JaLCDOI | 10.18926/AMO/30306 |
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FullText URL | fulltext.pdf |
Author | Tsutsumi, Koji| Nishibori, Masahiro| Saeki, Kiyomi| |
Abstract | In the presence of extracellular Ca2+, 6,7-dihydro-6,8,8, 10-tetramethyl-8H-pyrano [3, 2-g] chromone-2-carboxylic acid (EAA) had an inhibitory effect on the substance P-induced histamine release from rat peritoneal mast cells. Not only Ca2+ but also Mg2+, Sr2+ and Ba2+ were effective in enhancing the activity of EAA. Marked tachyphylaxis to EAA developed irrespective of the presence or absence of extracellular Ca2+. Cross-tachyphylaxis was observed between EAA and disodium cromoglycate (DSCG). These results indicate that the mode of action of EAA is similar, but not identical, with that of DSCG. |
Keywords | 6 7-dihydro-6 8 8 10-tetramethyl-8H-pyrano(3 2-g) chromone-2-carboxylic acid (EAA) disodium cromoglycate histamine release alkaline-earth metal ions substance P |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1984-08 |
Volume | volume38 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 367 |
End Page | 374 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
File Version | publisher |
Refereed | True |
PubMed ID | 6208753 |
Web of Science KeyUT | A1984TG25900006 |
Author | 西堀 正洋| |
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Published Date | 1985-12-31 |
Publication Title | |
Content Type | Thesis or Dissertation |
Author | 西堀 正洋| |
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Published Date | 2001-08-31 |
Publication Title | 岡山医学会雑誌 |
Volume | volume113 |
Issue | issue2 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/31987 |
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FullText URL | fulltext.pdf |
Author | Kawabata, Masahiro| Kawabata, Teruyuki| Nishibori, Masahiro| |
Abstract | DNA damage causes chromosomal instability leading to oncogenesis, apoptosis, and severe failure of cell functions. The DNA repair system includes base excision repair, nucleotide excision repair, mismatch repair, translesion replication, non-homologous end-joining, and recombinational repair. Homologous recombination performs the recombinational repair. The RAD51 gene is an ortholog of Esherichia coli recA, and the gene product Rad51 protein plays a central role in the homologous recombination. In mammals, 7 recA-like genes have been identified: RAD51, RAD51L1/B, RAD51L2/C, RAD51L3/D, XRCC2, XRCC3, and DMC1. These genes, with the exception of meiosis-specific DMC1, are essential for development in mammals. Disruption of the RAD51 gene leads to cell death, whereas RAD51L1/B, RAD51L2/C, RAD51L3/D, XRCC2, and XRCC3 genes (RAD51 paralogs) are not essential for viability of cells, but these gene-deficient cells exhibit a similar defective phenotype. Yeast two-hybrid analysis, co-immunoprecipitation, mutation analysis, and domain mapping of Rad51 and Rad51 paralogs have revealed protein-protein interactions among these gene products. Recent investigations have shown that Rad51 paralogs play a role not only in an early step, but also in a late step of homologous recombination. In addition, identification of alternative transcripts of some RAD51 paralogs may reflect the complexity of the homologous recombination system. |
Keywords | RAD51 RAD51 paralogs recA recombination DNA repair |
Amo Type | Review |
Publication Title | Acta Medica Okayama |
Published Date | 2005-02 |
Volume | volume59 |
Issue | issue1 |
Publisher | Okayama University Medical School |
Start Page | 1 |
End Page | 9 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
File Version | publisher |
Refereed | True |
PubMed ID | 15902993 |
Web of Science KeyUT | 000227263300001 |
Author | Liu, Keyue| Mori, Shuji| Takahashi, Hideo| Tomono, Yasuko| Wake, Hidenori| Kanke, Toru| Sato, Yasuharu| Hiraga, Norihito| Adachi, Naoto| Yoshino, Tadashi| Nishibori, Masahiro| |
