Updated on 2024/10/31

Information

 

写真a

 
YAMASHITA AKIKO
 
Organization
Faculty of Dental Science Department of Dental Science Assistant Professor
School of Dentistry Department of Dentistry（Concurrent）
Graduate School of Dental Science Department of Dental Science（Concurrent）
Title
Assistant Professor
Profile
糖尿病をはじめとする、さまざまな全身疾患と歯周病との関連に注目し、基礎、臨床研究を行っている。また、薬物性歯肉増殖症の基礎研究を行っている。歯学部第4年次学生対象の歯周病学１の講義、第５年次学生対象の歯周病学２の基礎実習ライター長を担当している。また、第5年次、第6年次学生対象の臨床実習では、歯科保存学、歯周治療学の臨床予備実習、臨床教育を担当している。また、大学院生の研究指導を行っている。 大学病院・歯科部門の歯科研修医の歯科臨床研修の指導や受託歯科衛生士臨床実習生の病因での実習時の指導を行っている。 副医局長、カルテ委員会歯科部門専門部会委員、口腔検査センター委員会委員、保険診療適正化推進委員会歯科部門専門部会委員、臨床研究トライアルマネージャー、デンタルマキシロフェイシャルセンター運営委員会委員などを担当している。
External link

Degree

  • PhD

Research History

  • 広島大学病院 広島大学大学院

Research Interests・Research Keywords

  • Research theme：Development of a novel therapeutic agent for drug induced gingival overgrowth by targeting miRNAs

    Keyword：periodontitis、 drug induced gingival overgrowth

    Research period： 2024.4 - 2027.3

  • Research theme：The study for signaling pathway of SPOCK1, a novel molecule involved in gingival overgrowth and obesity.

    Keyword：gingival overgrowth

    Research period： 2021.4 - 2024.3

  • Research theme：the study of the mechanism of gingival overgrowth

    Keyword：gingival overgrowth

    Research period： 2018.4 - 2021.3

  • Research theme：Study of the role of cathepsin in gingival hyperplasia

    Keyword：periodontitis, gingival hyperplsia

    Research period： 2014.10 - 2018.3

  • Research theme：miRNA

    Keyword：periodontitis

    Research period： 2012.4 - 2014.3

  • Research theme：Global analysis of adipocytes co-cultured with macrophages treated with anti-inflammatory substance

    Keyword：adipocytes co-cultured with macrophages

    Research period： 2010.4 - 2012.3

  • Research theme：The basic and clinical study of the relevance of periodontal disease and metabolic syndrome

    Keyword：periodontitis　metabolic syndrome

    Research period： 2008.4 - 2010.3

Awards

  • プレジデントポスター優秀演題賞

    2009.5   日本糖尿病学会  

  • 日本歯周病学会　奨励賞

    2007.7   日本歯周病学会  

Papers

  • Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development Reviewed

    Imagawa Mio, Shinjo Takanori, Sato Kohei, Kawakami Kentaro, Zeze Tatsuro, Nishimura Yuki, Toyoda Masaaki, Chen Shuang, Ryo Naoaki, Ahmed Al-kafee, Iwashita Misaki, Yamashita Akiko, Fukuda Takao, Sanui Terukazu, Nishimura Fusanori

