=== Generating (published_papers) ===
=== Generating (teaching_experience) ===
=== Generating (education) ===
=== Generating (research_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (awards) ===
=== Generating (association_memberships) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/published_papers.jsonl) ====
line:1, {"insert":{"user_id":"R000041357","type":"published_papers","id":"45564921"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119164","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=405032","label":"url"}],"paper_title":{"en":"Synthesis of secretory leukocyte protease inhibitor using cell-free protein synthesis system","ja":"Synthesis of secretory leukocyte protease inhibitor using cell-free protein synthesis system"},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Kido Rie"},{"name":"Kido Jun-ichi"},{"name":"Bandou Mika"},{"name":"Yoshida Kaya"},{"name":"Murakami Akikazu"},{"name":"Shinohara Yasuo"}],"ja":[{"name":"廣島 佑香"},{"name":"木戸 理恵"},{"name":"木戸 淳一"},{"name":"板東 美香"},{"name":"吉田 賀弥"},{"name":"村上 明一"},{"name":"篠原 康雄"}]},"publication_date":"2024-02","publication_name":{"en":"Odontology","ja":"Odontology"},"languages":["eng"],"referee":true,"identifiers":{"issn":["1618-1247"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118518","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36266256","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=393137","label":"url"}],"paper_title":{"en":"Porphyromonas gingivalis outer membrane vesicles in cerebral ventricles activate microglia in mice","ja":"Porphyromonas gingivalis outer membrane vesicles in cerebral ventricles activate microglia in mice"},"authors":{"en":[{"name":"Yoshida Kayo"},{"name":"Yoshida Kaya"},{"name":"Seyama Mariko"},{"name":"Hiroshima Yuka"},{"name":"Mekata Mana"},{"name":"Fujiwara Natsumi"},{"name":"Kudo Yasusei"},{"name":"Ozaki Kazumi"}],"ja":[{"name":"吉田 佳世"},{"name":"吉田 賀弥"},{"name":"瀬山 真莉子"},{"name":"廣島 佑香"},{"name":"芽形 真奈"},{"name":"藤原 奈津美"},{"name":"工藤 保誠"},{"name":"尾崎 和美"}]},"publication_date":"2023-11","publication_name":{"en":"Oral Diseases","ja":"Oral Diseases"},"volume":"Vol.29","number":"No.8","starting_page":"3688","ending_page":"3697","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/odi.14413"],"issn":["1601-0825"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119199","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36579753","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394011","label":"url"}],"paper_title":{"en":"Lipocalin 2, synthesized using a cell-free protein synthesis system and encapsulated into liposomes, inhibits the adhesion of Porphyromonas gingivalis to human oral epithelial cells.","ja":"Lipocalin 2, synthesized using a cell-free protein synthesis system and encapsulated into liposomes, inhibits the adhesion of Porphyromonas gingivalis to human oral epithelial cells."},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"Hiroshima Yuka"},{"name":"Kido Rie"},{"name":"Yoshida Kaya"},{"name":"Inagaki Yuji"},{"name":"Naruishi Koji"},{"name":"Kajimoto Kazuaki"},{"name":"Kataoka Masatoshi"},{"name":"Shinohara Yasuo"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"木戸 淳一"},{"name":"廣島 佑香"},{"name":"木戸 理恵"},{"name":"吉田 賀弥"},{"name":"稲垣 裕司"},{"name":"成石 浩司"},{"name":"Kajimoto Kazuaki"},{"name":"片岡 正俊"},{"name":"篠原 康雄"},{"name":"湯本 浩通"}]},"publication_date":"2023-04","publication_name":{"en":"Journal of Periodontal Research","ja":"Journal of Periodontal Research"},"volume":"Vol.58","number":"No.2","starting_page":"262","ending_page":"273","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/jre.13088"],"issn":["1600-0765"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36790046","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394014","label":"url"}],"paper_title":{"en":"Utility of a haemoglobin test of gingival crevicular fluid: A multicentre, observational study.","ja":"Utility of a haemoglobin test of gingival crevicular fluid: A multicentre, observational study."},"authors":{"en":[{"name":"Ito Hiroshi"},{"name":"Numabe Yukihiro"},{"name":"Hashimoto Shuichi"},{"name":"Sekino Satoshi"},{"name":"Murakashi Etsuko"},{"name":"Ishiguro Hitomi"},{"name":"Sasaki Daisuke"},{"name":"Yaegashi Takashi"},{"name":"Takai Hideki"},{"name":"Mezawa Masaru"},{"name":"Ogata Yorimasa"},{"name":"Watanabe Hisashi"},{"name":"Izumi Yuichi"},{"name":"Kido Jun-ichi"},{"name":"Hiroshima Yuka"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"Ito Hiroshi"},{"name":"Numabe Yukihiro"},{"name":"Hashimoto Shuichi"},{"name":"Sekino Satoshi"},{"name":"Murakashi Etsuko"},{"name":"Ishiguro Hitomi"},{"name":"Sasaki Daisuke"},{"name":"Yaegashi Takashi"},{"name":"Takai Hideki"},{"name":"Mezawa Masaru"},{"name":"Ogata Yorimasa"},{"name":"Watanabe Hisashi"},{"name":"Izumi Yuichi"},{"name":"木戸 淳一"},{"name":"廣島 佑香"},{"name":"永田 俊彦"}]},"publication_date":"2023-02-15","publication_name":{"en":"Oral Diseases","ja":"Oral Diseases"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/odi.14536"],"issn":["1601-0825"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118834","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36834667","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394204","label":"url"}],"paper_title":{"en":"Effects of Candidalysin Derived from Candida albicans on the Expression of Pro-Inflammatory Mediators in Human Gingival Fibroblasts","ja":"Effects of Candidalysin Derived from Candida albicans on the Expression of Pro-Inflammatory Mediators in Human Gingival Fibroblasts"},"authors":{"en":[{"name":"Nishikawa Yasufumi"},{"name":"Tomotake Yoritoki"},{"name":"Kawano Hiromichi"},{"name":"Naruishi Koji"},{"name":"Kido Jun-ichi"},{"name":"Hiroshima Yuka"},{"name":"Murakami Akikazu"},{"name":"Ichikawa Tetsuo"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"西川 泰史"},{"name":"友竹 偉則"},{"name":"川野 弘道"},{"name":"成石 浩司"},{"name":"木戸 淳一"},{"name":"廣島 佑香"},{"name":"村上 明一"},{"name":"市川 哲雄"},{"name":"湯本 浩通"}]},"publication_date":"2023-02-07","publication_name":{"en":"International Journal of Molecular Sciences","ja":"International Journal of Molecular Sciences"},"volume":"Vol.24","number":"No.4","starting_page":"3256","ending_page":"3256","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/ijms24043256"],"issn":["1422-0067"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119198","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36745267","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394013","label":"url"}],"paper_title":{"en":"β-defensin 2 synthesized by a cell-free protein synthesis system and encapsulated in liposomes inhibits adhesion of Porphyromonas gingivalis to oral epithelial cells.","ja":"β-defensin 2 synthesized by a cell-free protein synthesis system and encapsulated in liposomes inhibits adhesion of Porphyromonas gingivalis to oral epithelial cells."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Kido Rie"},{"name":"Yoshida Kaya"},{"name":"Bandou Mika"},{"name":"Kajimoto Kazuaki"},{"name":"Yumoto Hiromichi"},{"name":"Shinohara Yasuo"}],"ja":[{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"木戸 理恵"},{"name":"吉田 賀弥"},{"name":"板東 美香"},{"name":"Kajimoto Kazuaki"},{"name":"湯本 浩通"},{"name":"篠原 康雄"}]},"publication_date":"2023-02-06","publication_name":{"en":"Odontology","ja":"Odontology"},"volume":"Vol.111","starting_page":"830","ending_page":"838","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10266-023-00789-x"],"issn":["1618-1255"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:7, {"insert":{"user_id":"R000041357","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117616","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36289904","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=392564","label":"url"}],"paper_title":{"en":"Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways","ja":"Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways"},"authors":{"en":[{"name":"Uemura Yuta"},{"name":"Hiroshima Yuka"},{"name":"Tada Ayano"},{"name":"Murakami Keiji"},{"name":"Yoshida Kaya"},{"name":"Inagaki Yuji"},{"name":"Kuwahara Tomomi"},{"name":"Murakami Akikazu"},{"name":"Fujii Hideki"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"植村 勇太"},{"name":"廣島 佑香"},{"name":"Tada Ayano"},{"name":"村上 圭史"},{"name":"吉田 賀弥"},{"name":"稲垣 裕司"},{"name":"桑原 知巳"},{"name":"村上 明一"},{"name":"藤猪 英樹"},{"name":"湯本 浩通"}]},"description":{"en":"() is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. -OMVs are involved in the pathogenesis of periodontitis. -OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of -OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. -OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. -OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that -OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that -OMVs may play important roles in periodontitis exacerbation by stimulating various pathways.","ja":"() is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. -OMVs are involved in the pathogenesis of periodontitis. -OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of -OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. -OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. -OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that -OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that -OMVs may play important roles in periodontitis exacerbation by stimulating various pathways."},"publication_date":"2022-10-20","publication_name":{"en":"Biomedicines","ja":"Biomedicines"},"volume":"Vol.10","number":"No.10","starting_page":"2643","ending_page":"2643","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/biomedicines10102643"],"issn":["2227-9059"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:8, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657495"},"force":{"see_also":[{"@id":"https://doi.org/10.3390/antibiotics11060773","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117279","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35740179","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=385765","label":"url"}],"paper_title":{"en":"pruR and PA0065 Genes Are Responsible for Decreasing Antibiotic Tolerance by Autoinducer Analog-1 (AIA-1) in Pseudomonas aeruginosa","ja":"pruR and PA0065 Genes Are Responsible for Decreasing Antibiotic Tolerance by Autoinducer Analog-1 (AIA-1) in Pseudomonas aeruginosa"},"authors":{"en":[{"name":"Pahlevi Reza Muhammad"},{"name":"Murakami Keiji"},{"name":"Hiroshima Yuka"},{"name":"Murakami Akikazu"},{"name":"Fujii Hideki"}],"ja":[{"name":"MUHAMMAD REZA PAHLEVI"},{"name":"村上 圭史"},{"name":"廣島 佑香"},{"name":"村上 明一"},{"name":"藤猪 英樹"}]},"publication_date":"2022-06-06","publication_name":{"en":"Antibiotics","ja":"Antibiotics"},"volume":"Vol.11","number":"No.6","starting_page":"773","ending_page":"773","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/antibiotics11060773"],"issn":["2079-6382"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:9, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657496"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117210","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35052885","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85121669540&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383520","label":"url"}],"paper_title":{"en":"Autoinducer Analogs Can Provide Bactericidal Activity to Macrolides in Pseudomonas aeruginosa through Antibiotic Tolerance Reduction","ja":"Autoinducer Analogs Can Provide Bactericidal Activity to Macrolides in Pseudomonas aeruginosa through Antibiotic Tolerance Reduction"},"authors":{"en":[{"name":"Abe Mizuki"},{"name":"Murakami Keiji"},{"name":"Hiroshima Yuka"},{"name":"Amoh Takashi"},{"name":"Sebe Mayu"},{"name":"Kataoka Keiko"},{"name":"Fujii Hideki"}],"ja":[{"name":"Abe Mizuki"},{"name":"村上 圭史"},{"name":"廣島 佑香"},{"name":"Amoh Takashi"},{"name":"Sebe Mayu"},{"name":"片岡 佳子"},{"name":"藤猪 英樹"}]},"description":{"en":"Macrolide antibiotics are used in treating chronic biofilm infections despite their unsatisfactory antibacterial activity, because they display several special activities, such as modulation of the bacterial quorum sensing and immunomodulatory effects on the host. In this study, we investigated the effects of the newly synthesized quorum-sensing autoinducer analogs (AIA-1, -2) on the activity of azithromycin and clarithromycin against . In the killing assay of planktonic cells, AIA-1 and -2 enhanced the bactericidal ability of macrolides against PAO1; however, they did not affect the minimum inhibitory concentrations of macrolides. In addition, AIA-1 and -2 considerably improved the killing activity of azithromycin and clarithromycin in biofilm cells. The results indicated that AIA-1 and -2 could affect antibiotic tolerance. Moreover, the results of hydrocarbon adherence and cell membrane permeability assays suggested that AIA-1 and -2 changed bacterial cell surface hydrophobicity and accelerated the outer membrane permeability of the hydrophobic antibiotics such as azithromycin and clarithromycin. Our study demonstrated that the new combination therapy of macrolides and AIA-1 and -2 may improve the therapeutic efficacy of macrolides in the treatment of chronic biofilm infections.","ja":"Macrolide antibiotics are used in treating chronic biofilm infections despite their unsatisfactory antibacterial activity, because they display several special activities, such as modulation of the bacterial quorum sensing and immunomodulatory effects on the host. In this study, we investigated the effects of the newly synthesized quorum-sensing autoinducer analogs (AIA-1, -2) on the activity of azithromycin and clarithromycin against . In the killing assay of planktonic cells, AIA-1 and -2 enhanced the bactericidal ability of macrolides against PAO1; however, they did not affect the minimum inhibitory concentrations of macrolides. In addition, AIA-1 and -2 considerably improved the killing activity of azithromycin and clarithromycin in biofilm cells. The results indicated that AIA-1 and -2 could affect antibiotic tolerance. Moreover, the results of hydrocarbon adherence and cell membrane permeability assays suggested that AIA-1 and -2 changed bacterial cell surface hydrophobicity and accelerated the outer membrane permeability of the hydrophobic antibiotics such as azithromycin and clarithromycin. Our study demonstrated that the new combination therapy of macrolides and AIA-1 and -2 may improve the therapeutic efficacy of macrolides in the treatment of chronic biofilm infections."},"publication_date":"2021-12-22","publication_name":{"en":"Antibiotics","ja":"Antibiotics"},"volume":"Vol.11","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/antibiotics11010010"],"issn":["2079-6382"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:10, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657497"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114681","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32170733","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85081730917&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=363586","label":"url"}],"paper_title":{"en":"Advanced glycation end-products increase lipocalin 2 expression in human oral epithelial cells.","ja":"Advanced glycation end-products increase lipocalin 2 expression in human oral epithelial cells."},"authors":{"en":[{"name":"Kido Rie"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Ikuta Takahisa"},{"name":"Sakamoto Eijiro"},{"name":"Inagaki Yuji"},{"name":"Naruishi Koji"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"木戸 理恵"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"生田 貴久"},{"name":"坂本 英次郎"},{"name":"稲垣 裕司"},{"name":"成石 浩司"},{"name":"湯本 浩通"}]},"publication_date":"2020-03-13","publication_name":{"en":"Journal of Periodontal Research","ja":"Journal of Periodontal Research"},"volume":"Vol.55","number":"No.4","starting_page":"539","ending_page":"550","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/jre.12741"],"issn":["1600-0765"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:11, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657498"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114641","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32149126","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=363582","label":"url"}],"paper_title":{"en":"S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells.","ja":"S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells."},"authors":{"en":[{"name":"Takagi Ryosuke"},{"name":"Sakamoto Eijiro"},{"name":"Kido Jun-ichi"},{"name":"Inagaki Yuji"},{"name":"Hiroshima Yuka"},{"name":"Naruishi Koji"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"高木 亮輔"},{"name":"坂本 英次郎"},{"name":"木戸 淳一"},{"name":"稲垣 裕司"},{"name":"廣島 佑香"},{"name":"成石 浩司"},{"name":"湯本 浩通"}]},"publication_date":"2020-02-19","publication_name":{"en":"BioMed Research International","ja":"BioMed Research International"},"volume":"Vol.2020","number":"No.7149408","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1155/2020/7149408"],"issn":["2314-6141"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:12, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657499"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31394096","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=354464","label":"url"}],"paper_title":{"en":"Functional analysis of coiled-coil domains of MCU in mitochondrial calcium uptake","ja":"Functional analysis of coiled-coil domains of MCU in mitochondrial calcium uptake"},"authors":{"en":[{"name":"Yamamoto Takenori"},{"name":"Ozono Mizune"},{"name":"Watanabe Akira"},{"name":"Maeda Kosuke"},{"name":"Nara Atsushi"},{"name":"Hashida Mei"},{"name":"Ido Yusuke"},{"name":"Hiroshima Yuka"},{"name":"Yamada Akiko"},{"name":"Terada Hiroshi"},{"name":"Shinohara Yasuo"}],"ja":[{"name":"山本 武範"},{"name":"大園 瑞音"},{"name":"渡辺 朗"},{"name":"前田 康輔"},{"name":"奈良 篤"},{"name":"橋田 芽依"},{"name":"井戸 佑介"},{"name":"廣島 佑香"},{"name":"山田 安希子"},{"name":"寺田 弘"},{"name":"篠原 康雄"}]},"description":{"en":"The mitochondrial calcium uniporter (MCU) complex is a highly-selective calcium channel. This complex consists of MCU, mitochondrial calcium uptake proteins (MICUs), MCU regulator 1 (MCUR1), essential MCU regulator element (EMRE), etc. MCU, which is the pore-forming subunit, has 2 highly conserved coiled-coil domains (CC1 and CC2); however, their functional roles are unknown. The yeast expression system of mammalian MCU and EMRE enables precise reconstitution of the properties of the mammalian MCU complex in yeast mitochondria. Using the yeast expression system, we here showed that, when MCU mutant lacking CC1 or CC2 was expressed together with EMRE in yeast, their mitochondrial Ca-uptake function was lost. Additionally, point mutations in CC1 or CC2, which were expected to prevent the formation of the coiled coil, also disrupted the Ca-uptake function. Thus, it is essential for the Ca uptake function of MCU that the coiled-coil structure be formed in CC1 and CC2. The loss of function of those mutated MCUs was also observed in the mitochondria of a yeast strain lacking the yeast MCUR1 homolog. Also, in the D. discoideum MCU, which has EMRE-independent Ca-uptake function, the deletion of either CC1 or CC2 caused the loss of function. These results indicated that the critical functions of CC1 and CC2 were independent of other regulatory subunits such as MCUR1 and EMRE, suggesting that CC1 and CC2 might be essential for pore formation by MCUs themselves. Based on the tetrameric structure of MCU, we discussed the functional roles of the coiled-coil domains of MCU.","ja":"The mitochondrial calcium uniporter (MCU) complex is a highly-selective calcium channel. This complex consists of MCU, mitochondrial calcium uptake proteins (MICUs), MCU regulator 1 (MCUR1), essential MCU regulator element (EMRE), etc. MCU, which is the pore-forming subunit, has 2 highly conserved coiled-coil domains (CC1 and CC2); however, their functional roles are unknown. The yeast expression system of mammalian MCU and EMRE enables precise reconstitution of the properties of the mammalian MCU complex in yeast mitochondria. Using the yeast expression system, we here showed that, when MCU mutant lacking CC1 or CC2 was expressed together with EMRE in yeast, their mitochondrial Ca-uptake function was lost. Additionally, point mutations in CC1 or CC2, which were expected to prevent the formation of the coiled coil, also disrupted the Ca-uptake function. Thus, it is essential for the Ca uptake function of MCU that the coiled-coil structure be formed in CC1 and CC2. The loss of function of those mutated MCUs was also observed in the mitochondria of a yeast strain lacking the yeast MCUR1 homolog. Also, in the D. discoideum MCU, which has EMRE-independent Ca-uptake function, the deletion of either CC1 or CC2 caused the loss of function. These results indicated that the critical functions of CC1 and CC2 were independent of other regulatory subunits such as MCUR1 and EMRE, suggesting that CC1 and CC2 might be essential for pore formation by MCUs themselves. Based on the tetrameric structure of MCU, we discussed the functional roles of the coiled-coil domains of MCU."},"publication_date":"2019-08-03","publication_name":{"en":"Biochimica et Biophysica Acta (BBA) - Bioenergetics","ja":"Biochimica et Biophysica Acta (BBA) - Bioenergetics"},"starting_page":"148061","ending_page":"148061","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbabio.2019.148061"],"issn":["1879-2650"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:13, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657500"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29886045","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=339754","label":"url"}],"paper_title":{"en":"Polyethyleneimine renders mitochondrial membranes permeable by interacting with negatively charged phospholipids in them","ja":"Polyethyleneimine renders mitochondrial membranes permeable by interacting with negatively charged phospholipids in them"},"authors":{"en":[{"name":"Yamamoto Takenori"},{"name":"Tsunoda Moe"},{"name":"Ozono Mizune"},{"name":"Watanabe Akira"},{"name":"Kotake Kazumasa"},{"name":"Hiroshima Yuka"},{"name":"Yamada Akiko"},{"name":"Terada Hiroshi"},{"name":"Shinohara Yasuo"}],"ja":[{"name":"山本 武範"},{"name":"角田 萌"},{"name":"大園 瑞音"},{"name":"渡辺 朗"},{"name":"小武 和正"},{"name":"廣島 佑香"},{"name":"山田 安希子"},{"name":"寺田 弘"},{"name":"篠原 康雄"}]},"description":{"en":"Polyethyleneimines (PEIs) are used for transfection of cells with nucleic acids. Meanwhile, the interaction of PEI with mitochondria causes cytochrome c release prior to apoptosis; the mechanisms how PEI causes this permeabilization of mitochondrial membranes and the release of cytochrome c remain unclear. To clarify these mechanisms, we examined the effects of branched-type PEI and linear-type PEI, each of which was 25 kDa in size, on mitochondria. The permeabilization potency of mitochondrial membranes by branched PEI was stronger than that by linear PEI. The permeabilization by PEIs were insensitive to permeability-transition inhibitors, indicating that PEI-induced permeabilization was not attributed to permeability transition. Meanwhile, PEIs caused permeabilization of artificial lipid vesicles; again, the permeabilization potency of branched PEI was stronger than that of linear PEI. Such a difference in this potency was close to that in the case of isolated mitochondria, signifying that the PEI-induced permeabilization of mitochondrial membranes could be attributed to PEI's interaction with the phospholipid phase. Furthermore, this PEI-induced permeabilization of the lipid vesicles was observed only in the case of lipid vesicles including negatively charged phospholipids. These results indicate that PEIs interacted with negatively charged phospholipids in the mitochondrial membranes to directly lead to their permeabilization.","ja":"Polyethyleneimines (PEIs) are used for transfection of cells with nucleic acids. Meanwhile, the interaction of PEI with mitochondria causes cytochrome c release prior to apoptosis; the mechanisms how PEI causes this permeabilization of mitochondrial membranes and the release of cytochrome c remain unclear. To clarify these mechanisms, we examined the effects of branched-type PEI and linear-type PEI, each of which was 25 kDa in size, on mitochondria. The permeabilization potency of mitochondrial membranes by branched PEI was stronger than that by linear PEI. The permeabilization by PEIs were insensitive to permeability-transition inhibitors, indicating that PEI-induced permeabilization was not attributed to permeability transition. Meanwhile, PEIs caused permeabilization of artificial lipid vesicles; again, the permeabilization potency of branched PEI was stronger than that of linear PEI. Such a difference in this potency was close to that in the case of isolated mitochondria, signifying that the PEI-induced permeabilization of mitochondrial membranes could be attributed to PEI's interaction with the phospholipid phase. Furthermore, this PEI-induced permeabilization of the lipid vesicles was observed only in the case of lipid vesicles including negatively charged phospholipids. These results indicate that PEIs interacted with negatively charged phospholipids in the mitochondrial membranes to directly lead to their permeabilization."},"publication_date":"2018-06-07","publication_name":{"en":"Archives of Biochemistry and Biophysics","ja":"Archives of Biochemistry and Biophysics"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.abb.2018.06.003"],"issn":["1096-0384"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:14, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657501"},"force":{"see_also":[{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85041348582&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=339760","label":"url"}],"paper_title":{"en":"Synthesis and evaluation of simplified functionalized bongkrekic acid analogs.","ja":"Synthesis and evaluation of simplified functionalized bongkrekic acid analogs."},"authors":{"en":[{"name":"Fujita Satoshi"},{"name":"Suyama Masaki"},{"name":"Matsumoto Kenji"},{"name":"Yamamoto Atsushi"},{"name":"Yamamoto Takenori"},{"name":"Hiroshima Yuka"},{"name":"Iwata Takayuki"},{"name":"Kano Arihiro"},{"name":"Shinohara Yasuo"},{"name":"Shindo Mitsuru"}],"ja":[{"name":"Fujita Satoshi"},{"name":"Suyama Masaki"},{"name":"Matsumoto Kenji"},{"name":"Yamamoto Atsushi"},{"name":"山本 武範"},{"name":"廣島 佑香"},{"name":"Iwata Takayuki"},{"name":"Kano Arihiro"},{"name":"篠原 康雄"},{"name":"Shindo Mitsuru"}]},"publication_date":"2018-03-01","publication_name":{"en":"Tetrahedron","ja":"Tetrahedron"},"volume":"Vol.74","number":"No.9","starting_page":"962","ending_page":"969","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.tet.2018.01.018"],"issn":["0040-4020"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:15, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657502"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115598","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30023288","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=345432","label":"url"}],"paper_title":{"en":"Effects of cold exposure on metabolites in brown adipose tissue of rats.","ja":"Effects of cold exposure on metabolites in brown adipose tissue of rats."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Yamamoto Takenori"},{"name":"Watanabe Masahiro"},{"name":"Baba Yoshinobu"},{"name":"Shinohara Yasuo"}],"ja":[{"name":"廣島 佑香"},{"name":"山本 武範"},{"name":"Watanabe Masahiro"},{"name":"馬場 嘉信"},{"name":"篠原 康雄"}]},"description":{"en":"Brown adipose tissue (BAT) plays an important role in regulation of energy expenditure while adapting to a cold environment. BAT thermogenesis depends on uncoupling protein 1 (UCP1), which is expressed in the inner mitochondrial membranes of BAT. Gene expression profiles induced by cold exposure in BAT have been studied, but the metabolomic biological pathway that contributes to the activation of thermogenesis in BAT remains unclear. In this study, we comprehensively compared the relative levels of metabolites between the BAT of rats kept at room temperature (22 °C) and of those exposed to a cold temperature (4 °C) for 48 h using capillary electrophoresis (CE) time-of-flight mass spectrometry (TOFMS) and liquid chromatography (LC)-TOFMS. We identified 218 metabolites (137 cations and 81 anions) by CE-TOFMS and detected 81 metabolites (47 positive and 34 negative) by LC-TOFMS in BAT. We found that cold exposure highly influenced the BAT metabolome. We showed that the cold environment lead to lower levels of glycolysis and gluconeogenesis intermediates and higher levels of the tricarboxylic acid (TCA) cycle metabolites, fatty acids, and acyl-carnitine metabolites than control conditions in the BAT of rats. These results indicate that glycolysis and β-oxidation of fatty acids in BAT are positive biological pathways that contribute to the activation of thermogenesis by cold exposure, thereby facilitating the generation of heat by UCP1. These data provide useful information for understanding the basal metabolic functions of BAT thermogenesis in rats in response to cold exposure.","ja":"Brown adipose tissue (BAT) plays an important role in regulation of energy expenditure while adapting to a cold environment. BAT thermogenesis depends on uncoupling protein 1 (UCP1), which is expressed in the inner mitochondrial membranes of BAT. Gene expression profiles induced by cold exposure in BAT have been studied, but the metabolomic biological pathway that contributes to the activation of thermogenesis in BAT remains unclear. In this study, we comprehensively compared the relative levels of metabolites between the BAT of rats kept at room temperature (22 °C) and of those exposed to a cold temperature (4 °C) for 48 h using capillary electrophoresis (CE) time-of-flight mass spectrometry (TOFMS) and liquid chromatography (LC)-TOFMS. We identified 218 metabolites (137 cations and 81 anions) by CE-TOFMS and detected 81 metabolites (47 positive and 34 negative) by LC-TOFMS in BAT. We found that cold exposure highly influenced the BAT metabolome. We showed that the cold environment lead to lower levels of glycolysis and gluconeogenesis intermediates and higher levels of the tricarboxylic acid (TCA) cycle metabolites, fatty acids, and acyl-carnitine metabolites than control conditions in the BAT of rats. These results indicate that glycolysis and β-oxidation of fatty acids in BAT are positive biological pathways that contribute to the activation of thermogenesis by cold exposure, thereby facilitating the generation of heat by UCP1. These data provide useful information for understanding the basal metabolic functions of BAT thermogenesis in rats in response to cold exposure."},"publication_date":"2018-02-03","publication_name":{"en":"Molecular Genetics and Metabolism Reports","ja":"Molecular Genetics and Metabolism Reports"},"volume":"Vol.15","starting_page":"36","ending_page":"42","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ymgmr.2018.01.005"],"issn":["2214-4269"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:16, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657503"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119200","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28771806","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=327751","label":"url"}],"paper_title":{"en":"Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells.","ja":"Advanced glycation end-products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Sakamoto Eijiro"},{"name":"Yoshida Kaya"},{"name":"Abe Kaori"},{"name":"Naruishi Koji"},{"name":"Yamamoto Takenori"},{"name":"Shinohara Yasuo"},{"name":"Kido Jun-ichi"},{"name":"Geczy L Carolyn"}],"ja":[{"name":"廣島 佑香"},{"name":"坂本 英次郎"},{"name":"吉田 賀弥"},{"name":"阿部 佳織"},{"name":"成石 浩司"},{"name":"山本 武範"},{"name":"篠原 康雄"},{"name":"木戸 淳一"},{"name":"Geczy L Carolyn"}]},"description":{"en":"Accumulation of advanced glycation end-products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA-9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE + PgLPS co-stimulation amplified their expression in OBA-9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA-treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE-induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE-specific siRNA. In contrast, PgLPS-induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2-specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF-κB attenuated AGE- and PgLPS-induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF-κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis. This article is protected by copyright. All rights reserved.","ja":"Accumulation of advanced glycation end-products (AGEs) in periodontal tissues of patients with diabetes mellitus aggravates periodontitis, but the mechanisms are unknown. Calprotectin, a heterocomplex of S100A8 and S100A9 proteins, is a constitutive cytoplasmic component of healthy gingival epithelial cells. This study aimed at investigating the effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin expression in the human gingival epithelial cell line OBA-9. AGE and PgLPS increased the expression of S100A8 and S100A9 mRNAs, and AGE + PgLPS co-stimulation amplified their expression in OBA-9 cells. A higher concentration of calprotectin in cell lysates was also induced by stimulation with AGE and/or PgLPS. S100A8 was mainly translocated from the nucleus to the cytoplasm by AGE stimulation, while cytoplasmic localization of S100A9 was not altered following stimulation with AGE and/or PgLPS. Calprotectin was found in the cytoplasm of BSA-treated cells, but cytoplasmic and nuclear localization was observed following stimulation with AGE and/or PgLPS. AGE-induced S100A8, and S100A9 mRNA expression was partially suppressed by RAGE-specific siRNA. In contrast, PgLPS-induced S100A8 and S100A9 mRNA expression was strongly suppressed by TLR2-specific siRNA. Furthermore, the inhibition of p38, JNK MAPK, and NF-κB attenuated AGE- and PgLPS-induced S100A8 and S100A9 mRNA expression. Taken together, these results demonstrate that AGE acts in synergy with PgLPS to stimulate RAGE and TLR2 expression and activate p38, JNK MAPK, and NF-κB signaling pathways, resulting in increased activation of calprotectin (S100A8/S100A9) in human gingival epithelial cells. Our results suggest that calprotectin may be involved in the pathogenesis of diabetic periodontitis. This article is protected by copyright. All rights reserved."