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Published Date | 2008-12-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume120 |
Issue | issue3 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/31855 |
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FullText URL | fulltext.pdf |
Author | Nishibori, Masahiro| Takahashi, Hide K.| Katayama, Hiroshi| Mori, Shuji| Saito, Shinya| Iwagaki, Hiromi| Tanaka, Noriaki| Morita, Kiyoshi| Ohtsuka, Aiji| |
Abstract | Lipopolysaccharide (LPS) is one of the major causes of septic shock. The polymyxin B-immobilized filter column (PMX) was developed for the adsorption of endotoxin by direct hemoperfusion and has been used for the treatment of LPS-induced septic shock. In this study, we demonstrated that PMX also specifically bound monocytes from the peripheral blood leukocytes of septic patients by mean of an analysis of bound cells using immunocytochemical and electron microscopic techniques. The specific removal of monocytes from septic patients may produce beneficial effects by reducing the interaction between monocytes and functionally associated cells including vascular endothelial cells. |
Keywords | septic shock polymixin B-immobilized column monocyte adsorptive removal |
Amo Type | Short Communication |
Publication Title | Acta Medica Okayama |
Published Date | 2009-02 |
Volume | volume63 |
Issue | issue1 |
Publisher | Okayama University Medical School |
Start Page | 65 |
End Page | 69 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
File Version | publisher |
Refereed | True |
Web of Science KeyUT | 000263730300009 |
JaLCDOI | 10.18926/AMO/31812 |
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FullText URL | fulltext.pdf |
Author | Liu, Rui| Mori, Shuji| Wake, Hidenori| Zhang, Jiyong| Liu, Keyue| Izushi, Yasuhisa| Takahashi, Hideo K.| Peng, Bo| Nishibori, Masahiro| |
Abstract | Interaction between the receptor for advanced glycation end products (RAGE) and its ligands has been implicated in the pathogenesis of various inflammatory disorders. In this study, we establish an in vitro binding assay in which recombinant human high-mobility group box 1 (rhHMGB1) or recombinant human S100A12 (rhS100A12) immobilized on the microplate binds to recombinant soluble RAGE (rsRAGE). The rsRAGE binding to both rhHMGB1 and rhS100A12 was saturable and dependent on the immobilized ligands. The binding of rsRAGE to rhS100A12 depended on Ca2 and Zn2, whereas that to rhHMGB1 was not. Scatchard plot analysis showed that rsRAGE had higher affinity for rhHMGB1 than for rhS100A12. rsRAGE was demonstrated to bind to heparin, and rhS100A12, in the presence of Ca2, was also found to bind to heparin. We examined the effects of heparin preparations with different molecular sizesunfractionated native heparin (UFH), low molecular weight heparin (LMWH) 5000Da, and LMWH 3000Da on the binding of rsRAGE to rhHMGB1 and rhS100A12. All 3 preparations concentration-dependently inhibited the binding of rsRAGE to rhHMGB1 to a greater extent than did rhS100A12. These results suggested that heparin's anti-inflammatory effects can be partly explained by its blocking of the interaction between HMGB1 or S100A12 and RAGE. On the other hand, heparin would be a promising effective remedy against RAGE-related inflammatory disorders. |
Keywords | RAGE HMGB1 S100A12 heparin inflammation |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2009-08 |
Volume | volume63 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 203 |
End Page | 211 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
File Version | publisher |
Refereed | True |
PubMed ID | 19727205 |
Web of Science KeyUT | 000269228400006 |
JaLCDOI | 10.18926/AMO/31845 |
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FullText URL | fulltext.pdf |
Author | Wake, Hidenori| Mori, Shuji| Liu, Keyue| Takahashi, Hideo K.| Nishibori, Masahiro| |