    Frontiers in Physiology   14   2023.12   （ eISSN:1664042X ）

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    Drug-induced gingival overgrowth (DIGO), induced by certain immunosuppressive drugs, antihypertensive agents, and antiepileptic drugs, may contribute to the formation of deeper periodontal pockets and intractableness in periodontitis. To date, multiple factors such as enhanced matrix production, inflammation, and reduced matrix degradation might be involved in the pathogenesis of DIGO. We have previously reported that SPOCK-1, a heparan sulfate proteoglycan, could affect gingival thickening by promoting epithelial-to-mesenchymal transition (EMT) in gingival keratinocytes. However, few studies have investigated whether a combination of these factors enhances the DIGO phenotype in animal models. Therefore, we investigated whether SPOCK-1, periodontal inflammation, and cyclosporin-A (CsA) could cooperatively promote gingival overgrowth. We first confirmed that Spock-1 overexpressing (Spock1-Tg) mice showed significantly thicker gingiva and greater alveolar bone loss than WT mice in response to ligature-induced experimental periodontitis. DIGO was induced by the combination of CsA administration and experimental periodontitis was significantly enhanced in Spock1-Tg mice compared to that in WT mice. Ligature-induced alveolar bone loss in CsA-treated Spock1-Tg mice was also significantly greater than that in CsA-treated WT mice, while being accompanied by an increase in Rankl and Col1a1 levels and a reduction in matrix metalloprotease expression. Lastly, SPOCK-1 promoted RANKL-induced osteoclast differentiation in both human peripheral blood mononuclear cells and murine macrophages, while peritoneal macrophages from Spock1-Tg mice showed less TNFα and IL-1β secretion than WT mice in response to Escherichia coli lipopolysaccharide. These results suggest that EMT, periodontal inflammation, and subsequent enhanced collagen production and reduced proteinase production contribute to CsA-induced DIGO pathogenesis.

    CiNii Research

  • A Case Report of Improved Palmoplantar Pustulosis following Periodontal Treatment and Possible association with Diminished Systemic Subclinical Inflammation Reviewed International journal

    Case Reports in Dermatological Medicine   2021.10

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： https://doi.org/10.1155/2021/5548760

    Repository Public URL： https://hdl.handle.net/2324/7183064

  • Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development Reviewed International journal

    Mio Imagawa , Takanori Shinjo , Kohei Sato, Kentaro Kawakami, Tatsuro Zeze Yuki Nishimura , Masaaki Toyoda , Shuang Chen, Naoaki Ryo, Al-Kafee Ahmed , Misaki Iwashita , Akiko Yamashita, Takao Fukuda , Terukazu Sanui , Fusanori Nishimura

    Front Physiol   14   1298813   2024.11   （ ISSN:1664-042X eISSN:1664-042X ）

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.3389/fphys.2023.1298813

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    Repository Public URL： https://hdl.handle.net/2324/7174516

  • Effect of Periodontal Treatment on Reducing Chronic Inflammation in Systemically Healthy Patients With Periodontal Disease Reviewed International journal

    Shinji Matsuda, Tomoaki Shintani, Tsuyoshi Miyagawa, Hiromichi Yumoto, Yasutaka Komatsu, Nanae Dewake, Takanori Iwata, Takatoshi Nagano, Toshiya Morozumi, Ryoma Goto, Satsuki Kato, Masahiro Kitamura, Kitetsu Shin, Satoshi Sekino, Akiko Yamashita, Keiko Yamashita, Atsutoshi Yoshimura, Tsutomu Sugaya , Shogo Takashiba, Yoichiro Taguchi , Eiji Nemoto , Hiromi Nishi , Noriyoshi Mizuno , Yukihiro Numabe , Hiroyuki Kawaguchi.

    Am J Med   137 ( 3 )   273 - 279.e2   2024.3   （ ISSN:0002-9343 eISSN:1555-7162 ）

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.amjmed.2023.11.001

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    Repository Public URL： https://hdl.handle.net/2324/7183038

  • Effect of Periodontal Treatment on Reducing Chronic Inflammation in Systemically Healthy Patients With Periodontal Disease Reviewed

    Matsuda Shinji, Shintani Tomoaki, Miyagawa Tsuyoshi, Yumoto Hiromichi, Komatsu Yasutaka, Dewake Nanae, Iwata Takanori, Nagano Takatoshi, Morozumi Toshiya, Goto Ryoma, Kato Satsuki, Kitamura Masahiro, Shin Kitetsu, Sekino Satoshi, Yamashita Akiko, Yamashita Keiko, Yoshimura Atsutoshi, Sugaya Tsutomu, Takashiba Shogo, Taguchi Yoichiro, Nemoto Eiji, Nishi Hiromi, Mizuno Noriyoshi, Numabe Yukihiro, Kawaguchi Hiroyuki

