-inflammatory cytokine interleukin (IL)-6 to the increased resistance of mucosal T cells against apoptosis in Crohn disease indicates that a pathway of T-cell activation driven by IL-6–sIL-6R contributes to the perpetuation of chronic intestinal inflammation.
Abstract: The pro-inflammatory cytokine interleukin (IL)-6 (refs. 1-5) can bind to cells lacking the IL-6 receptor (IL-6R) when it forms a complex with the soluble IL-6R (sIL-6R) (trans signaling). Here, we have assessed the contribution of this system to the increased resistance of mucosal T cells against apoptosis in Crohn disease (CD), a chronic inflammatory disease of the gastrointestinal tract. A neutralizing antibody against IL-6R suppressed established experimental colitis in various animal models of CD mediated by type 1 T-helper cells, by inducing apoptosis of lamina propria T cells. Similarly, specific neutralization of sIL-6R in vivo by a newly designed gp130-Fc fusion protein caused suppression of colitis activity and induction of apoptosis, indicating that sIL-6R prevents mucosal T-cell apoptosis. In patients with CD, mucosal T cells showed strong evidence for IL-6 trans signaling, with activation of signal transducer and activator of transcription 3, bcl-2 and bcl-xl. Blockade of IL-6 trans signaling caused T-cell apoptosis, indicating that the IL-6-sIL-6R system mediates the resistance of T cells to apoptosis in CD. These data indicate that a pathway of T-cell activation driven by IL-6-sIL-6R contributes to the perpetuation of chronic intestinal inflammation. Specific targeting of this pathway may be a promising new approach for the treatment of CD.

1,248 citations

Journal ArticleDOI
TL;DR: In this paper, the state-of-the-art technologies on photonics-based terahertz communications are compared with competing technologies based on electronics and free-space optical communications.
Abstract: This Review covers the state-of-the-art technologies on photonics-based terahertz communications, which are compared with competing technologies based on electronics and free-space optical communications. Future prospects and challenges are also discussed. Almost 15 years have passed since the initial demonstrations of terahertz (THz) wireless communications were made using both pulsed and continuous waves. THz technologies are attracting great interest and are expected to meet the ever-increasing demand for high-capacity wireless communications. Here, we review the latest trends in THz communications research, focusing on how photonics technologies have played a key role in the development of first-age THz communication systems. We also provide a comparison with other competitive technologies, such as THz transceivers enabled by electronic devices as well as free-space lightwave communications.

1,238 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