},"publication_date":"2018","publication_name":{"en":"Journal of Cellular Biochemistry","ja":"Journal of Cellular Biochemistry"},"volume":"Vol.119","number":"No.2","starting_page":"1591","ending_page":"1603","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/jcb.26319"],"issn":["1097-4644"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:17, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657504"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111349","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28341446","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=324013","label":"url"}],"paper_title":{"en":"PKR induces the expression of NLRP3 by regulating the NF-κB pathway in Porphyromonas gingivalis-infected osteoblasts","ja":"PKR induces the expression of NLRP3 by regulating the NF-κB pathway in Porphyromonas gingivalis-infected osteoblasts"},"authors":{"en":[{"name":"Yoshida Kaya"},{"name":"Okamura Hirohiko"},{"name":"Hiroshima Yuka"},{"name":"Abe Kaori"},{"name":"Kido Jun-ichi"},{"name":"Shinohara Yasuo"},{"name":"Ozaki Kazumi"}],"ja":[{"name":"吉田 賀弥"},{"name":"岡村 裕彦"},{"name":"廣島 佑香"},{"name":"阿部 佳織"},{"name":"木戸 淳一"},{"name":"篠原 康雄"},{"name":"尾崎 和美"}]},"description":{"en":"The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases.","ja":"The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases."},"publication_date":"2017-05-01","publication_name":{"en":"Experimental Cell Research","ja":"Experimental Cell Research"},"volume":"Vol.354","number":"No.1","starting_page":"57","ending_page":"64","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.yexcr.2017.03.028"],"issn":["1090-2422"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:18, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657505"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115146","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28074060","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=322120","label":"url"}],"paper_title":{"en":"S100A8/A9 and S100A9 reduce acute lung injury.","ja":"S100A8/A9 and S100A9 reduce acute lung injury."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Hsu Kenneth"},{"name":"Tedla Nicodemus"},{"name":"Wong Wing Sze"},{"name":"Chow Sharron"},{"name":"Kawaguchi Naomi"},{"name":"Geczy L Carolyn"}],"ja":[{"name":"廣島 佑香"},{"name":"Hsu Kenneth"},{"name":"Tedla Nicodemus"},{"name":"Wong Wing Sze"},{"name":"Chow Sharron"},{"name":"Kawaguchi Naomi"},{"name":"Geczy L Carolyn"}]},"description":{"en":"S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-, IL-1, IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury (ALI) provoked by LPS challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1, SAA3 and IL-10. Novel common pathways including increased induction of an NAD(+)-dependent protein deacetylase sirtuin-1 (SIRT1) that may reduce NF-B signalling, and increased STAT3 activation may reduce LPS activation. Results suggest a role for these proteins in normal homeostasis and protective mechanisms in the lung.Immunology and Cell Biology accepted article preview online, 11 January 2017. doi:10.1038/icb.2017.2.","ja":"S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-, IL-1, IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury (ALI) provoked by LPS challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1, SAA3 and IL-10. Novel common pathways including increased induction of an NAD(+)-dependent protein deacetylase sirtuin-1 (SIRT1) that may reduce NF-B signalling, and increased STAT3 activation may reduce LPS activation. Results suggest a role for these proteins in normal homeostasis and protective mechanisms in the lung.Immunology and Cell Biology accepted article preview online, 11 January 2017. doi:10.1038/icb.2017.2."},"publication_date":"2017-01-11","publication_name":{"en":"Immunology and Cell Biology","ja":"Immunology and Cell Biology"},"volume":"Vol.95","number":"No.5","starting_page":"461","ending_page":"472","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/icb.2017.2"],"issn":["1440-1711"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:19, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657506"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27468797","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=321797","label":"url"}],"paper_title":{"en":"Correlation Between Gingival Crevicular Fluid Hemoglobin Content and Periodontal Clinical Parameters.","ja":"Correlation Between Gingival Crevicular Fluid Hemoglobin Content and Periodontal Clinical Parameters."},"authors":{"en":[{"name":"Ito Hiroshi"},{"name":"Numabe Yukihiro"},{"name":"Hashimoto Shuichi"},{"name":"Sekino Satoshi"},{"name":"Murakashi Etsuko"},{"name":"Ishiguro Hitomi"},{"name":"Sasaki Daisuke"},{"name":"Yaegashi Takashi"},{"name":"Takai Hideki"},{"name":"Mezawa Masaru"},{"name":"Ogata Yorimasa"},{"name":"Watanabe Hisashi"},{"name":"Hagiwara Satsuki"},{"name":"Izumi Yuichi"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"},{"name":"Kunimatsu Kazushi"}],"ja":[{"name":"Ito Hiroshi"},{"name":"Numabe Yukihiro"},{"name":"Hashimoto Shuichi"},{"name":"Sekino Satoshi"},{"name":"Murakashi Etsuko"},{"name":"Ishiguro Hitomi"},{"name":"Sasaki Daisuke"},{"name":"Yaegashi Takashi"},{"name":"Takai Hideki"},{"name":"Mezawa Masaru"},{"name":"Ogata Yorimasa"},{"name":"Watanabe Hisashi"},{"name":"Hagiwara Satsuki"},{"name":"Izumi Yuichi"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"},{"name":"Kunimatsu Kazushi"}]},"description":{"en":"Hb was observed in more than 60% of GCF samples in BOP(-) gingival sulci in both periodontally stable and periodontal-management-required groups. These results suggest inspection of Hb derived from microbleeding in gingival sulci may serve as an index for preclinical diagnosis.","ja":"Hb was observed in more than 60% of GCF samples in BOP(-) gingival sulci in both periodontally stable and periodontal-management-required groups. These results suggest inspection of Hb derived from microbleeding in gingival sulci may serve as an index for preclinical diagnosis."},"publication_date":"2016-07-29","publication_name":{"en":"Journal of Periodontology","ja":"Journal of Periodontology"},"volume":"Vol.87","number":"No.11","starting_page":"1314","ending_page":"1319","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1902/jop.2016.160092"],"issn":["1943-3670"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:20, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657507"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25649126","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=298099","label":"url"}],"paper_title":{"en":"Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells.","ja":"Effect of Hangeshashinto on calprotectin expression in human oral epithelial cells."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Bandou Mika"},{"name":"Inagaki Yuji"},{"name":"Kido Reiko"},{"name":"Kataoka Masatoshi"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"廣島 佑香"},{"name":"板東 美香"},{"name":"稲垣 裕司"},{"name":"木戸 玲子"},{"name":"片岡 正俊"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"Oral epithelial cells produce antimicrobial peptides (AMPs) to prevent microbial infection. Calprotectin (S100A8/S100A9) is one of these AMPs in oral epithelial cells, the expression of which is up-regulated by interleukin-1α (IL-1α). Hangeshashinto (HST) is a traditional Japanese herbal medicine that has anti-inflammatory effects. The purpose of this study was to investigate the effect of HST on the expression of calprotectin through the regulation of IL-1α in oral epithelial cells. Human oral epithelial cells (TR146) were cultured with HST in the presence or absence of anti-IL-1α antibody or IL-1 receptor antagonist, or with six major components of HST (3,4-dihydroxybenzaldehyde, baicalin, ginsenoside Rb1, glycyrrhizin, oleanolic acid and berberine). The expression of S100A8, S100A9, other AMPs and cytokine mRNAs was examined by RT-PCR and quantitative real-time PCR. Calprotectin expression and IL-1α secretion were investigated by ELISA. HST (6 μg/ml) increased the expression of S100A8/S100A9 mRNAs and calprotectin protein, and also up-regulated β-defensin 2 (DEFB4) and S100A7 expression. The expression of IL-1α mRNA and its protein was slightly but significantly increased by HST. A neutralizing antibody against IL-1α and IL-1 receptor antagonist inhibited HST-up-regulated S100A8/S100A9 mRNA expression. Although 3,4-dihydroxybenzaldehyde, baicalin and ginsenoside Rb1 as HST components increased S100A8/S100A9 expression, oleanolic acid and berberine decreased their expression. These results suggest that HST increases the expression of calprotectin, DEFB4 and S100A7 in oral epithelial cells. In response to HST, up-regulation of calprotectin expression may be partially induced via IL-1α.","ja":"Oral epithelial cells produce antimicrobial peptides (AMPs) to prevent microbial infection. Calprotectin (S100A8/S100A9) is one of these AMPs in oral epithelial cells, the expression of which is up-regulated by interleukin-1α (IL-1α). Hangeshashinto (HST) is a traditional Japanese herbal medicine that has anti-inflammatory effects. The purpose of this study was to investigate the effect of HST on the expression of calprotectin through the regulation of IL-1α in oral epithelial cells. Human oral epithelial cells (TR146) were cultured with HST in the presence or absence of anti-IL-1α antibody or IL-1 receptor antagonist, or with six major components of HST (3,4-dihydroxybenzaldehyde, baicalin, ginsenoside Rb1, glycyrrhizin, oleanolic acid and berberine). The expression of S100A8, S100A9, other AMPs and cytokine mRNAs was examined by RT-PCR and quantitative real-time PCR. Calprotectin expression and IL-1α secretion were investigated by ELISA. HST (6 μg/ml) increased the expression of S100A8/S100A9 mRNAs and calprotectin protein, and also up-regulated β-defensin 2 (DEFB4) and S100A7 expression. The expression of IL-1α mRNA and its protein was slightly but significantly increased by HST. A neutralizing antibody against IL-1α and IL-1 receptor antagonist inhibited HST-up-regulated S100A8/S100A9 mRNA expression. Although 3,4-dihydroxybenzaldehyde, baicalin and ginsenoside Rb1 as HST components increased S100A8/S100A9 expression, oleanolic acid and berberine decreased their expression. These results suggest that HST increases the expression of calprotectin, DEFB4 and S100A7 in oral epithelial cells. In response to HST, up-regulation of calprotectin expression may be partially induced via IL-1α."},"publication_date":"2016-05","publication_name":{"en":"Odontology","ja":"Odontology"},"volume":"Vol.104","number":"No.2","starting_page":"152","ending_page":"162","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10266-015-0196-3"],"issn":["1618-1255"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:21, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657508"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25740558","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84930271794&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=339758","label":"url"}],"paper_title":{"en":"YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes","ja":"YKL-40 level in gingival crevicular fluid from patients with periodontitis and type 2 diabetes"},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"Bandou Yukiko"},{"name":"Bandou Mika"},{"name":"Kajiura Yukari"},{"name":"Hiroshima Yuka"},{"name":"Inagaki Yuji"},{"name":"Murata Hiromi"},{"name":"Ikuta Takahisa"},{"name":"Kido Reiko"},{"name":"Naruishi Koji"},{"name":"Funaki Makoto"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"木戸 淳一"},{"name":"坂東 由記子"},{"name":"板東 美香"},{"name":"梶浦 由加里"},{"name":"廣島 佑香"},{"name":"稲垣 裕司"},{"name":"村田 裕美"},{"name":"生田 貴久"},{"name":"木戸 玲子"},{"name":"成石 浩司"},{"name":"船木 真理"},{"name":"永田 俊彦"}]},"description":{"en":"YKL-40 is a chitin-binding glycoprotein, the level of which increases in inflammatory diseases, diabetes mellitus (DM), cardiovascular diseases, and tumors. Gingival crevicular fluid (GCF) contains many proteins and markers of periodontitis. The purpose of this study was to investigate YKL-40 level in GCF from patients with periodontitis and DM and the association between YKL-40 level and chronic periodontitis (CP) or DM. The subjects were 121 patients with DM, CP, DM and periodontitis (DM-P), and healthy subjects (H). GCF was collected using paper strips after the sites for GCF collection were clinically evaluated for probing depth (PD), gingival index (GI), and bleeding on probing (BOP). YKL-40 in GCF was identified by Western blotting, and its level was determined by ELISA. YKL-40 was contained in GCF samples from H, DM, CP, and DM-P sites, and its levels (amount and concentration) in CP and DM-P were significantly higher than those in H and DM. GCF YKL-40 level significantly correlated with PD and GI, and its level in BOP-positive sites was significantly higher than that in BOP-negative ones. GCF YKL-40 level was elevated in periodontitis, but not DM. YKL-40 in GCF may be an inflammatory marker for periodontitis.","ja":"YKL-40 is a chitin-binding glycoprotein, the level of which increases in inflammatory diseases, diabetes mellitus (DM), cardiovascular diseases, and tumors. Gingival crevicular fluid (GCF) contains many proteins and markers of periodontitis. The purpose of this study was to investigate YKL-40 level in GCF from patients with periodontitis and DM and the association between YKL-40 level and chronic periodontitis (CP) or DM. The subjects were 121 patients with DM, CP, DM and periodontitis (DM-P), and healthy subjects (H). GCF was collected using paper strips after the sites for GCF collection were clinically evaluated for probing depth (PD), gingival index (GI), and bleeding on probing (BOP). YKL-40 in GCF was identified by Western blotting, and its level was determined by ELISA. YKL-40 was contained in GCF samples from H, DM, CP, and DM-P sites, and its levels (amount and concentration) in CP and DM-P were significantly higher than those in H and DM. GCF YKL-40 level significantly correlated with PD and GI, and its level in BOP-positive sites was significantly higher than that in BOP-negative ones. GCF YKL-40 level was elevated in periodontitis, but not DM. YKL-40 in GCF may be an inflammatory marker for periodontitis."