    The American Journal of Medicine   137 ( 3 )   273 - 279.e2   2024.3   （ ISSN:00029343 eISSN:15557162 ）

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    Background: / We determined the effects and an accurate marker of periodontal treatment on serum interleukin (IL)-6 and high-sensitivity C-reactive protein (HsCRP) levels in systemically healthy individuals with periodontal disease. / Methods: / This multicenter study included systemically healthy individuals with periodontal disease who received initial periodontal treatment and had no periodontal treatment history. Periodontal parameters, including periodontal inflamed surface area, masticatory efficiency, and periodontal disease classification; serum IL-6 and HsCRP levels; and serum immunoglobulin (Ig)G titers against periodontal pathogens were evaluated at baseline and after treatment. Subjects were classified as low or high responders (group) based on periodontal inflamed surface area changes. / Results: / There were 153 participants. Only periodontal inflamed surface area changes were markedly different between low and high responders. Periodontal treatment (time point) decreased both serum IL-6 and HsCRP levels. The interaction between group and time point was remarkable only for serum IL-6 levels. Changes in serum immunoglobulin (Ig)G titers against periodontal pathogens were not associated with IL-6 changes in high responders. We analyzed the indirect effect of serum anti-Porphyromonas gingivalis type 2 IgG titer changes using mediation analysis and found no significance. However, the direct effect of group (low or high responder) on IL-6 changes was considerable. / Conclusions: / Periodontal treatment effectively decreased serum IL-6 levels, independent of periodontal pathogen infection, in systemically healthy individuals with periodontal disease.

    CiNii Research

  • Luteolin Is a Potential Immunomodulating Natural Compound against Pulpal Inflammation Reviewed

    Kawakami Kentaro, Fukuda Takao, Toyoda Masaaki, Nakao Yuki, Hayashi Chikako, Watanabe Yukari, Aoki Tsukasa, Shinjo Takanori, Iwashita Misaki, Yamashita Akiko, Shida Miyu, Sanui Terukazu, Uchiumi Takeshi, Nishimura Fusanori

    BioMed Research International   2024   8864513   2024.1   （ ISSN:23146133 eISSN:23146141 ）

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    Language：English  

    Aim. The present study evaluated the therapeutic effects of luteolin in alleviating pulpitis of dental pulp- (DP-) derived microvesicles (MVs) via the inhibition of protein kinase R- (PKR-) mediated inflammation. Methodology. Proteomic analysis of immortalized human dental pulp (DP-1) cell-derived MVs was performed to identify PKR-associated molecules. The effect of luteolin on PKR phosphorylation in DP-1 cells and the expression of tumor necrosis factor-α (TNF-α) in THP-1 macrophage-like cells were validated. The effect of luteolin on cell proliferation was compared with that of chemical PKR inhibitors (C16 and 2-AP) and the unique commercially available sedative guaiacol-parachlorophenol. In the dog experimental pulpitis model, the pulps were treated with (1) saline, (2) guaiacol-parachlorophenol, and (3) luteolin. Sixteen teeth from four dogs were extracted, and the pulp tissues were analyzed using hematoxylin and eosin staining. Immunohistochemical staining was performed to analyze the expression of phosphorylated PKR (pPKR), myeloperoxidase (MPO), and CD68. Experimental endodontic-periodontal complex lesions were established in mouse molar through a silk ligature and simultaneous MV injection. MVs were prepared from DP-1 cells with or without pretreatment with 2-AP or luteolin. A three-dimensional microcomputed tomography analysis was performed on day 7 (n=6). Periodontal bone resorption volumes were calculated for each group (nonligated–ligated), and the ratio of bone volume to tissue volume was measured. Results. Proteomic analysis identified an endogenous PKR activator, and a protein activator of interferon-induced PKR, also known as PACT, was included in MVs. Luteolin inhibited the expressions of pPKR in DP-1 cells and TNF-α in THP-1 cells with the lowest suppression of cell proliferation. In the dog model of experimental pulpitis, luteolin treatment suppressed the expression of pPKR-, MPO-, and CD68-positive cells in pulp tissues, whereas guaiacol-parachlorophenol treatment caused coagulative necrosis and disruption. In a mouse model of endodontic-periodontal complex lesions, luteolin treatment significantly decreased MV-induced alveolar bone resorption. Conclusion. Luteolin is an effective and safe compound that inhibits PKR activation in DP-derived MVs, enabling pulp preservation.