Abstract | Angiogenesis involves complex processes mediated by several factors and is associated with inflammation and wound healing. High mobility group box 1 (HMGB1) is released from necrotic cells as well as macrophages and plays proinflammatory roles. In the present study, we examined whether HMGB1 would exhibit angiogenic activity in a matrigel plug assay in mice. HMGB1 in combination with heparin strongly induced angiogenesis, whereas neither HMGB1 nor heparin alone showed such angiogenic activity. The heparin-dependent induction of angiogenesis by HMGB1 was accompanied by increases in the expression of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor-A120 (VEGF-A120). It is likely that the dependence of the angiogenic activity of HMGB1 on heparin was due to the efficiency of the diffusion of the HMGB1-heparin complex from matrigel to the surrounding areas. VEGF-A165 possessing a heparin-binding domain showed a pattern of heparin-dependent angiogenic activity similar to that of HMGB1. The presence of heparin also inhibited the degradation of HMGB1 by plasmin in vitro. Taken together, these results suggested that HMGB1 in complex with heparin possesses remarkable angiogenic activity, probably through the induction of TNF-alpha and VEGF-A120. |
Keywords | angiogenesis HMGB1 heparin |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2009-10 |
Volume | volume63 |
Issue | issue5 |
Publisher | Okayama University Medical School |
Start Page | 249 |
End Page | 262 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
File Version | publisher |
Refereed | True |
PubMed ID | 19893601 |
Web of Science KeyUT | 000271132000005 |
Author | Nishibori, Masahiro| |
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Published Date | 2010-12-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume122 |
Issue | issue3 |
Content Type | Article |
JaLCDOI | 10.18926/AMO/47262 |
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FullText URL | 65_6_369.pdf |
Author | Terada, Chuji| Yoshida, Aki| Nasu, Yoshihisa| Mori, Shuji| Tomono, Yasuko| Tanaka, Masato| Takahashi, Hideo K.| Nishibori, Masahiro| Ozaki, Toshifumi| Nishida, Keiichiro| |
Abstract | We investigated the expression and localization of high-mobility group box chromosomal protein-1 (HMGB-1) in human osteoarthritic (OA) cartilage in relation to the histopathological grade of cartilage destruction, and examined the role of HMGB-1 in the regulation of proinflammatory cytokine expression in chondrocytes. An immunohistochemical study demonstrated that total HMGB-1-positive cell ratios increase as the Osteoarthritis Research Society International (OARSI) histological grade increased. The population of cytoplasmic HMGB-1-positive chondrocytes was especially increased in the deep layers of higher-grade cartilage. The ratios and localization of receptors for advanced glycation end products (RAGE) expression by chondrocytes in Grade 2, 3, and 4 were significantly higher than those in Grade 1. In vitro stimulation with IL-1β, but not TNFα, significantly upregulated the expression of HMGB-1 mRNA by human OA chondrocytes. Both IL-1β and TNFα promoted the translocation of HMGB-1 from nuclei to cytoplasm. IL-1β and TNFα secretions were stimulated at higher levels of HMGB-1. The results of our study suggest the involvement of HMGB-1 in the pathogenesis of cartilage destruction in OA. |
Keywords | HMGB-1 RAGE chondrocyte osteoarthritis cartilage |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-12 |
Volume | volume65 |
Issue | issue6 |
Publisher | Okayama University Medical School |
Start Page | 369 |
End Page | 377 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 22189477 |
Web of Science KeyUT | 000298516900003 |
Author | Okuma, Yu| Liu, Keyue| Wake, Hidenori| Haruma, Jun| Yoshino, Tadashi| Ohtsuka, Aiji| Takahashi, Hideo| Mori, Shuji| Nishibori, Masahiro| Date, Isao| |
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Published Date | 2013-08-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume125 |
Issue | issue2 |
Content Type | Journal Article |