},"publication_date":"2015-04-06","publication_name":{"en":"Oral Diseases","ja":"Oral Diseases"},"volume":"Vol.21","number":"No.5","starting_page":"667","ending_page":"673","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/odi.12334"],"issn":["1601-0825"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:22, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657509"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25767333","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84924215816&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=298091","label":"url"}],"paper_title":{"en":"ISU201 enhances the resolution of airway inflammation in a mouse model of an acute exacerbation of asthma.","ja":"ISU201 enhances the resolution of airway inflammation in a mouse model of an acute exacerbation of asthma."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Garthwaite Linda"},{"name":"Hsu Kenneth"},{"name":"Yoo Hyouna"},{"name":"Park Sang-Ho"},{"name":"Geczy Carolyn L"},{"name":"Kumar Rakesh K"},{"name":"Herbert Cristan"}],"ja":[{"name":"廣島 佑香"},{"name":"Garthwaite Linda"},{"name":"Hsu Kenneth"},{"name":"Yoo Hyouna"},{"name":"Park Sang-Ho"},{"name":"Geczy Carolyn L"},{"name":"Kumar Rakesh K"},{"name":"Herbert Cristan"}]},"description":{"en":"Glucocorticoids are commonly used for treating asthma and its exacerbations but have well-recognised adverse effects and are not always effective. Few alternative treatments exist. Using a murine model of an acute exacerbation of asthma, we assessed the ability of ISU201, a novel protein drug, to suppress the inflammatory response when administered after induction of an exacerbation. Sensitised mice were chronically challenged with a low mass concentration of aerosolised ovalbumin, and then received a single moderate-level challenge to simulate an allergen-induced exacerbation. ISU201 was administered to mice 2 and 8 hours later, while pulmonary inflammation and expression of mRNA for chemokines and proinflammatory cytokines were assessed after 4, 12, and 24 hours. Relative to vehicle-treated controls, ISU201 suppressed accumulation of pulmonary neutrophils and eosinophils, while accelerating the decline in CXCL1, TNF-, and IL-6 in lavage fluid and lung tissue. ISU201 significantly reduced peak expression of mRNA for the chemokines Cxcl9 and Cxcl10, the adhesion molecules Icam1 and Vcam1, and the proinflammatory cytokines Il1b, Il12p40, and Csf1. The ability of ISU201 to promote resolution of inflammation suggests that it may have potential as an alternative to glucocorticoids in the management of asthma, including when administered after the onset of an acute exacerbation.","ja":"Glucocorticoids are commonly used for treating asthma and its exacerbations but have well-recognised adverse effects and are not always effective. Few alternative treatments exist. Using a murine model of an acute exacerbation of asthma, we assessed the ability of ISU201, a novel protein drug, to suppress the inflammatory response when administered after induction of an exacerbation. Sensitised mice were chronically challenged with a low mass concentration of aerosolised ovalbumin, and then received a single moderate-level challenge to simulate an allergen-induced exacerbation. ISU201 was administered to mice 2 and 8 hours later, while pulmonary inflammation and expression of mRNA for chemokines and proinflammatory cytokines were assessed after 4, 12, and 24 hours. Relative to vehicle-treated controls, ISU201 suppressed accumulation of pulmonary neutrophils and eosinophils, while accelerating the decline in CXCL1, TNF-, and IL-6 in lavage fluid and lung tissue. ISU201 significantly reduced peak expression of mRNA for the chemokines Cxcl9 and Cxcl10, the adhesion molecules Icam1 and Vcam1, and the proinflammatory cytokines Il1b, Il12p40, and Csf1. The ability of ISU201 to promote resolution of inflammation suggests that it may have potential as an alternative to glucocorticoids in the management of asthma, including when administered after the onset of an acute exacerbation."},"publication_date":"2015-02-12","publication_name":{"en":"Mediators of Inflammation","ja":"Mediators of Inflammation"},"volume":"Vol.2015","starting_page":"405629","ending_page":"405629","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1155/2015/405629"],"issn":["1466-1861"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:23, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657510"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=307805","label":"url"}],"paper_title":{"en":"Expression and LPS-Induced Elevation of Nod2 and Calprotectin in the Submandibular Gland of Wild-Type and TLR4-Knockout Male Mice","ja":"Expression and LPS-Induced Elevation of Nod2 and Calprotectin in the Submandibular Gland of Wild-Type and TLR4-Knockout Male Mice"},"authors":{"en":[{"name":"Purevjav Javkhlan"},{"name":"Guangfei Xu"},{"name":"Gang Chen"},{"name":"Yao Chenjuan"},{"name":"Hiroshima Yuka"},{"name":"Yoshimura Hiroshi"},{"name":"Nagata Toshihiko"},{"name":"Hosoi Kazuo"}],"ja":[{"name":"Purevjav Javkhlan"},{"name":"Guangfei Xu"},{"name":"Gang Chen"},{"name":"姚 陳娟"},{"name":"廣島 佑香"},{"name":"吉村 弘"},{"name":"永田 俊彦"},{"name":"細井 和雄"}]},"publication_date":"2015","publication_name":{"en":"Journal of Research and Practice in Dentistry","ja":"Journal of Research and Practice in Dentistry"},"volume":"Vol.2015","number":"No.290259","languages":["eng"],"referee":true,"identifiers":{"doi":["10.5171/2015.290259"],"issn":["2333-3650"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:24, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657511"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23179356","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84892874741&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=297848","label":"url"}],"paper_title":{"en":"Evaluation of bleeding on probing and gingival crevicular fluid enzyme activity for detection of periodontally active sites during supportive periodontal therapy","ja":"Evaluation of bleeding on probing and gingival crevicular fluid enzyme activity for detection of periodontally active sites during supportive periodontal therapy"},"authors":{"en":[{"name":"Ito Hiroshi"},{"name":"Numabe Yukihiro"},{"name":"Sekino Satoshi"},{"name":"Murakashi Etsuko"},{"name":"Iguchi Hitomi"},{"name":"Hashimoto Shuichi"},{"name":"Sasaki Daisuke"},{"name":"Yaegashi Takashi"},{"name":"Kunimatsu Kazushi"},{"name":"Takai Hideki"},{"name":"Mezawa Masaru"},{"name":"Ogata Yorimasa"},{"name":"Watanabe Hisashi"},{"name":"Hagiwara Satsuki"},{"name":"Izumi Yuichi"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"伊藤 博"},{"name":"沼部 幸博"},{"name":"関野 愉"},{"name":"村樫 悦子"},{"name":"井口 一美"},{"name":"橋本 修一"},{"name":"佐々木 大輔"},{"name":"八重柏 隆"},{"name":"國松 和司"},{"name":"高井 英樹"},{"name":"目澤 優"},{"name":"小方 頼昌"},{"name":"渡辺 久"},{"name":"萩原 さつき"},{"name":"和泉 雄一"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"}]},"description":{"en":"This study aimed to analyze the enzyme activity in gingival crevicular fluid (GCF) and its association with clinical parameters, especially bleeding on probing (BOP), and thus reconsider the significance and accuracy of recording BOP. A total of 184 patients who had entered supportive periodontal therapy were selected and GCF was collected from 401 sites before recording the clinical parameters, probing pocket depth (PPD), BOP, clinical attachment level, gingival index and plaque index. The enzyme activity of neutrophil elastase and aspartate aminotransferase and amount of protein in GCF were also analyzed. In the clinical parameters for biochemical data, amount of GCF showed the most correlation. A cut-off value for BOP and PPD were determined by the ROC curve and Youden index. Analysis was performed with all clinical parameters and biochemical data. Of the 401 sites, 51 were less than the cut-off value and were BOP-negative. On the other hand, 29 sites had values more than the cut-off value, with 14 BOP-negative sites and 15 BOP-positive sites. A conclusion is as follows: twenty-nine sites with values more than the cut-off value were diagnosed as sites requiring periodontal management, however, 14 of these were BOP-negative. These results suggest that combining other biochemical tests with examination of BOP and PPD may improve the validity of periodontal disease diagnosis. In future studies, it will be essential to find a marker that can precisely detect periodontal disease activity, and to develop a diagnostic tool for chair-side use.","ja":"This study aimed to analyze the enzyme activity in gingival crevicular fluid (GCF) and its association with clinical parameters, especially bleeding on probing (BOP), and thus reconsider the significance and accuracy of recording BOP. A total of 184 patients who had entered supportive periodontal therapy were selected and GCF was collected from 401 sites before recording the clinical parameters, probing pocket depth (PPD), BOP, clinical attachment level, gingival index and plaque index. The enzyme activity of neutrophil elastase and aspartate aminotransferase and amount of protein in GCF were also analyzed. In the clinical parameters for biochemical data, amount of GCF showed the most correlation. A cut-off value for BOP and PPD were determined by the ROC curve and Youden index. Analysis was performed with all clinical parameters and biochemical data. Of the 401 sites, 51 were less than the cut-off value and were BOP-negative. On the other hand, 29 sites had values more than the cut-off value, with 14 BOP-negative sites and 15 BOP-positive sites. A conclusion is as follows: twenty-nine sites with values more than the cut-off value were diagnosed as sites requiring periodontal management, however, 14 of these were BOP-negative. These results suggest that combining other biochemical tests with examination of BOP and PPD may improve the validity of periodontal disease diagnosis. In future studies, it will be essential to find a marker that can precisely detect periodontal disease activity, and to develop a diagnostic tool for chair-side use."},"publication_date":"2014-11-22","publication_name":{"en":"Odontology","ja":"Odontology"},"volume":"Vol.102","number":"No.1","starting_page":"50","ending_page":"56","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10266-012-0090-1"],"issn":["1618-1255"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:25, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657512"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24532576","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=298092","label":"url"}],"paper_title":{"en":"S100A8 induces IL-10 and protects against acute lung injury.","ja":"S100A8 induces IL-10 and protects against acute lung injury."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Hsu Kenneth"},{"name":"Tedla Nicodemus"},{"name":"Chung Yuen Ming"},{"name":"Chow Sharron"},{"name":"Herbert Cristan"},{"name":"Geczy Carolyn L"}],"ja":[{"name":"廣島 佑香"},{"name":"Hsu Kenneth"},{"name":"Tedla Nicodemus"},{"name":"Chung Yuen Ming"},{"name":"Chow Sharron"},{"name":"Herbert Cristan"},{"name":"Geczy Carolyn L"}]},"description":{"en":"S100A8 is considered proinflammatory by activating TLR4 and/or the receptor for advanced glycation end products. The aim was to investigate inflammatory effects of S100A8 in murine lung. S100A8 was administered to BALB/c mice by nasal inhalation and genes induced over a time-course assessed. LPS was introduced intranasally either alone or 2 h after pretreatment of mice with intranasal application of S100A8 or dexamethasone. A Cys(42)-Ala(42) mutant S100A8 mutant was used to assess whether S100A8's effects were via pathways that were dependent on reactive oxygen species. S100A8 induced IL-10 mRNA, and expression was apparent only in airway epithelial cells. Importantly, it suppressed acute lung injury provoked by LPS inhalation by suppressing mast-cell activation and induction of mediators orchestrating leukocyte recruitment, possibly by reducing NF-B activation via an IB/Akt pathway and by downmodulating pathways generating oxidative stress. The Cys(42)-Ala(42) S100A8 mutant did not induce IL-10 and was less immunosuppressive, indicating modulation by scavenging oxidants. S100A8 inhibition of LPS-mediated injury was as potent, and outcomes were remarkably similar to immunosuppression by dexamethasone. We challenge the notion that S100A8 is an agonist for TLR4 or the receptor for advanced glycation end products. S100A8 induced IL-10 in vivo and initiates a feedback loop that attenuates acute lung injury.","ja":"S100A8 is considered proinflammatory by activating TLR4 and/or the receptor for advanced glycation end products. The aim was to investigate inflammatory effects of S100A8 in murine lung. S100A8 was administered to BALB/c mice by nasal inhalation and genes induced over a time-course assessed. LPS was introduced intranasally either alone or 2 h after pretreatment of mice with intranasal application of S100A8 or dexamethasone. A Cys(42)-Ala(42) mutant S100A8 mutant was used to assess whether S100A8's effects were via pathways that were dependent on reactive oxygen species. S100A8 induced IL-10 mRNA, and expression was apparent only in airway epithelial cells. Importantly, it suppressed acute lung injury provoked by LPS inhalation by suppressing mast-cell activation and induction of mediators orchestrating leukocyte recruitment, possibly by reducing NF-B activation via an IB/Akt pathway and by downmodulating pathways generating oxidative stress. The Cys(42)-Ala(42) S100A8 mutant did not induce IL-10 and was less immunosuppressive, indicating modulation by scavenging oxidants. S100A8 inhibition of LPS-mediated injury was as potent, and outcomes were remarkably similar to immunosuppression by dexamethasone. We challenge the notion that S100A8 is an agonist for TLR4 or the receptor for advanced glycation end products. S100A8 induced IL-10 in vivo and initiates a feedback loop that attenuates acute lung injury."},"publication_date":"2014-02-14","publication_name":{"en":"The Journal of Immunology","ja":"The Journal of Immunology"},"volume":"Vol.192","number":"No.6","starting_page":"2800","ending_page":"2811","languages":["eng"],"referee":true,"identifiers":{"doi":["10.4049/jimmunol.1302556"],"issn":["1550-6606"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:26, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657513"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24389598","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=298093","label":"url"}],"paper_title":{"en":"Calgranulins may contribute vascular protection in atherogenesis.","ja":"Calgranulins may contribute vascular protection in atherogenesis."},"authors":{"en":[{"name":"Geczy Carolyn L"},{"name":"Chung Yuen Ming"},{"name":"Hiroshima Yuka"}],"ja":[{"name":"Geczy Carolyn L"},{"name":"Chung Yuen Ming"},{"name":"廣島 佑香"}]},"description":{"en":"S100A8, S100A9 and S100A12 are considered proinflammatory mediators of atherosclerosis. Known as calgranulins, they are major components of neutrophils and are upregulated in macrophages and foam cells. They influence leukocyte recruitment, and may propagate inflammation by binding TLR4 and/or receptor for advanced glycation endproducts (RAGE). However, the receptors for calgranulins remain an enigma; we have no evidence for TLR4 or RAGE activation by S100A8 or S100A12. Moreover, gene regulation studies suggest antiinflammatory functions for S100A8 and emerging reports indicate pleiotropic roles. Unlike S100A9, S100A8 effectively scavenges oxidants generated by the myeloperoxidase system in vivo, forming novel thiol modifications. S100A8 is also readily S-nitrosylated, stabilizing nitric oxide and transporting it to hemoglobin. S100A8-SNO reduces leukocyte transmigration in the vasculature. S-glutathionylation of S100A9 modifies its effects on leukocyte adhesion. Both S100A8 forms inhibit mast cell activation, at least partially by scavenging reactive oxygen species required for signaling. Conversely, S100A12 activates and sequesters mast cells. However S100A12 suppresses proinflammatory cytokine induction by SAA-activated monocytes and macrophages, and inhibits matrix metalloprotease activity. We propose that the abundance and types of cells expressing calgranulins in particular microenvironments, their relative concentrations and post-translational modifications may have distinct functional outcomes, including those that are protective, at different stages of atherogenesis.","ja":"S100A8, S100A9 and S100A12 are considered proinflammatory mediators of atherosclerosis. Known as calgranulins, they are major components of neutrophils and are upregulated in macrophages and foam cells. They influence leukocyte recruitment, and may propagate inflammation by binding TLR4 and/or receptor for advanced glycation endproducts (RAGE). However, the receptors for calgranulins remain an enigma; we have no evidence for TLR4 or RAGE activation by S100A8 or S100A12. Moreover, gene regulation studies suggest antiinflammatory functions for S100A8 and emerging reports indicate pleiotropic roles. Unlike S100A9, S100A8 effectively scavenges oxidants generated by the myeloperoxidase system in vivo, forming novel thiol modifications. S100A8 is also readily S-nitrosylated, stabilizing nitric oxide and transporting it to hemoglobin. S100A8-SNO reduces leukocyte transmigration in the vasculature. S-glutathionylation of S100A9 modifies its effects on leukocyte adhesion. Both S100A8 forms inhibit mast cell activation, at least partially by scavenging reactive oxygen species required for signaling. Conversely, S100A12 activates and sequesters mast cells. However S100A12 suppresses proinflammatory cytokine induction by SAA-activated monocytes and macrophages, and inhibits matrix metalloprotease activity. We propose that the abundance and types of cells expressing calgranulins in particular microenvironments, their relative concentrations and post-translational modifications may have distinct functional outcomes, including those that are protective, at different stages of atherogenesis."