    CiNii Research

  • Luteolin Is a Potential Immunomodulating Natural Compound against Pulpal Inflammation Reviewed

    Kawakami, K; Fukuda, T; Toyoda, M; Nakao, Y; Hayashi, C; Watanabe, Y; Aoki, T; Shinjo, T; Iwashita, M; Yamashita, A; Shida, M; Sanui, T; Uchiumi, T; Nishimura, F

    BIOMED RESEARCH INTERNATIONAL   2024   8864513   2024.1   （ ISSN:2314-6133 eISSN:2314-6141 ）

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    Language：English   Publisher：BioMed Research International  

    Aim. The present study evaluated the therapeutic effects of luteolin in alleviating pulpitis of dental pulp- (DP-) derived microvesicles (MVs) via the inhibition of protein kinase R- (PKR-) mediated inflammation. Methodology. Proteomic analysis of immortalized human dental pulp (DP-1) cell-derived MVs was performed to identify PKR-associated molecules. The effect of luteolin on PKR phosphorylation in DP-1 cells and the expression of tumor necrosis factor-α (TNF-α) in THP-1 macrophage-like cells were validated. The effect of luteolin on cell proliferation was compared with that of chemical PKR inhibitors (C16 and 2-AP) and the unique commercially available sedative guaiacol-parachlorophenol. In the dog experimental pulpitis model, the pulps were treated with (1) saline, (2) guaiacol-parachlorophenol, and (3) luteolin. Sixteen teeth from four dogs were extracted, and the pulp tissues were analyzed using hematoxylin and eosin staining. Immunohistochemical staining was performed to analyze the expression of phosphorylated PKR (pPKR), myeloperoxidase (MPO), and CD68. Experimental endodontic-periodontal complex lesions were established in mouse molar through a silk ligature and simultaneous MV injection. MVs were prepared from DP-1 cells with or without pretreatment with 2-AP or luteolin. A three-dimensional microcomputed tomography analysis was performed on day 7 (n=6). Periodontal bone resorption volumes were calculated for each group (nonligated-ligated), and the ratio of bone volume to tissue volume was measured. Results. Proteomic analysis identified an endogenous PKR activator, and a protein activator of interferon-induced PKR, also known as PACT, was included in MVs. Luteolin inhibited the expressions of pPKR in DP-1 cells and TNF-α in THP-1 cells with the lowest suppression of cell proliferation. In the dog model of experimental pulpitis, luteolin treatment suppressed the expression of pPKR-, MPO-, and CD68-positive cells in pulp tissues, whereas guaiacol-parachlorophenol treatment caused coagulative necrosis and disruption. In a mouse model of endodontic-periodontal complex lesions, luteolin treatment significantly decreased MV-induced alveolar bone resorption. Conclusion. Luteolin is an effective and safe compound that inhibits PKR activation in DP-derived MVs, enabling pulp preservation.

    DOI： 10.1155/2024/8864513

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  • Endothelial Insulin Resistance Exacerbates Experimental Peeriodontitis Reviewed International journal

    Zeze T, Shinjo T, Sato K, Nishimura Y, Imagawa M, Chen S, Ahmed A-K, Iwashita M, Yamashita A, Fukuda T, Sanui T, Park K, King GL, Nishimura F

    J Dent Res   102 ( 10 )   1152 - 1161   2023.7   （ ISSN:0022-0345 eISSN:1544-0591 ）

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1177/00220345231181539

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  • miR-582-5p targets Skp1 and regulates NF-κB signaling-mediated inflammation Reviewed International journal

    Rongzhi Li, Tomomi Sano, Akiko Mizokami, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Yusuke Nakatsu, Yusuke Sotomaru, Tomoichiro Asano, Takashi Kanematsu, Fusanori Nishimura

