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Institution

Kumamoto University

EducationKumamoto, Kumamoto, Japan
About: Kumamoto University is a education organization based out in Kumamoto, Kumamoto, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 19602 authors who have published 35513 publications receiving 901260 citations. The organization is also known as: Kumamoto Daigaku.


Papers
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Journal ArticleDOI
TL;DR: Osteoclasts are bone-resorbing, multinucleated giant cells that are essential for bone remodeling and are formed through cell fusion of mononuclear precursor cells and DC-STAMP directly induced the expression of the osteoclast marker tartrate-resistant acid phosphatase, demonstrating for the first time that DC- STAMP has an essential role in osteoc lastogenesis.
Abstract: Osteoclasts are bone-resorbing, multinucleated giant cells that are essential for bone remodeling and are formed through cell fusion of mononuclear precursor cells. Although receptor activator of nuclear factor–κB ligand (RANKL) has been demonstrated to be an important osteoclastogenic cytokine, the cell surface molecules involved in osteoclastogenesis are mostly unknown. Here, we report that the seven-transmembrane receptor-like molecule, dendritic cell–specific transmembrane protein (DC-STAMP) is involved in osteoclastogenesis. Expression of DC-STAMP is rapidly induced in osteoclast precursor cells by RANKL and other osteoclastogenic stimulations. Targeted inhibition of DC-STAMP by small interfering RNAs and specific antibody markedly suppressed the formation of multinucleated osteoclast-like cells. Overexpression of DC-STAMP enhanced osteoclastogenesis in the presence of RANKL. Furthermore, DC-STAMP directly induced the expression of the osteoclast marker tartrate-resistant acid phosphatase. These data demonstrate for the first time that DC-STAMP has an essential role in osteoclastogenesis.

344 citations

Journal ArticleDOI
TL;DR: The CD144-positive EMP exist in human plasma, and plasmaCD144-EMP levels can be a clinically specific and quantitative marker of EC dysfunction and/or injury and may be useful for identifying DM patients with increased risk of CAD.

344 citations

Journal ArticleDOI
TL;DR: The response of left coronary arteries to intracoronary injection of acetylcholine (ACh) 50 micrograms in 74 patients was examined by measuring the diameter changes with a videodensitometric analysis system and the dilator response to ACh was significantly greater in the distal segment than in the proximal segment.
Abstract: We examined the response of left coronary arteries to intracoronary injection of acetylcholine (ACh) 50 micrograms in 74 patients by measuring the diameter changes with a videodensitometric analysis system. Patients with angiographically normal coronary arteries were subdivided into a younger group of 26 patients (age, 9-29 years) and an older group of 23 patients (age, 31-68 years). In the younger group, the diameter at the distal segment of the left anterior descending artery (LAD) and at the proximal, middle, and distal segments of the left circumflex artery (LCx) increased significantly (16.7 +/- 19.3%, p less than 0.01, for LAD and 8.0 +/- 18.8%, p less than 0.05; 11.0 +/- 16.1%, p less than 0.01; and 19.8 +/- 17.5%, p less than 0.01, for LCx segments, respectively) in response to ACh. In the older group, on the other hand, the diameter at the proximal and middle segments of LAD and LCx decreased significantly (-20.8 +/- 16.9%, p less than 0.01; and -17.9 +/- 28.4%, p less than 0.01, for LAD segments and -14.6 +/- 17.4%, p less than 0.01; and -11.3 +/- 21.4%, p less than 0.05, for LCx segments, respectively). The dilator response to ACh in the younger group was significantly greater in the distal segment than in the proximal segment in both LAD and LCx (p less than 0.01 for LAD and p less than 0.05 for LCx). The constrictor response to ACh in the older group was significantly greater in the proximal than the distal segment in both LAD and LCx (p less than 0.05 for LAD and LCx, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

344 citations

Journal Article
TL;DR: The result suggests that the number of colorectal polyps in FAP patients may be associated with a difference in the stability or biological function of the truncated APC protein.
Abstract: Recently we have isolated the adenomatous polyposis coli (APC) gene which causes familial adenomatous polyposis (FAP), and its germ-line mutations in a substantial number of FAP patients have been identified. On the basis of this information, we compared the location of germ-line mutations in the APC gene in 22 unrelated patients (12 of whom have been reported previously) with the number of colorectal polyps developed in FAP patients; 17 were sparse types and five were profuse types. All but one of the mutations were considered to cause truncation of the gene product by frame-shift due to deletion (14 cases) or nonsense mutation (seven cases). The location of the germ-line mutations seems to correlate with the two clinical types; germ-line mutations in five FAP patients with profuse polyps were observed between codon 1250 and codon 1464, whereas mutations in 17 FAP patients with fewer polyps were observed in the other regions of the APC gene. The result suggests that the number of colorectal polyps in FAP patients may be associated with a difference in the stability or biological function of the truncated APC protein.

344 citations

Journal ArticleDOI
TL;DR: The present review discusses recent findings regarding the nature of drug binding sites, drug-albumin binding in certain diseased states or in the presence of co administered drugs, and the potential of utilizing albumin-drug interactions in clinical applications.

344 citations


Authors

Showing all 19645 results

NameH-indexPapersCitations
Fred H. Gage216967185732
George D. Yancopoulos15849693955
Kenji Kangawa1531117110059
Tasuku Honjo14171288428
Hideo Yagita13794670623
Masashi Yanagisawa13052483631
Kazuwa Nakao128104170812
Kouji Matsushima12459056995
Thomas E. Mallouk12254952593
Toshio Hirano12040155721
Eisuke Nishida11234945918
Hiroaki Shimokawa11194948822
Bernd Bukau11127138446
Kazuo Tsubota105137948991
Toshio Suda10458041069
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202315
202297
20211,701
20201,654
20191,511
20181,330