Author | Nakamura, Yoki| Morioka, Norimitsu| Abe, Hiromi| Zhang, Fang Fang| Hisaoka-Nakashima, Kazue| Liu, Keyue| Nishibori, Masahiro| Nakata, Yoshihiro| |
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Published Date | 2013-08-21 |
Publication Title | PLOS ONE |
Volume | volume8 |
Issue | issue8 |
Content Type | Journal Article |
FullText URL | fulltext.pdf |
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Author | Chen, Youyi| Sumardika, I Wayan| Tomonobu, Nahoko| Kinoshita, Rie| Inoue, Yusuke| Iioka, Hidekazu| Mitsui, Yosuke| Saito, Ken| Ruma, I Made Winarsa| Sato, Hiroki| Yamauchi, Akira| Murata, Hitoshi| Yamamoto, Ken-ichi| Tomida, Shuta| Shien, Kazuhiko| Yamamoto, Hiromasa| Soh, Junichi| Futami, Junichiro| Kubo, Miyoko| Putranto, Endy Widya| Murakami, Takashi| Liu, Ming| Hibino, Toshihiko| Nishibori, Masahiro| Kondo, Eisaku| Toyooka, Shinichi| Sakaguchi, Masakiyo| |
Published Date | 2019-07 |
Publication Title | Neoplasia |
Volume | volume21 |
Issue | issue7 |
Start Page | 627 |
End Page | 640 |
ISSN | 1522-8002 |
NCID | AA11470191 |
Content Type | Journal Article |
language | English |
OAI-PMH Set | 岡山大学 |
Copyright Holders | © 2019 The Authors. |
File Version | publisher |
PubMed ID | 31100639 |
DOI | 10.1016/j.neo.2019.04.006 |
Web of Science KeyUT | 000472189700001 |
Related Url | isVersionOf https://doi.org/10.1016/j.neo.2019.04.006 |
Title Alternative | The 9th International DAMPs and Alarmins Symposium (9th iDEAs) |
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FullText URL | 132_39.pdf |
Author | Nishibori, Masahiro| |
Publication Title | Journal of Okayama Medical Association |
Published Date | 2020-04-01 |
Volume | volume132 |
Issue | issue1 |
Start Page | 39 |
End Page | 40 |
ISSN | 0030-1558 |
Related Url | isVersionOf https://doi.org/10.4044/joma.132.39 |
language | Japanese |
Copyright Holders | Copyright (c) 2020 岡山医学会 |
File Version | publisher |
DOI | 10.4044/joma.132.39 |
NAID | 130007840312 |
FullText URL | fulltext.pdf |
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Author | Nishibori, Masahiro| Wang, Dengli| Ousaka, Daiki| Wake, Hidenori| |
Keywords | high mobility group box-1 blood-brain barrier inflammation stroke trauma vascular endothelial cell pericyte monoclonal antibody |
Published Date | 2020-12-10 |
Publication Title | Cells |
Volume | volume9 |
Issue | issue12 |
Publisher | MDPI |
Start Page | 2650 |
ISSN | 2073-4409 |
Content Type | Journal Article |
language | English |
OAI-PMH Set | 岡山大学 |
Copyright Holders | © 2020 by the authors. |
File Version | publisher |
PubMed ID | 33321691 |
DOI | 10.3390/cells9122650 |
Web of Science KeyUT | 000601700200001 |
Related Url | isVersionOf https://doi.org/10.3390/cells9122650 |
Title Alternative | Novel understanding of septic pathophysiology and neutrophil extracellular traps |
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FullText URL | 133_10.pdf |
Author | Nishibori, Masahiro| Wake, Hidenori| |
Keywords | 敗血症 histidine-rich glycoprotein(HRG) 好中球 NETs 血管内皮細胞 |
Publication Title | Journal of Okayama Medical Association |
Published Date | 2021-04-01 |
Volume | volume133 |
Issue | issue1 |
Start Page | 10 |
End Page | 22 |
ISSN | 0030-1558 |
Related Url | isVersionOf https://doi.org/10.4044/joma.133.10 |
language | Japanese |
Copyright Holders | Copyright (c) 2021 岡山医学会 |
File Version | publisher |
DOI | 10.4044/joma.133.10 |
NAID | 130008034811 |
FullText URL | fulltext.pdf |
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Author | Kuroda, Kosuke| Ishii, Kenzo| Mihara, Yuko| Kawanoue, Naoya| Wake, Hidenori| Mori, Shuji| Yoshida, Michihiro| Nishibori, Masahiro| Morimatsu, Hiroshi| |
Published Date | 2021-05-13 |
Publication Title | Scientific Reports |
Volume | volume11 |
Issue | issue1 |
Publisher | Nature Research |
Start Page | 10223 |
ISSN | 2045-2322 |
Content Type | Journal Article |
language | English |
OAI-PMH Set | 岡山大学 |
Copyright Holders | © The Author(s) 2021 |