    Archives of Biochemistry and Biophysics   734   109501 - 109501   2023.1   （ ISSN:0003-9861 eISSN:1096-0384 ）

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.abb.2022.109501

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  • XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis Invited Reviewed International journal

    Nishimura Yuki、Iwashita Misaki、Hayashi Masato、Shinjo Takanori、Watanabe Yukari、Zeze Tatsuro、Yamashita Akiko、Fukuda Takao、Sanui Terukazu、Sano Tomomi、Asano Tomoichiro、 Nishimura Fusanori

    2022.10

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

  • XAF1 overexpression exacerbates diabetes by promoting pancreatic β-cell apoptosis Reviewed

    Yuki Nishimura, Misaki Iwashita, Masato Hayashi, Takanori Shinjo, Yukari Watanabe, Tatsuro Zeze, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomomi Sano, Tomoichiro Asano, Fusanori Nishimura

    Acta Diabetologica   59 ( 10 )   1275 - 1286   2022.10   （ ISSN:0940-5429 eISSN:1432-5233 ）

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Abstract

    Aims

    Pancreatic β-cell apoptosis may be involved in the onset and progression of type 2 diabetes mellitus, although its mechanism remains unclear. We previously demonstrated that macrophage-derived interferon (IFN) β induced X-linked inhibitor of apoptosis–associated factor 1 (XAF1) expression in β-cells and accelerated β-cell apoptosis in vitro. Here, we explored the effects of XAF1 on β-cell function and progression of diabetes in vivo.

    Methods

    Pancreatic β-cell-selective XAF1 overexpressing (Xaf1 Tg) mice were generated. Xaf1 Tg mice and their wild-type (WT) littermates were fed either a normal diet or a 40% or 60% high-fat diet (HFD). The effects of β-cell XAF1 on β-cell apoptosis and exacerbation of diabetes were investigated.

    Results

    Palmitic acid induced IFNβ expression in macrophages, and HFD intake promoted macrophage infiltration in pancreatic islets, both of which cooperatively upregulated XAF1 expression in mouse islets. Furthermore, HFD-fed Xaf1 Tg mice demonstrated increased β-cell apoptosis, lowered insulin expression, and impaired glucose tolerance compared with WT mice fed the same diet. These effects were more pronounced in the 60%HFD group than in the 40%HFD group.

    Conclusions

    Pancreatic β-cell XAF1 expression was enhanced via HFD-induced, macrophage-derived IFNβ, which promoted β-cell apoptosis and led to a reduction in insulin secretion and progression of diabetes. To our knowledge, this is the first report to demonstrate an association between pancreatic β-cell XAF1 overexpression and exacerbation of diabetes, thus providing insight into the mechanism of β-cell mass reduction in diabetes.

    DOI： 10.1007/s00592-022-01930-y

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    Other Link： https://link.springer.com/article/10.1007/s00592-022-01930-y/fulltext.html

  • SPOCK1 induces adipose tissue maturation: New insights into the function of SPOCK1 in metabolism Reviewed International journal

    #Rehab Alshargabi, @Takanori Shinjo, @Misaki Iwashita, @Akiko Yamashita, @Tomomi Sano, #Yuki Nishimura, @Masato Hayashi , #Tatsuro Zeze, @Takao Fukuda, @Terukazu Sanui, @Fusanori Nishimura

    Biochem Biophys Res Commun.   17 ( 533(4) )   1076 - 1082   2020.11

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues Reviewed

    Taiki Sanada, Tomomi Sano, Yusuke Sotomaru, Rehab Alshargabi, Yosuke Yamawaki, Akiko Yamashita, Hiroaki Matsunaga, Misaki Iwashita, Takanori Shinjo, Takashi Kanematsu, Tomoichiro Asano, Fusanori Nishimura

    Biochemistry and Biophysics Reports   22   2020.7

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrep.2020.100757

  • SPOCK1 is a novel inducer of　epithelial to mesenchymal　transition in drug-induced gingival　overgrowth Reviewed International journal

