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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 & Population. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Population, Catalysis, Thin film, Gene


Papers
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Journal ArticleDOI
TL;DR: In this paper, phase diagrams of lead-free alloy systems have been intensively examined by using careful thermal and microstructural analysis combined with the thermodynamic calculation such as the CLAPHAD method.
Abstract: Lead-free soldering has emerged as one of the key technologies for assembling in environmental-conscious electronics. Among several candidate alloys, the Sn–Ag–Cu alloy family is believed to be the first choice with the combination of other alloys such as Sn–Zn–Bi, Sn–Cu and Sn–Bi–Ag. Phase diagrams of lead-free alloy systems have been intensively examined by using careful thermal and microstructural analysis combined with the thermodynamic calculation such as the CLAPHAD method. The Cu6Sn5/Cu3Sn layers are formed at most lead-free solder alloy/Cu interfaces, while Cu–Zn compound layers are formed in the Sn–Zn/Cu system. Growth kinetics of intermetallic layers both in solid-state and in soldering are also discussed. Creep and fatigue phenomena are also reviewed. In many aspects of lead-free soldering, much more work is required to establish a sound scientific basis to promote their applications.

665 citations

Journal ArticleDOI
25 Oct 2002-Science
TL;DR: By a comparative analysis of ion relaxations and valence charge redistributions in aluminum and copper, this work arrives at contrasting descriptions of bonding characteristics in these two metals that can explain their relative strength and deformation behavior.
Abstract: Although aluminum has a smaller modulus in [111] shear than that of copper, we find by first-principles calculation that its ideal shear strength is larger because of a more extended deformation range before softening. This fundamental behavior, along with an abnormally high intrinsic stacking fault energy and a different orientation dependence on pressure hardening, are traced to the directional nature of its bonding. By a comparative analysis of ion relaxations and valence charge redistributions in aluminum and copper, we arrive at contrasting descriptions of bonding characteristics in these two metals that can explain their relative strength and deformation behavior.

665 citations

Book ChapterDOI
TL;DR: In this paper, a signal orchestration model was proposed to explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances, which can be seen as a consequence of the orchestration of diverse signaling pathways generated by a given ligand.
Abstract: Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.

664 citations

Journal ArticleDOI
31 Mar 2011-Nature
TL;DR: It is reported that SHARPIN functions as a novel component of the linear ubiquitin chain assembly complex (LUBAC) and that the absence of SHARPin causes dysregulation of NF-κB and apoptotic signalling pathways, explaining the severe phenotypes displayed by chronic proliferative dermatitis (cpdm) in SHARPIn-deficient mice.
Abstract: SHARPIN is a ubiquitin-binding and ubiquitin-like-domain-containing protein which, when mutated in mice, results in immune system disorders and multi-organ inflammation. Here we report that SHARPIN functions as a novel component of the linear ubiquitin chain assembly complex (LUBAC) and that the absence of SHARPIN causes dysregulation of NF-κB and apoptotic signalling pathways, explaining the severe phenotypes displayed by chronic proliferative dermatitis (cpdm) in SHARPIN-deficient mice. Upon binding to the LUBAC subunit HOIP (also known as RNF31), SHARPIN stimulates the formation of linear ubiquitin chains in vitro and in vivo. Coexpression of SHARPIN and HOIP promotes linear ubiquitination of NEMO (also known as IKBKG), an adaptor of the IκB kinases (IKKs) and subsequent activation of NF-κB signalling, whereas SHARPIN deficiency in mice causes an impaired activation of the IKK complex and NF-κB in B cells, macrophages and mouse embryonic fibroblasts (MEFs). This effect is further enhanced upon concurrent downregulation of HOIL-1L (also known as RBCK1), another HOIP-binding component of LUBAC. In addition, SHARPIN deficiency leads to rapid cell death upon tumour-necrosis factor α (TNF-α) stimulation via FADD- and caspase-8-dependent pathways. SHARPIN thus activates NF-κB and inhibits apoptosis via distinct pathways in vivo.

663 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
20216,914
20206,865
20196,462
20186,189