File Version | publisher |
PubMed ID | 33986340 |
NAID | 120007053368 |
DOI | 10.1038/s41598-021-89555-z |
Web of Science KeyUT | 000656946100013 |
Related Url | isVersionOf https://doi.org/10.1038/s41598-021-89555-z |
JaLCDOI | 10.18926/AMO/62805 |
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FullText URL | 75_6_671.pdf |
Author | Gao, Shangze| Nishibori, Masahiro| |
Abstract | Histidine-rich glycoprotein (HRG) is a 75 kDa plasma protein that is synthesized in the liver of many verte-brates and present in their plasma at relatively high concentrations of 100-150 μg/mL. HRG is an abundant and well-characterized protein having a multidomain structure that enable it to interact with many ligands, func-tion as an adaptor molecule, and participate in numerous physiological and pathological processes. As a plasma protein, HRG has been reported to regulate vascular biology, including coagulation, fibrinolysis and angiogenesis, through its binding with several ligands (heparin, FXII, fibrinogen, thrombospondin, and plas-minogen) and interaction with many types of cells (endothelial cells, erythrocytes, neutrophils and platelets). This review aims to summarize the roles of HRG in maintaining vascular homeostasis and regulating angiogen-esis in various pathological conditions. |
Keywords | histidine-rich glycoprotein vascular biology coagulation angiogenesis |
Amo Type | Review |
Publication Title | Acta Medica Okayama |
Published Date | 2021-12 |
Volume | volume75 |
Issue | issue6 |
Publisher | Okayama University Medical School |
Start Page | 671 |
End Page | 675 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | Copyright Ⓒ 2021 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 34955533 |
Web of Science KeyUT | 000735297900001 |
NAID | 120007180287 |
FullText URL | fulltext20210831-4.pdf |
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Author | Masai, Kaori| Kuroda, Keita| Isooka, Nami| Kikuoka, Ryo| Murakami, Shinki| Kamimai, Sunao| Wang, Dengli| Liu, Keyue| Miyazaki, Ikuko| Nishibori, Masahiro| Asanuma, Masato| |
Keywords | methamphetamine dopamine neuron high mobility group box-1 hyperthermia inflammation neurotoxicity |
Note | This is a post-peer-review, pre-copyedit version of an article published in Neurotoxicity Research. The final authenticated version is available online at: https://doi.org/10.1007/s12640-021-00402-5 This fulltext is available in Aug. 2022.| |
Published Date | 2021-8-21 |
Publication Title | Neurotoxicity Research |
Volume | volume39 |
Publisher | Springer Science and Business Media LLC |
Start Page | 1511 |
End Page | 1523 |
ISSN | 1029-8428 |
NCID | AA11570800 |
Content Type | Journal Article |
language | English |
OAI-PMH Set | 岡山大学 |
Copyright Holders | © 2021 Springer Nature Switzerland AG |
File Version | author |
PubMed ID | 34417986 |
DOI | 10.1007/s12640-021-00402-5 |
Web of Science KeyUT | 000687003700001 |
Related Url | isVersionOf https://doi.org/10.1007/s12640-021-00402-5 |
FullText URL | fulltext20210908-1.pdf figure20210908-1.pdf |
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Author | Namba, Takahiro| Tsuge, Mitsuru| Yashiro, Masato| Saito, Yukie| Liu, Keyue| Nishibori, Masahiro| Morishima, Tsuneo| Tsukahara, Hirokazu| |
Keywords | Influenza Acute respiratory distress syndrome High mobility group box 1 Human pulmonary microvascular endothelial cell Cytokine Tumor necrosis factor-α |
Note | This is an Accepted Manuscript of an article published by Springer Science. This fulltext is available in Aug. 2022.| |
Published Date | 2021-8-29 |
Publication Title | Inflammation Research |
Publisher | Springer Science and Business Media LLC |
ISSN | 1023-3830 |
Content Type | Journal Article |
language | English |
OAI-PMH Set | 岡山大学 |
File Version | author |
PubMed ID | 34455489 |
DOI | 10.1007/s00011-021-01496-5 |
Web of Science KeyUT | 000690802000001 |
Related Url | isVersionOf https://doi.org/10.1007/s00011-021-01496-5 |