},"publication_date":"2013-12-27","publication_name":{"en":"Circulation Journal","ja":"Circulation Journal"},"volume":"Vol.78","number":"No.2","starting_page":"271","ending_page":"280","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1253/circj.CJ-13-1505"],"issn":["1347-4820"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:27, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657514"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23563247","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84880346974&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=280272","label":"url"}],"paper_title":{"en":"Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line","ja":"Mechanism of interleukin-1α transcriptional regulation of S100A9 in a human epidermal keratinocyte cell line"},"authors":{"en":[{"name":"Bandou Mika"},{"name":"Zou Xianqiong"},{"name":"Hiroshima Yuka"},{"name":"Kataoka Masatoshi"},{"name":"Ross F. Karen"},{"name":"Shinohara Yasuo"},{"name":"Nagata Toshihiko"},{"name":"Herzberg C. Mark"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"板東 美香"},{"name":"Zou Xianqiong"},{"name":"廣島 佑香"},{"name":"片岡 正俊"},{"name":"Ross F. Karen"},{"name":"篠原 康雄"},{"name":"永田 俊彦"},{"name":"Herzberg C. Mark"},{"name":"木戸 淳一"}]},"description":{"en":"S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -94 to -53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity.","ja":"S100A9 is a calcium-binding protein and subunit of antimicrobial calprotectin complex (S100A8/A9). Produced by neutrophils, monocytes/macrophages and keratinocytes, S100A9 expression increases in response to inflammation. For example, IL-1α produced by epithelial cells acts autonomously on the same cells to induce the expression of S100A8/A9 and cellular differentiation. Whereas it is well known that IL-1α and members of the IL-10 family of cytokines upregulate S100A8 and S100A9 in several cell lineages, the pathway and mechanism of IL-1α-dependent transcriptional control of S100A9 in epithelial cells are not established. Modeled using human epidermal keratinocytes (HaCaT cells), IL-1α stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor. Transcription of S100A9 in HaCaT cells depended on nucleotides -94 to -53 in the upstream promoter region, based upon the use of deletion constructs and luciferase reporter activity. Within the responsive promoter region, IL-1α increased the binding activity of CCAAT/enhancer binding protein β (C/EBPβ). Mutated C/EBPβ binding sequences or C/EBPβ-specific siRNA inhibited the S100A9 transcriptional response. Hence, IL-1α is strongly suggested to increase S100A9 expression in a human epidermal keratinocyte cell line by signaling through the IL-1 receptor and p38 MAPK, increasing C/EBPβ-dependent transcriptional activity."},"publication_date":"2013-04-03","publication_name":{"en":"Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms","ja":"Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms"},"volume":"Vol.1829","number":"No.9","starting_page":"954","ending_page":"962","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.bbagrm.2013.03.010"],"issn":["1874-9399"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:28, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657515"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23326472","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84872235277&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=280269","label":"url"}],"paper_title":{"en":"Simultaneous immunoassay analysis of plasma IL-6 and TNF-α on a microchip.","ja":"Simultaneous immunoassay analysis of plasma IL-6 and TNF-α on a microchip."},"authors":{"en":[{"name":"Abe Kaori"},{"name":"Hashimoto Y"},{"name":"Yatsushiro S"},{"name":"Yamamura S"},{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Tanaka M"},{"name":"Shinohara Yasuo"},{"name":"Ooie Toshihiko"},{"name":"Baba Yoshinobu"},{"name":"Kataoka Masatoshi"}],"ja":[{"name":"阿部 佳織"},{"name":"Hashimoto Y"},{"name":"Yatsushiro S"},{"name":"Yamamura S"},{"name":"板東 美香"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"Tanaka M"},{"name":"篠原 康雄"},{"name":"大家 利彦"},{"name":"馬場 嘉信"},{"name":"片岡 正俊"}]},"description":{"en":"Sandwich enzyme-linked immunosorbant assay (ELISA) using a 96-well plate is frequently employed for clinical diagnosis, but is time-and sample-consuming. To overcome these drawbacks, we performed a sandwich ELISA on a microchip. The microchip was made of cyclic olefin copolymer with 4 straight microchannels. For the construction of the sandwich ELISA for interleukin-6 (IL-6) or tumor necrosis factor-α (TNF-α), we used a piezoelectric inkjet printing system for the deposition and fixation of the 1st anti-IL-6 antibody or 1st anti-TNF-α antibody on the surface of the each microchannel. After the infusion of 2 µl of sample to the microchannel and a 20 min incubation, 2 µl of biotinylated 2nd antibody for either antigen was infused and a 10 min incubation. Then 2 µl of avidin-horseradish peroxidase was infused; and after a 5 min incubation, the substrate for peroxidase was infused, and the luminescence intensity was measured. Calibration curves were obtained between the concentration and luminescence intensity over the range of 0 to 32 pg/ml (IL-6: R(2) = 0.9994, TNF-α: R(2) = 0.9977), and the detection limit for each protein was 0.28 pg/ml and 0.46 pg/ml, respectively. Blood IL-6 and TNF-α concentrations of 5 subjects estimated from the microchip data were compared with results obtained by the conventional method, good correlations were observed between the methods according to linear regression analysis (IL-6: R(2) = 0.9954, TNF-α: R(2) = 0.9928). The reproducibility of the presented assay for the determination of the blood IL-6 and TNF-α concentration was comparable to that obtained with the 96-well plate. Simultaneous detection of blood IL-6 and TNF-α was possible by the deposition and fixation of each 1st antibody on the surface of a separate microchannel. This assay enabled us to determine simultaneously blood IL-6 and TNF-α with accuracy, satisfactory sensitivity, time saving ability, and low consumption of sample and reagents, and will be applicable to clinic diagnosis.","ja":"Sandwich enzyme-linked immunosorbant assay (ELISA) using a 96-well plate is frequently employed for clinical diagnosis, but is time-and sample-consuming. To overcome these drawbacks, we performed a sandwich ELISA on a microchip. The microchip was made of cyclic olefin copolymer with 4 straight microchannels. For the construction of the sandwich ELISA for interleukin-6 (IL-6) or tumor necrosis factor-α (TNF-α), we used a piezoelectric inkjet printing system for the deposition and fixation of the 1st anti-IL-6 antibody or 1st anti-TNF-α antibody on the surface of the each microchannel. After the infusion of 2 µl of sample to the microchannel and a 20 min incubation, 2 µl of biotinylated 2nd antibody for either antigen was infused and a 10 min incubation. Then 2 µl of avidin-horseradish peroxidase was infused; and after a 5 min incubation, the substrate for peroxidase was infused, and the luminescence intensity was measured. Calibration curves were obtained between the concentration and luminescence intensity over the range of 0 to 32 pg/ml (IL-6: R(2) = 0.9994, TNF-α: R(2) = 0.9977), and the detection limit for each protein was 0.28 pg/ml and 0.46 pg/ml, respectively. Blood IL-6 and TNF-α concentrations of 5 subjects estimated from the microchip data were compared with results obtained by the conventional method, good correlations were observed between the methods according to linear regression analysis (IL-6: R(2) = 0.9954, TNF-α: R(2) = 0.9928). The reproducibility of the presented assay for the determination of the blood IL-6 and TNF-α concentration was comparable to that obtained with the 96-well plate. Simultaneous detection of blood IL-6 and TNF-α was possible by the deposition and fixation of each 1st antibody on the surface of a separate microchannel. This assay enabled us to determine simultaneously blood IL-6 and TNF-α with accuracy, satisfactory sensitivity, time saving ability, and low consumption of sample and reagents, and will be applicable to clinic diagnosis."},"publication_date":"2013-02","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.8","number":"No.1","starting_page":"e53620","ending_page":"e53620","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0053620"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:29, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657516"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23791254","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84879412695&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=280273","label":"url"}],"paper_title":{"en":"Advanced glycation end-products enhance calcification in cultured rat dental pulp cells","ja":"Advanced glycation end-products enhance calcification in cultured rat dental pulp cells"},"authors":{"en":[{"name":"Nakajima Yukiko"},{"name":"Inagaki Yuji"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"中島 由紀子"},{"name":"稲垣 裕司"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"}]},"description":{"en":"Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues.","ja":"Amorphous calcification frequently appears in dental pulp tissues of diabetic patients; however, its pathologic process has not been fully elucidated. We previously found that pulp stones and thickened predentin occurred more frequently in diabetic rats. Recent findings demonstrated that accumulation of advanced glycation end-products (AGE) might be involved in vascular calcification complicated with diabetes. The aim of this study was to determine the effect of AGE on calcified nodule formation by rat dental pulp cells in culture. Rat dental pulp cells and gingival fibroblasts were independently cultured with 50 and 100 μg/mL AGE. Alkaline phosphatase activity and calcified nodule formation were measured. Expressions of receptor for AGE, osteopontin (OPN), and osteocalcin (OCN) mRNA were determined by quantitative real-time polymerase chain reaction. Protein levels of OPN and OCN secreted in culture medium were quantified by enzyme-linked immunosorbent assay. AGE (50 and 100 μg/mL) markedly increased both alkaline phosphatase activity and calcified nodule formation in dental pulp cells (P < .01), whereas it did not affect those in gingival fibroblasts. Real-time polymerase chain reaction analysis revealed that AGE increased mRNA expressions of receptor for AGE, OPN, and OCN in dental pulp cells (P < .05). Enzyme-linked immunosorbent assay analysis revealed that the protein levels of OPN and OCN produced by dental pulp cells were higher in AGE-treated than in untreated cells (P < .05). AGE enhanced the calcification potentials of rat dental pulp cells, suggesting that it may stimulate pathologic calcification of diabetic dental pulp tissues."},"publication_date":"2013-01-16","publication_name":{"en":"Journal of Endodontics","ja":"Journal of Endodontics"},"volume":"Vol.39","starting_page":"873","ending_page":"878","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.joen.2012.11.027"],"issn":["1878-3554"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:30, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657517"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10030799485/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679391110400/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=269430","label":"url"}],"paper_title":{"en":"Topical injection of osteoprotegerin prevents alveolar bone loss in rat experimental periodontitis","ja":"ラット実験的歯周炎におけるオステオプロテジェリンの局所投与による歯槽骨吸収抑制効果"},"authors":{"en":[{"name":"Wada -Mihara Chie"},{"name":"徳永 格"},{"name":"Seto Hiroyuki"},{"name":"Sakamoto Eijiro"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"美原(和田) 智恵"},{"name":"徳永 格"},{"name":"瀬戸 浩行"},{"name":"坂本 英次郎"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"}]},"publication_date":"2012-05","publication_name":{"en":"Journal of the Japanese Association of Periodontology","ja":"日本歯周病学会会誌"},"volume":"Vol.54","number":"No.2","starting_page":"167","ending_page":"174","languages":["jpn"],"referee":true,"identifiers":{"doi":["10.2329/perio.54.167"],"issn":["0385-0110"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:31, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657518"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22609893","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=264444","label":"url"}],"paper_title":{"en":"Determination of calprotectin in gingival crevicular fluid by immunoassay on a microchip","ja":"Determination of calprotectin in gingival crevicular fluid by immunoassay on a microchip"},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"Abe Kaori"},{"name":"Yatsushiro Shouki"},{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"},{"name":"Nagata Toshihiko"},{"name":"Ooie Toshihiko"},{"name":"Tanaka Masato"},{"name":"Kataoka Masatoshi"}],"ja":[{"name":"木戸 淳一"},{"name":"阿部 佳織"},{"name":"八代 聖基"},{"name":"板東 美香"},{"name":"廣島 佑香"},{"name":"永田 俊彦"},{"name":"大家 利彦"},{"name":"田中 正人"},{"name":"片岡 正俊"}]},"description":{"en":"Gingival crevicular fluid (GCF) contains calprotectin, which appears to be a useful biomarker for periodontal diseases because of its high level in GCF from periodontally diseased pockets. To determine calprotectin in GCF that has a very small volume, sandwich enzyme-linked immunosorbent assay (ELISA) on a microchip was performed and its utility was estimated. Anti-calprotectin primary antibody was discharged on a microchip using a piezoelectric inkjet printing system. Calprotectin standard and calprotectin in GCF samples from eleven subjects were determined by the ELISA method with the prepared microchip and their values were compared with those obtained by conventional ELISA. Using the ELISA on a microchip, a reasonable standard curve of calprotectin protein (1.56-100 ng/mL) was obtained. Calprotectin in GCF samples was quantified and showed reasonable values in accordance with the condition of periodontal diseases. The values determined by the microchip method and conventional ELISA showed a significant linear relationship (R(2)=0.981). Calprotectin in GCF was determined using the ELISA on a microchip with high efficiency and this ELISA method for calprotectin determination may become a useful method for diagnosing periodontal diseases.","ja":"Gingival crevicular fluid (GCF) contains calprotectin, which appears to be a useful biomarker for periodontal diseases because of its high level in GCF from periodontally diseased pockets. To determine calprotectin in GCF that has a very small volume, sandwich enzyme-linked immunosorbent assay (ELISA) on a microchip was performed and its utility was estimated. Anti-calprotectin primary antibody was discharged on a microchip using a piezoelectric inkjet printing system. Calprotectin standard and calprotectin in GCF samples from eleven subjects were determined by the ELISA method with the prepared microchip and their values were compared with those obtained by conventional ELISA. Using the ELISA on a microchip, a reasonable standard curve of calprotectin protein (1.56-100 ng/mL) was obtained. Calprotectin in GCF samples was quantified and showed reasonable values in accordance with the condition of periodontal diseases. The values determined by the microchip method and conventional ELISA showed a significant linear relationship (R(2)=0.981). Calprotectin in GCF was determined using the ELISA on a microchip with high efficiency and this ELISA method for calprotectin determination may become a useful method for diagnosing periodontal diseases."},"publication_date":"2012-05-17","publication_name":{"en":"Clinical Biochemistry","ja":"Clinical Biochemistry"},"volume":"Vol.45","number":"No.15","starting_page":"1239","ending_page":"1244","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.clinbiochem.2012.05.009"],"issn":["1873-2933"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:32, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657519"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22309231","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84865553635&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=264439","label":"url"}],"paper_title":{"en":"Resistin in gingival crevicular fluid and induction of resistin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils","ja":"Resistin in gingival crevicular fluid and induction of resistin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils"},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Bandou Mika"},{"name":"Inagaki Yuji"},{"name":"Wada -Mihara Chie"},{"name":"Kataoka Masatoshi"},{"name":"Murata Hiromi"},{"name":"Shinohara Yasuo"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"廣島 佑香"},{"name":"板東 美香"},{"name":"稲垣 裕司"},{"name":"美原(和田) 智恵"},{"name":"片岡 正俊"},{"name":"村田 裕美"},{"name":"篠原 康雄"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"Resistin is an adipocytokine that induces insulin resistance and is predominantly expressed in adipocytes and peripheral blood mononuclear cells. Resistin expression increases in inflammatory diseases as well as diabetes mellitus, and is upregulated by bacterial pathogens and proinflammatory cytokines. The aim of this study was to identify resistin in human gingival crevicular fluid, to compare the resistin levels in gingival crevicular fluid between subjects with and without periodontitis and diabetes mellitus and to investigate the regulation of resistin release from human neutrophils by Porphyromonas gingivalis lipopolysaccharide (P-LPS). Gingival crevicular fluid samples were collected from patients with chronic periodontitis (n = 24), patients with diabetes mellitus-related periodontitis (n = 18) and healthy subjects (n = 21). Resistin in gingival crevicular fluid was determined using western blot analysis and an ELISA kit. The glycated hemoglobin (HbA(1c)) value was obtained from patients with diabetes mellitus-related periodontitis by a medical interview. Human neutrophils were cultured with P-LPS (0-1000 ng/mL), or incubated with inhibitors of actin or microtubule polymerization in the absence or presence of P-LPS. The medium and cellular fractions were used for determination of resistin by ELISA. The resistin level in gingival crevicular fluid from patients with periodontitis or diabetes mellitus-related periodontitis was significantly higher than that of healthy subjects. The resistin level in gingival crevicular fluid was correlated with gingival index score, but not blood HbA(1c) value. The P-LPS increased resistin release from human neutrophils, and its induction was decreased by actin polymerization inhibitors. We show, for the first time, the presence of resistin in gingival crevicular fluid. A high resistin level in gingival crevicular fluid samples from periodontitis patients may to some extent be related to P-LPS-induced resistin release from neutrophils.","ja":"Resistin is an adipocytokine that induces insulin resistance and is predominantly expressed in adipocytes and peripheral blood mononuclear cells. Resistin expression increases in inflammatory diseases as well as diabetes mellitus, and is upregulated by bacterial pathogens and proinflammatory cytokines. The aim of this study was to identify resistin in human gingival crevicular fluid, to compare the resistin levels in gingival crevicular fluid between subjects with and without periodontitis and diabetes mellitus and to investigate the regulation of resistin release from human neutrophils by Porphyromonas gingivalis lipopolysaccharide (P-LPS). Gingival crevicular fluid samples were collected from patients with chronic periodontitis (n = 24), patients with diabetes mellitus-related periodontitis (n = 18) and healthy subjects (n = 21). Resistin in gingival crevicular fluid was determined using western blot analysis and an ELISA kit. The glycated hemoglobin (HbA(1c)) value was obtained from patients with diabetes mellitus-related periodontitis by a medical interview. Human neutrophils were cultured with P-LPS (0-1000 ng/mL), or incubated with inhibitors of actin or microtubule polymerization in the absence or presence of P-LPS. The medium and cellular fractions were used for determination of resistin by ELISA. The resistin level in gingival crevicular fluid from patients with periodontitis or diabetes mellitus-related periodontitis was significantly higher than that of healthy subjects. The resistin level in gingival crevicular fluid was correlated with gingival index score, but not blood HbA(1c) value. The P-LPS increased resistin release from human neutrophils, and its induction was decreased by actin polymerization inhibitors. We show, for the first time, the presence of resistin in gingival crevicular fluid. A high resistin level in gingival crevicular fluid samples from periodontitis patients may to some extent be related to P-LPS-induced resistin release from neutrophils."},"publication_date":"2012-02-06","publication_name":{"en":"Journal of Periodontal Research","ja":"Journal of Periodontal Research"},"volume":"Vol.47","number":"No.5","starting_page":"554","ending_page":"562","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/j.1600-0765.2011.01466.x"],"issn":["1600-0765"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:33, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657520"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22220998","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=264440","label":"url"}],"paper_title":{"en":"Analysis of proteins in human gingival crevicular fluid by mass spectrometry","ja":"Analysis of proteins in human gingival crevicular fluid by mass spectrometry"},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"},{"name":"Iwasaka Hiroyuki"},{"name":"Yamada Keisuke"},{"name":"Ohgami Naoto"},{"name":"Namubu Toshiyuki"},{"name":"Kataoka Masatoshi"},{"name":"Yamamoto Takenori"},{"name":"Shinohara Yasuo"},{"name":"Sagawa Ikuko"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"木戸 淳一"},{"name":"板東 美香"},{"name":"廣島 佑香"},{"name":"岩坂 博之"},{"name":"山田 圭佑"},{"name":"大上 直人"},{"name":"南部 敏之"},{"name":"片岡 正俊"},{"name":"山本 武範"},{"name":"篠原 康雄"},{"name":"佐川 幾子"},{"name":"永田 俊彦"}]},"description":{"en":"Gingival crevicular fluid is a bodily fluid transuded from periodontal tissues into the gingival crevice and periodontal pocket, and contains many species of components. Proteins in gingival crevicular fluid have been studied as markers for periodontal diseases. Mass spectrometric analysis is used for the analyses of proteins, lipids, saccharides and metals, and expected as an approach for disease diagnosis. For better analysis of the protein components in gingival crevicular fluid, we investigated proteins in gingival crevicular fluid samples from the healthy gingival crevice and periodontal pocket using mass spectrometry. Gingival crevicular fluid samples were collected from subjects who gave their informed consent and were periodontally healthy or had diseased pockets. These samples were electrophoretically separated, and each fraction on the gels was analysed by nano liquid chromatography coupled with tandem mass spectrometry. Antimicrobial peptides detected in gingival crevicular fluid were confirmed by western blotting. One hundred and four proteins were detected in gingival crevicular fluid samples from both healthy sites and sites of periodontitis; 64 proteins were contained only in gingival crevicular fluid from healthy sites and 63 proteins were observed only in gingival crevicular fluid from periodontitis sites. These proteins were blood-, cytoskeleton-, immunity-, inflammation- and lipid-related proteins and enzymes. Some proteins, including ceruloplasmin, glycogen phosphorylase, glutathione S-transferase, phosphoglycerate mutase, psoriasin, S100A11 and resistin, were identified for the first time in gingival crevicular fluid. Antimicrobial peptides, such as lactoferrin, α1-antitrypsin, lipocalin, S100A7, S100A8, S100A9 and cathelicidin, were observed by mass spectrometry and western blotting. Multiple protein components in gingival crevicular fluid were analysed at the same time using mass spectrometry, and this approach may be useful for the diagnosis of periodontal diseases.","ja":"Gingival crevicular fluid is a bodily fluid transuded from periodontal tissues into the gingival crevice and periodontal pocket, and contains many species of components. Proteins in gingival crevicular fluid have been studied as markers for periodontal diseases. Mass spectrometric analysis is used for the analyses of proteins, lipids, saccharides and metals, and expected as an approach for disease diagnosis. For better analysis of the protein components in gingival crevicular fluid, we investigated proteins in gingival crevicular fluid samples from the healthy gingival crevice and periodontal pocket using mass spectrometry. Gingival crevicular fluid samples were collected from subjects who gave their informed consent and were periodontally healthy or had diseased pockets. These samples were electrophoretically separated, and each fraction on the gels was analysed by nano liquid chromatography coupled with tandem mass spectrometry. Antimicrobial peptides detected in gingival crevicular fluid were confirmed by western blotting. One hundred and four proteins were detected in gingival crevicular fluid samples from both healthy sites and sites of periodontitis; 64 proteins were contained only in gingival crevicular fluid from healthy sites and 63 proteins were observed only in gingival crevicular fluid from periodontitis sites. These proteins were blood-, cytoskeleton-, immunity-, inflammation- and lipid-related proteins and enzymes. Some proteins, including ceruloplasmin, glycogen phosphorylase, glutathione S-transferase, phosphoglycerate mutase, psoriasin, S100A11 and resistin, were identified for the first time in gingival crevicular fluid. Antimicrobial peptides, such as lactoferrin, α1-antitrypsin, lipocalin, S100A7, S100A8, S100A9 and cathelicidin, were observed by mass spectrometry and western blotting. Multiple protein components in gingival crevicular fluid were analysed at the same time using mass spectrometry, and this approach may be useful for the diagnosis of periodontal diseases."},"publication_date":"2012-01-03","publication_name":{"en":"Journal of Periodontal Research","ja":"Journal of Periodontal Research"},"volume":"Vol.47","number":"No.4","starting_page":"488","ending_page":"499","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/j.1600-0765.2011.01458.x"],"issn":["1600-0765"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:34, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657521"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=264445","label":"url"}],"paper_title":{"en":"Diagnosis of periodontal diseases by biomarkers","ja":"Diagnosis of periodontal diseases by biomarkers"},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"Hino Mami"},{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"}],"ja":[{"name":"木戸 淳一"},{"name":"日野 真美"},{"name":"板東 美香"},{"name":"廣島 佑香"}]},"publication_date":"2012","publication_name":{"en":"Electrical Engineering in Japan","ja":"Electrical Engineering in Japan"},"volume":"Vol.179","number":"No.1","starting_page":"40","ending_page":"45","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/eej.21150"],"issn":["1520-6416"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:35, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657522"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21125321","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=213378","label":"url"}],"paper_title":{"en":"Lipopolysaccharide-mediated induction of calprotectin in the submandibular and parotid glands of mice","ja":"Lipopolysaccharide-mediated induction of calprotectin in the submandibular and parotid glands of mice"},"authors":{"en":[{"name":"Javkhlan, Purevjav"},{"name":"Hiroshima Yuka"},{"name":"Azlina, Ahmad"},{"name":"Hasegawa Takahiro"},{"name":"Yao Chenjuan"},{"name":"Akamatsu Tetsuya"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"},{"name":"Hosoi Kazuo"}],"ja":[{"name":"Javkhlan, Purevjav"},{"name":"廣島 佑香"},{"name":"Azlina, Ahmad"},{"name":"長谷川 敬展"},{"name":"姚 陳娟"},{"name":"赤松 徹也"},{"name":"木戸 淳一"},{"name":"永田 俊彦"},{"name":"細井 和雄"}]},"description":{"en":"S100A8 and S100A9 constitute a heterodimeric protein, calprotectin. The mRNAs of S100A8 and S100A9, being expressed at minimal levels in the submandibular and parotid glands (SMG and PG, respectively) of C3H/HeN mice, were induced strongly and transiently by lipopolysaccharide (LPS). Among the mRNAs of members of the S100 protein family examined, those of S100A8 and S100A9 were specifically induced by LPS in the salivary glands. The induction was assumed to be mediated via toll-like receptor 4 (TLR4), since their elevation was limited in C3H/HeJ mice, a TLR4-mutant strain. These proteins became expressed in the granular convoluted tubular cells and striated duct cells in the SMG, and in both acinar and duct cells in the PG (all in the cytoplasm). The salivary calprotectin level was not increased by LPS treatment, implying that elevated calprotectin was not secreted into the saliva and that they may function in microcellular environment of the salivary gland.","ja":"S100A8 and S100A9 constitute a heterodimeric protein, calprotectin. The mRNAs of S100A8 and S100A9, being expressed at minimal levels in the submandibular and parotid glands (SMG and PG, respectively) of C3H/HeN mice, were induced strongly and transiently by lipopolysaccharide (LPS). Among the mRNAs of members of the S100 protein family examined, those of S100A8 and S100A9 were specifically induced by LPS in the salivary glands. The induction was assumed to be mediated via toll-like receptor 4 (TLR4), since their elevation was limited in C3H/HeJ mice, a TLR4-mutant strain. These proteins became expressed in the granular convoluted tubular cells and striated duct cells in the SMG, and in both acinar and duct cells in the PG (all in the cytoplasm). The salivary calprotectin level was not increased by LPS treatment, implying that elevated calprotectin was not secreted into the saliva and that they may function in microcellular environment of the salivary gland."},"publication_date":"2011-12","publication_name":{"en":"Inflammation","ja":"Inflammation"},"volume":"Vol.34","number":"No.6","starting_page":"668","ending_page":"680","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10753-010-9277-1"],"issn":["1573-2576"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:36, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657523"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21316034","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=234781","label":"url"}],"paper_title":{"en":"Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α","ja":"Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α"},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Bandou Mika"},{"name":"Kataoka, Masatoshi"},{"name":"Inagaki Yuji"},{"name":"Herzberg, C. Mark"},{"name":"Ross, F. Karen"},{"name":"Hosoi Kazuo"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"廣島 佑香"},{"name":"板東 美香"},{"name":"Kataoka, Masatoshi"},{"name":"稲垣 裕司"},{"name":"Herzberg, C. Mark"},{"name":"Ross, F. Karen"},{"name":"細井 和雄"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection.","ja":"In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection."},"publication_date":"2011-02-11","publication_name":{"en":"Archives of Oral Biology","ja":"Archives of Oral Biology"},"volume":"Vol.56","number":"No.8","starting_page":"761","ending_page":"767","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.archoralbio.2011.01.004"],"issn":["1879-1506"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:37, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657524"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20689061","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=219833","label":"url"}],"paper_title":{"en":"Roles of lysosomal proteolytic systems in AQP5 degradation in the submandibular gland of rats following chorda tympani parasympathetic denervation","ja":"Roles of lysosomal proteolytic systems in AQP5 degradation in the submandibular gland of rats following chorda tympani parasympathetic denervation"},"authors":{"en":[{"name":"Azlina, Ahmad"},{"name":"Javkhlan, Purevjav"},{"name":"Hiroshima Yuka"},{"name":"Hasegawa Takahiro"},{"name":"Yao Chenjuan"},{"name":"Akamatsu Tetsuya"},{"name":"Hosoi Kazuo"}],"ja":[{"name":"Azlina, Ahmad"},{"name":"Javkhlan, Purevjav"},{"name":"廣島 佑香"},{"name":"長谷川 敬展"},{"name":"姚 陳娟"},{"name":"赤松 徹也"},{"name":"細井 和雄"}]},"description":{"en":"Chorda tympani denervation (CTD) of rats was earlier shown to result in loss of submandibular gland (SMG) weight (at only 1 wk) and in continued reduction in aquaporin 5 (AQP5) protein expression (until 4 wk), without affecting its mRNA synthesis (Li X, Azlina A, Karabasil MR, Purwanti N, Hasegawa T, Yao C, Akamatsu T, Hosoi K. Am J Physiol Gastrointest Liver Physiol 295: G112-G123, 2008). The present study indicated that despite elevation of bax, a proapoptosis protein, by CTD, the operation also increased the level of bcl-2, an antiapoptosis protein, in the SMG. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL assay) showed no increase in the number of apoptotic cells in the SMG. CTD, however, induced strongly and transiently (at 1-3 days) the protein expression of LC3B-II, a marker protein of autophagosomes, suggesting that the reduction in the gland weight was due to onset of autophagy by CTD. Upon CTD, Lamp2, a lysosomal marker, gradually increased in amount, reaching a peak at the 14th day. Immunohistochemical analysis revealed an increase in the number of lysosome-like structures positive for both AQP5 and Lamp2 in the acinar cells of the SMG after CTD; similar changes were observed also for AQP5 and LC3Bs. These data suggest that AQP5 in the SMG entered autophagosomes and/or lysosomes for degradation upon CTD. In vitro AQP5-degrading activity was found in the SMG extracts, and such activity was shown to be increased by CTD. Inhibitor experiments implied cathepsins B and L to be candidate enzymes for this degradation under normal and CTD conditions, respectively.","ja":"Chorda tympani denervation (CTD) of rats was earlier shown to result in loss of submandibular gland (SMG) weight (at only 1 wk) and in continued reduction in aquaporin 5 (AQP5) protein expression (until 4 wk), without affecting its mRNA synthesis (Li X, Azlina A, Karabasil MR, Purwanti N, Hasegawa T, Yao C, Akamatsu T, Hosoi K. Am J Physiol Gastrointest Liver Physiol 295: G112-G123, 2008). The present study indicated that despite elevation of bax, a proapoptosis protein, by CTD, the operation also increased the level of bcl-2, an antiapoptosis protein, in the SMG. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL assay) showed no increase in the number of apoptotic cells in the SMG. CTD, however, induced strongly and transiently (at 1-3 days) the protein expression of LC3B-II, a marker protein of autophagosomes, suggesting that the reduction in the gland weight was due to onset of autophagy by CTD. Upon CTD, Lamp2, a lysosomal marker, gradually increased in amount, reaching a peak at the 14th day. Immunohistochemical analysis revealed an increase in the number of lysosome-like structures positive for both AQP5 and Lamp2 in the acinar cells of the SMG after CTD; similar changes were observed also for AQP5 and LC3Bs. These data suggest that AQP5 in the SMG entered autophagosomes and/or lysosomes for degradation upon CTD. In vitro AQP5-degrading activity was found in the SMG extracts, and such activity was shown to be increased by CTD. Inhibitor experiments implied cathepsins B and L to be candidate enzymes for this degradation under normal and CTD conditions, respectively."},"publication_date":"2010-11","publication_name":{"en":"American Journal of Physiology, Gastrointestinal and Liver Physiology","ja":"American Journal of Physiology, Gastrointestinal and Liver Physiology"},"volume":"Vol.299","number":"No.5","starting_page":"G1106","ending_page":"G1117","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajpgi.00194.2010"],"issn":["1522-1547"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:38, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657525"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/110008006906/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001205520972544/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=232094","label":"url"}],"paper_title":{"en":"Osmotic Stress Affects Calcium Deposition and Osteopontin Expression in Cultured Rat Dental Pulp Cells","ja":"オスモティックストレスが培養歯髄細胞の硬組織形成能とオステオポンチン産生に及ぼす影響"},"authors":{"en":[{"name":"Inagaki Yuji"},{"name":"Bandou Mika"},{"name":"中島 由紀子"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"稲垣 裕司"},{"name":"板東 美香"},{"name":"中島 由紀子"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"}]},"description":{"en":"Osmotic stress is a stimulus caused by osmotic pressure, which is known to affect physiological functions in various tissues and cells. However, there is little information on the effect of osmotic stress on dental pulp tissues and cells. In this study, we investigated the relationship between osmotic stress and calcium deposition in cultured rat dental pulp cells. We also analyzed the effect of osmotic stress on the expression and phosphorylation of osteopontin (OPN), a multi-functional bone matrix protein, in the dental pulp cells. Both hypo- and hyper-osmotic stress affected cell-shape and -growth, and decreased calcium deposition in cultured rat dental pulp cells. Hypoosmotic stress increased OPN secretion and its protein ratio in the culture medium. Also, the secreted OPN was highly phosphorylated. On the other hand, hyper-osmotic stress decreased OPN secretion and its protein ratio and most of the OPN in the hypertoinc medium was dephosphorylated. Both hypo- and hyper-osmotic stress decreased calcium deposition in the cultured rat dental pulp cells. However, the mechanism of the inhibitory action seemed to be different in the two groups, because the amount and phosphorylation pattern of OPN were not similar between the hypo- and hyper-osmotic conditions. We concluded that osmotic stress affects calcium deposition in cultured rat dental pulp cells and that OPN expression and its phosphorylation may be a control factor of osmotic stress-associated mineralization.","ja":"浸透圧変化が惹起する刺激源は一般にオスモティックストレス(osmotic stress)と呼ばれており,種々の組織や細胞に影響をもたらすことが知られている.しかし,オスモティックストレスが歯髄の組織や細胞にどのような影響を与えるのかを論じた成書や研究報告はぼとんどない.本研究ではラット由来の歯髄細胞培養系を用いて,オスモティックストレスと歯髄細胞の硬組織形成の関連性を検証した.また,オスモティックストレスによって硬組織形成関連タンパクであるオステオポンチン(OPN)の発現やリン酸化に変化が生じるかも検証した.その結果,歯髄細胞培養系においては,低張および高張のいずれのオスモティックストレスによっても細胞の形態や増殖に影響が認められ,硬組織形成も低下した.低張ストレスを付与するとOPNの発現量や総タンパク量に対するOPNの比率は上昇し,また発現したOPNはリン酸化されていた.一方,高張ストレスを付与するとOPNの発現量や総タンパク量に対するOPNの比率は低下し,脱リン酸化されたOPNが主に発現した.このように低張と高張のオスモティックストレスではOPNの発現量やリン酸化による修飾の程度が異なっていたことから,低張および高張のいずれのオスモティックストレスによっても石灰化は抑制されたが,その抑制のメカニズムは一様でないことが明らかとなった.以上より,オスモティックストレスは歯髄細胞の硬組織形成に影響を与え,OPNの発現およびそのリン酸化が制御因子として機能している可能性が示唆された."},"publication_date":"2010-08","publication_name":{"en":"The Japanese Journal of Conservative Dentistry","ja":"日本歯科保存学雑誌"},"volume":"Vol.53","number":"No.4","starting_page":"367","ending_page":"375","languages":["jpn"],"referee":true,"identifiers":{"issn":["0387-2343"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:39, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657526"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19602113","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209453","label":"url"}],"paper_title":{"en":"Shosaikoto increases calprotectin expression in human oral epithelial cells.","ja":"Shosaikoto increases calprotectin expression in human oral epithelial cells."},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Bandou Mika"},{"name":"Kataoka Masatoshi"},{"name":"Shinohara Yasuo"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"Inagaki Yuji"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"廣島 佑香"},{"name":"板東 美香"},{"name":"片岡 正俊"},{"name":"篠原 康雄"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"稲垣 裕司"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"BACKGROUND AND OBJECTIVE: Oral epithelial cells help to prevent against bacterial infection in the oral cavity by producing antimicrobial peptides (AMPs). A broad-spectrum AMP, calprotectin (a complex of S100A8 and S100A9 proteins), is expressed by oral epithelial cells and is up-regulated by interleukin-1alpha (IL-1alpha). Shosaikoto (SST) is a traditional Japanese herbal medicine that has immunomodulatory effects and is reported to enhance the levels of IL-1alpha in epithelial cells. The purpose of this study was to investigate the effect of SST on the expression of calprotectin and other AMPs through the regulation of IL-1alpha in oral epithelial cells. MATERIAL AND METHODS: Human oral epithelial cells (TR146) were cultured with SST (at concentrations ranging from 10 to 250 microg/mL) in the presence or absence of anti-IL-1alpha or IL-1 receptor antagonist. The expression of S100A8- and S100A9-specific mRNAs was examined by northern blotting. Calprotectin expression and IL-1alpha secretion were investigated by immunofluorescent staining or ELISA. The expression of other AMPs and IL-1alpha was analyzed by RT-PCR and by quantitative real-time PCR. RESULTS: Shosaikoto (25 microg/mL) significantly increased the expression of S100A8- and S100A9-specific mRNAs and calprotectin protein. Shosaikoto increased S100A7 expression, but had no effect on the expression of other AMPs. The expression of IL-1alpha-specific mRNA and its protein were slightly increased by SST. A neutralizing antibody against IL-1alpha or IL-1 receptor antagonist inhibited SST up-regulated S100A8/S100A9 mRNA expression. CONCLUSION: These results suggest that SST increases the expression of calprotectin and S100A7 in oral epithelial cells. In response to SST, up-regulation of calprotectin may be partially induced via IL-1alpha.","ja":"BACKGROUND AND OBJECTIVE: Oral epithelial cells help to prevent against bacterial infection in the oral cavity by producing antimicrobial peptides (AMPs). A broad-spectrum AMP, calprotectin (a complex of S100A8 and S100A9 proteins), is expressed by oral epithelial cells and is up-regulated by interleukin-1alpha (IL-1alpha). Shosaikoto (SST) is a traditional Japanese herbal medicine that has immunomodulatory effects and is reported to enhance the levels of IL-1alpha in epithelial cells. The purpose of this study was to investigate the effect of SST on the expression of calprotectin and other AMPs through the regulation of IL-1alpha in oral epithelial cells. MATERIAL AND METHODS: Human oral epithelial cells (TR146) were cultured with SST (at concentrations ranging from 10 to 250 microg/mL) in the presence or absence of anti-IL-1alpha or IL-1 receptor antagonist. The expression of S100A8- and S100A9-specific mRNAs was examined by northern blotting. Calprotectin expression and IL-1alpha secretion were investigated by immunofluorescent staining or ELISA. The expression of other AMPs and IL-1alpha was analyzed by RT-PCR and by quantitative real-time PCR. RESULTS: Shosaikoto (25 microg/mL) significantly increased the expression of S100A8- and S100A9-specific mRNAs and calprotectin protein. Shosaikoto increased S100A7 expression, but had no effect on the expression of other AMPs. The expression of IL-1alpha-specific mRNA and its protein were slightly increased by SST. A neutralizing antibody against IL-1alpha or IL-1 receptor antagonist inhibited SST up-regulated S100A8/S100A9 mRNA expression. CONCLUSION: These results suggest that SST increases the expression of calprotectin and S100A7 in oral epithelial cells. In response to SST, up-regulation of calprotectin may be partially induced via IL-1alpha."},"publication_date":"2010-07-08","publication_name":{"en":"Journal of Periodontal Research","ja":"Journal of Periodontal Research"},"volume":"Vol.45","number":"No.1","starting_page":"79","ending_page":"86","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/j.1600-0765.2009.01203.x"],"issn":["1600-0765"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:40, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657527"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20065999","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209454","label":"url"}],"paper_title":{"en":"Modulation of calprotectin in human keratinocytes by keratinocyte growth factor and interleukin-1alpha.","ja":"Modulation of calprotectin in human keratinocytes by keratinocyte growth factor and interleukin-1alpha."},"authors":{"en":[{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"},{"name":"Kataoka Masatoshi"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"Shinohara Yasuo"},{"name":"Yamamoto Takenori"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"板東 美香"},{"name":"廣島 佑香"},{"name":"片岡 正俊"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"篠原 康雄"},{"name":"山本 武範"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"Calprotectin is an antimicrobial complex composed of the S100A8 and S100A9 protein family subunits. Contributing to innate immunity, calprotectin expression is increased by interleukin-1alpha (IL-1alpha), which modulates keratinocyte differentiation. Keratinocyte growth factor (KGF) is produced by mesenchymal cells and has a mitogenic activity for epithelial cells. In this study, we investigated the effect of KGF on calprotectin expression in keratinocytes and modulation by IL-1alpha. Human keratinocytes were cultured with KGF in the presence or absence of a KGF receptor (KGFR) inhibitor or mitogen-activated protein kinase (MAPK) inhibitors. Calprotectin (S100A8/S100A9) expression was determined by northern blotting and enzyme-linked immunosorbent assay, respectively, whereas MAPK phosphorylation was analyzed by western blot analysis. KGF significantly decreased the expression of S100A8/S100A9-specific mRNAs and calprotectin protein. In the presence of KGF, KGFR inhibitor or extracellular-regulated kinase inhibitor restored KGF-downregulated expression of S100A8/S100A9. KGF increased IL-1alpha expression in keratinocytes, whereas IL-1alpha increased KGF expression in fibroblasts. Cocultured fibroblast and keratinocytes showed lower S100A8/S100A9 mRNA expression than keratinocytes alone in the presence or absence of IL-1alpha or KGF. These results suggest that fibroblast-derived KGF reduces or restricts calprotectin expression in keratinocytes, which supports our hypothesis that calprotectin expression in keratinocytes is modulated by factors associated with epithelial-mesenchymal interactions.","ja":"Calprotectin is an antimicrobial complex composed of the S100A8 and S100A9 protein family subunits. Contributing to innate immunity, calprotectin expression is increased by interleukin-1alpha (IL-1alpha), which modulates keratinocyte differentiation. Keratinocyte growth factor (KGF) is produced by mesenchymal cells and has a mitogenic activity for epithelial cells. In this study, we investigated the effect of KGF on calprotectin expression in keratinocytes and modulation by IL-1alpha. Human keratinocytes were cultured with KGF in the presence or absence of a KGF receptor (KGFR) inhibitor or mitogen-activated protein kinase (MAPK) inhibitors. Calprotectin (S100A8/S100A9) expression was determined by northern blotting and enzyme-linked immunosorbent assay, respectively, whereas MAPK phosphorylation was analyzed by western blot analysis. KGF significantly decreased the expression of S100A8/S100A9-specific mRNAs and calprotectin protein. In the presence of KGF, KGFR inhibitor or extracellular-regulated kinase inhibitor restored KGF-downregulated expression of S100A8/S100A9. KGF increased IL-1alpha expression in keratinocytes, whereas IL-1alpha increased KGF expression in fibroblasts. Cocultured fibroblast and keratinocytes showed lower S100A8/S100A9 mRNA expression than keratinocytes alone in the presence or absence of IL-1alpha or KGF. These results suggest that fibroblast-derived KGF reduces or restricts calprotectin expression in keratinocytes, which supports our hypothesis that calprotectin expression in keratinocytes is modulated by factors associated with epithelial-mesenchymal interactions."},"publication_date":"2010-01-12","publication_name":{"en":"Immunology and Cell Biology","ja":"Immunology and Cell Biology"},"volume":"Vol.88","number":"No.3","starting_page":"328","ending_page":"333","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/icb.2009.104"],"issn":["1440-1711"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:41, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657528"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10023999637/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679582732032/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209457","label":"url"}],"paper_title":{"en":"バイオマーカーを用いた歯周病診断","ja":"バイオマーカーを用いた歯周病診断"},"authors":{"en":[{"name":"Kido Jun-ichi"},{"name":"日野 真美"},{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"}],"ja":[{"name":"木戸 淳一"},{"name":"日野 真美"},{"name":"板東 美香"},{"name":"廣島 佑香"}]},"publication_date":"2009-02-01","publication_name":{"en":"IEEJ Transactions on Electronics, Information and Systems","ja":"電気学会論文誌C (電子，情報，システム部門誌)"},"volume":"Vol.129","number":"No.2","starting_page":"233","ending_page":"237","languages":["jpn"],"referee":true,"identifiers":{"doi":["10.1541/ieejeiss.129.233"],"issn":["0385-4221"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:42, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657529"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/110007151262/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282680499131392/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209458","label":"url"}],"paper_title":{"en":"Long-term Observation of Marked Overfilling in Root Canal Therapy : A Report of Three Cases","ja":"著明な過剰根管充填の経過を長期観察した3症例"},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Inagaki Yuji"},{"name":"Bandou Mika"},{"name":"Kido Jun-ichi"},{"name":"Nagata Toshihiko"}],"ja":[{"name":"廣島 佑香"},{"name":"稲垣 裕司"},{"name":"板東 美香"},{"name":"木戸 淳一"},{"name":"永田 俊彦"}]},"description":{"en":"In endodontic therapy, overfilling of gutta-percha point in root canals sometimes occurs due to wrong measurement of working length and overextension of gutta-percha point. Although a slight overfilling to periapical tissues (within 2 mm past the apical foramen) is tolerable, marked overfilling should be checked by postoperative recheck radiographs and/or clinical symptoms. In this report, three clinical cases of marked overfilling are described and long-term radiographic observation (6-14 years) was continued. Overfilled gutta-percha points on the radiographic observation were 3.0 (case 1), 2.5 (case 2), and 3.5 mm (case 3) in the left maxillary molar of a 47-year-old woman, in the left mandibular molar of a 45-year-old woman, and in the left mandibular premolar of a 39-year-old woman, respectively. In case 1, an overfilled point was cut after 1.5 years and disappeared after 3.5 years, and then apical radiolucency was improved after 6 years. In case 2, overfilled points started to minimize after 3 years and disappeared after 14 years. In case 3, an overfilled point was minimized after 13 years accompanied with improvement of apical lesion. None of the cases showed any significant clinical symptoms after the overfilling. These observations are interesting to longitudinally evaluate the disappearance of overfilled gutta-percha and the improvement of apical lesion.","ja":"歯内治療において,ときどき過剰根管充填(過剰根充)に遭遇する.一般に,過剰根充は作業長の測定ミスや根充操作時のガッタパーチャポイントの根尖孔外への突き出しが主な原因であるといわれている.根尖孔から2mm以内のわずかな過剰根充であれば根尖歯周組織に為害性はないが,それ以上の著しい過剰根充の場合は,術後の症状やX線写真によるチェックを行い注意深く対応する必要がある.本報告では,X線写真上で2.5∼3.5mmのポイントの突出が認められた3症例(症例1:上顎第二大臼歯,3.0mm,症例2:下顎第一大臼歯,2.5mm,症例3:下顎第一小臼歯,3.5mm)について,最長6∼14年の経過観察を行った結果を提示した.症例1では,突出ポイントは1年5カ月後に切断され3年8カ月後に消失し,6年8カ月後に根尖透過像も改善した.症例2では,突出ポイントは3年後に縮小傾向を示し,14年7カ月後には消失しており,根尖透過像の消失,歯槽硬線の明瞭化が観察された.症例3では,突出ポイントは13年6カ月後にわずかな部分を残して,ほとんどが吸収しており,同時に根尖透過像も消失していた.臨床症状は,症例1で打診痛が長期残存したほかには特記事項はほとんど認められなかった.当該歯は現在も健常に機能している.今回の症例は,術前診断,術中術後の情報を詳細に提示しながら過剰根充されたガッタパーチャポイントの経過と根尖病巣の治癒経過を長期間追跡したものであり,過剰根充の転帰を知るうえで興味深い臨床報告である."},"publication_date":"2008-10","publication_name":{"en":"The Japanese Journal of Conservative Dentistry","ja":"日本歯科保存学雑誌"},"volume":"Vol.51","number":"No.5","starting_page":"485","ending_page":"492","languages":["jpn"],"referee":true,"identifiers":{"issn":["0387-2343"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:43, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657530"},"force":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10027094494/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282679388561152/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209456","label":"url"}],"paper_title":{"en":"Regulation of calprotectin expression in human keratinocytes in vitro","ja":"Regulation of calprotectin expression in human keratinocytes in vitro"},"authors":{"en":[{"name":"Hiroshima Yuka"},{"name":"Bandou Mika"},{"name":"Kataoka Masatoshi"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"廣島 佑香"},{"name":"板東 美香"},{"name":"片岡 正俊"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"Calprotectin, a heterodimeric complex of S100A8 and S100A9, is an antimicrobial peptide (AMP) expressed in healthy or inflamed epithelium and epidermis. The expression of calprotectin and other AMPs in keratinocytes is regulated by proinflammatory cytokines, bacterial products and keratinocyte differentiation modulators. Interleukin-1α (IL-1α), an autonomous cytokine in keratinocytes, induces keratinocyte differentiation and up-regulates calprotectin expression. Since keratinocyte differentiation is also specified<KG>by interactions with the basement membrane and connective tissue proteins, we sought to learn whether calprotectin expression is affected by extracellular matrix (ECM) proteins in the presence or absence of IL-1α. Human immortalized epidermal keratinocytes (HaCaT cells) were grown in vitro on different ECM substrates including type I collagen (Col I), type IV collagen (Col IV), fibronectin (FN) and laminin (LM) with or without IL-1α and were then cultured in basement membrane extract (Matrigel)-coated dishes or on a feeder layer of fibroblasts. Calprotectin expression in the cultured cells was investigated using immunohistochemical and northern blot analyses, and an enzyme-linked immunosorbent assay. The four ECM proteins (Col I, Col IV, FN and LM) had little effect on calprotectin expression. IL-1α significantly increased the expression of S100A8/ S100A9 mRNAs and calprotecin protein in the cells cultured on each of the ECM(Col I, Col IV, FN and LM)-coated dishes,but these ECM protein substrates did not show a further effect on calprotectin expression in the presence of IL-1α. On the other hand, Matrigel and the fibroblast-feeder layer slightly decreased the expression of S100A8/S100A9 mRNAs in HaCaT cells. These results suggest that calprotectin expression in keratinocytes is regulated by cytokines during epithelial-mesenchymal interactions.<KG>Nihon Shishubyo Gakkai Kaishi (J Jpn Periodontol) 49 : 224-232,2007.","ja":"カルプロテクチンはS100A8とS100A9の2つの蛋白複合体から構成される抗菌ペプチドであり，上皮において発現している．カルプロテクチン発現は，炎症性サイトカイン，細菌産物や上皮細胞分化調節因子により調節されている．上皮細胞で恒常的に産生されるインターロイキン-1α( IL-1α) は上皮細胞分化を誘導し，カルプロテクチン発現を上昇させる．上皮細胞の分化は基底膜や結合組織の相互作用により制御されている．本研究では，細胞外基質(ECM)蛋白やIL-1αによるカルプロテクチン発現について検討した．ヒト上皮細胞株HaCaTをECM蛋白(I型とIV型コラーゲン，フィブロネクチン，ラミニン)コートディッシュに播種し，IL-1αの存在，非存在下で培養した．また，基底膜抽出物(マトリゲル)コートディッシュや線維芽細胞フィーダー層でも培養した．カルプロテクチンの発現は，免疫組織染色，ノーザンブロット法およびELISA法により分析した．その結果，4種のECM蛋白ディッシュで培養を行った場合，カルプロテクチン発現に変化は認められなかった．一方，IL-1αは培養ディッシュに関わらずカルプロテクチン発現を有意に上昇させたが，ECM蛋白はこの効果に影響を及ぼさなかった．また，マトリゲルや線維芽細胞フィーダー層ではカルプロテクチン発現の軽度の減少が認められた．これらの結果より，上皮細胞でのカルプロテクチン発現は上皮-間葉系においてサイトカインにより調節されていることが示唆された．"},"publication_date":"2007-09-28","publication_name":{"en":"Journal of the Japanese Association of Periodontology","ja":"Journal of the Japanese Association of Periodontology"},"volume":"Vol.49","number":"No.3","starting_page":"224","ending_page":"232","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2329/perio.49.224"],"issn":["0385-0110"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:44, {"insert":{"user_id":"R000041357","type":"published_papers","id":"39657531"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/17549071","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209455","label":"url"}],"paper_title":{"en":"Interleukin-1alpha regulates antimicrobial peptide expression in human keratinocytes.","ja":"Interleukin-1alpha regulates antimicrobial peptide expression in human keratinocytes."},"authors":{"en":[{"name":"Bandou Mika"},{"name":"Hiroshima Yuka"},{"name":"Kataoka Masatoshi"},{"name":"Shinohara Yasuo"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"Nagata Toshihiko"},{"name":"Kido Jun-ichi"}],"ja":[{"name":"板東 美香"},{"name":"廣島 佑香"},{"name":"片岡 正俊"},{"name":"篠原 康雄"},{"name":"Herzberg MC"},{"name":"Ross KF"},{"name":"永田 俊彦"},{"name":"木戸 淳一"}]},"description":{"en":"Human epidermis and epithelium serve as physiologic barriers to protect against noxious and infectious agents. Contributing to the defense against infection, epithelial cells express antimicrobial peptides (AMPs). The expression of AMPs in keratinocytes is generally regulated directly by bacteria and indirectly by proinflammatory cytokines. Bacteria may also regulate AMP expression by inducing keratinocyte expression of the autonomous proinflammatory cytokine, interleukin-1alpha (IL-1alpha). To test the hypothesis that AMP expression may be regulated by cell autonomous cytokines, we investigated the effect of IL-1alpha on the expression of AMPs in human keratinocytes (HaCaT cells) by microarray, northern blot, reverse transcriptase (RT)-PCR and western blot analyses. IL-1alpha increased expression of mRNA in a dose- and time-dependent manner specific for lipocalin 2, S100A8, S100A9 and secretory leukocyte protease inhibitor (SLPI) more than twofold relative to nonstimulated cells (control), and slightly upregulated S100A7 and beta-defensin-2. Furthermore, the expression of lipocalin 2, S100A7, S100A8, S100A9 and SLPI proteins were upregulated by IL-1alpha. On the other hand, HaCaT cells expressed mRNA specific for other AMPs, including cystatin 3, adrenomedullin, RNase-7 and mucin 5, which were unaffected by IL-1alpha treatment. These results suggest that the autonomous keratinocyte cytokine, IL-1alpha, selectively upregulates the expression of AMPs which may modulate innate epithelial cell immunity in skin and mucosa.","ja":"Human epidermis and epithelium serve as physiologic barriers to protect against noxious and infectious agents. Contributing to the defense against infection, epithelial cells express antimicrobial peptides (AMPs). The expression of AMPs in keratinocytes is generally regulated directly by bacteria and indirectly by proinflammatory cytokines. Bacteria may also regulate AMP expression by inducing keratinocyte expression of the autonomous proinflammatory cytokine, interleukin-1alpha (IL-1alpha). To test the hypothesis that AMP expression may be regulated by cell autonomous cytokines, we investigated the effect of IL-1alpha on the expression of AMPs in human keratinocytes (HaCaT cells) by microarray, northern blot, reverse transcriptase (RT)-PCR and western blot analyses. IL-1alpha increased expression of mRNA in a dose- and time-dependent manner specific for lipocalin 2, S100A8, S100A9 and secretory leukocyte protease inhibitor (SLPI) more than twofold relative to nonstimulated cells (control), and slightly upregulated S100A7 and beta-defensin-2. Furthermore, the expression of lipocalin 2, S100A7, S100A8, S100A9 and SLPI proteins were upregulated by IL-1alpha. On the other hand, HaCaT cells expressed mRNA specific for other AMPs, including cystatin 3, adrenomedullin, RNase-7 and mucin 5, which were unaffected by IL-1alpha treatment. These results suggest that the autonomous keratinocyte cytokine, IL-1alpha, selectively upregulates the expression of AMPs which may modulate innate epithelial cell immunity in skin and mucosa."},"publication_date":"2007-06-05","publication_name":{"en":"Immunology and Cell Biology","ja":"Immunology and Cell Biology"},"volume":"Vol.85","number":"No.7","starting_page":"532","ending_page":"537","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/sj.icb.7100078"],"issn":["0818-9641"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/published_papers.jsonl, LwE5HI8B7kacV6CWSkQr) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/misc.jsonl) ====
line:1, {"insert":{"user_id":"R000041357","type":"misc","id":"39657351"},"force":{"see_also":[{"@id":"https://ci.nii.ac.jp/naid/130007960320/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1391975831222787968/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=373137","label":"url"}],"paper_title":{"en":"Various roles of calprotectin in periodontal disease and its possibility as a diagnostic marker for periodontal disease","ja":"カルプロテクチンの歯周病病態における多様な役割と歯周病診断マーカーとしての可能性"},"authors":{"en":[{"name":"Sakamoto Eijiro"},{"name":"Hiroshima Yuka"},{"name":"Kido Jun-ichi"},{"name":"Nishikawa Yasufumi"},{"name":"Naruishi Koji"},{"name":"Kido Rie"},{"name":"Yumoto Hiromichi"}],"ja":[{"name":"坂本 英次郎"},{"name":"廣島 佑香"},{"name":"木戸 淳一"},{"name":"西川 泰史"},{"name":"成石 浩司"},{"name":"木戸 理恵"},{"name":"湯本 浩通"}]},"publication_date":"2020-12","publication_name":{"en":"Journal of the Japanese Association of Periodontology","ja":"日本歯周病学会会誌"},"volume":"Vol.62","number":"No.4","starting_page":"193","ending_page":"199","languages":["jpn"],"identifiers":{"doi":["10.2329/perio.62.193"],"issn":["0385-0110"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/misc.jsonl, PgE5HI8B7kacV6CWS0QB) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/awards.jsonl) ====
line:1, {"insert":{"user_id":"R000041357","type":"awards","id":"39657372"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=209452","label":"url"}],"award_name":{"en":"日本歯科保存学会奨励賞","ja":"日本歯科保存学会奨励賞"},"winners":{"en":[{"name":"Hiroshima Yuka"}],"ja":[{"name":"廣島 佑香"}]},"award_title":{"en":"Shosaikoto increases calprotectin expression in human oral epithelial cells","ja":"Shosaikoto increases calprotectin expression in human oral epithelial cells"},"association":{"en":"The Japanese Society of Conservative Dentistry","ja":"日本歯科保存学会"},"award_date":"2010-06-04"},"priority":"input_data"}
line:2, {"insert":{"user_id":"R000041357","type":"awards","id":"39657373"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=349398","label":"url"}],"award_name":{"en":"第24回高田充歯科基礎医学奨励賞","ja":"第24回高田充歯科基礎医学奨励賞"},"winners":{"en":[{"name":"Hiroshima Yuka"}],"ja":[{"name":"廣島 佑香"}]},"association":{"en":"徳島大学歯学部","ja":"徳島大学歯学部"},"award_date":"2019-02-07"},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/awards.jsonl, TAE5HI8B7kacV6CWS0TP) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/204938/researchmap/presentations.jsonl) ====
line:1, {"insert":{"user_id":"R000041357","type":"presentations","id":"39657374"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=237695","label":"url"}],"presentation_title":{"en":"Topical application of osteoprotegerin inhibits alveolar bone loss in rat experimental periodontitis","ja":"Topical application of osteoprotegerin inhibits alveolar bone loss in rat experimental periodontitis"},"presenters":{"en":[{"name":"Sakamoto E"},{"name":"Wada -Mihara Chie"},{"name":"Tokunaga K"},{"name":"Seto H"},{"name":"Hiroshima Yuka"}],"ja":[{"name":"Sakamoto E"},{"name":"美原(和田) 智恵"},{"name":"Tokunaga K"},{"name":"Seto H"},{"name":"廣島 佑香"}]},"event":{"en":"International Joint Symposium on Oral Science, Bali, Indonesia, Dec 17-19, 2010","ja":"International Joint Symposium on Oral Science, Bali, Indonesia, Dec 17-19, 2010"},"languages":["eng"],"is_international_presentation":true},"priority":"input_data"}
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