    2020.6

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    Repository Public URL： https://hdl.handle.net/2324/7183062

  • Anti-inflammatory Effects of miRNA-146a Induced in Adipose and Periodontal Tissues Reviewed International journal

    #Taiki Sanada, @Tomomi Sano, Yusuke Sotomaru, #Rehab Alshargabi, Yosuke Yamawaki, @Akiko Yamashita, Hiroaki Matsunaga, @Misaki Iwashita, @Takanori Shinjo, @Takashi Kanematsu, Tomoichiro Asano, @Fusanori Nishimura

    Biochemistry and Biophysics Reports   2020.4

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  • Dental pulp cell-derived powerful inducer of TNF-α comprises PKR containing stress granule rich microvesicles Reviewed

    9 ( 1 )   2019.12

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    It is well known that dental pulp tissue can evoke some of the most severe acute inflammation observed in the human body. We found that dental pulp cells secrete a factor that induces tumor necrosis factor-α production from macrophages, and designated this factor, dental pulp cell-derived powerful inducer of TNF-α (DPIT). DPIT was induced in dental pulp cells and transported to recipient cells via microvesicles. Treatment of dental pulp cells with a PKR inhibitor markedly suppressed DPIT activity, and weak interferon signals were constitutively activated inside the cells. In recipient macrophages, stimulation with DPIT-containing supernatants from pulp cells resulted in activation of both nuclear factor-κB and MAP kinases like JNK and p38. Proteomics analyses revealed that many stress granule-related proteins were present in supernatants from dental pulp cells as well as microvesicle marker proteins like GAPDH, β-actin, HSPA8, HSPB1, HSPE1, and HSPD1. Furthermore, giant molecule AHNAK and PKR were detected in microvesicles derived from dental pulp cells, and gene silencing of AHNAK in dental pulp cells led to reduced DPIT activity. Thus, it appeared that the core protein of DPIT was PKR, and that PKR was maintained in an active state in stress granule aggregates with AHNAK and transported via microvesicles. The activity of DPIT for TNF-α induction was far superior to that of gram-negative bacterial endotoxin. Therefore, we, report for the first time, that active PKR is transported via microvesicles as stress granule aggregates and induces powerful inflammatory signals in macrophages.

    DOI： 10.1038/s41598-019-40046-2

  • Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure Reviewed

    Tomomi Sano, Taiki Sanada, Yusuke Sotomaru, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomoichiro Asano, Takashi Kanematsu, Fusanori Nishimura

    Nutrition and Metabolism   16 ( 1 )   2019.7

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1186/s12986-019-0372-5

  • Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure. Reviewed International journal

    Sano T, Sanada T, Sotomaru Y, Shinjo T, Iwashita M, Yamashita A, Fukuda T, Sanui T, Asano T, Kanematsu T, Nishimura F.

    Nutr Metab (Lond)   2019.7

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  • Dental pulp cell-derived powerful inducer of TNF-α comprises PKR containing stress granule rich microvesicles. Reviewed International journal

    2019.3

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  • Metabolic Endotoxemia-Activated Macrophages Promote Pancreatic β Cell Death via IFNβ-Xaf1 Pathway Reviewed

    50 ( 2 )   160 - 167   2018.2

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    Metabolic endotoxemia has been implicated in the pathogenesis of type 2 diabetes. In addition to adipose tissue inflammation, inflammatory cell infiltration is also observed in islets, although its effect on islets is largely unknown. We hypothesized that macrophage infiltration into islets leads to impairment of α or β cell function, which ultimately act to exacerbate the pathophysiology of diabetes. Gene expression in a murine α cell line, αTC1, and β cell line, βTC6, was investigated by DNA microarray after co-culturing the cells with a murine macrophage cell line, RAW 264.7, in the presence or absence of bacterial endotoxin. Among the genes showing highly upregulated expression, genes specifically upregulated only in β cells were evaluated to determine the roles of the gene products on the cellular function of β cells. In both α and β cells, expression of type I interferon-responsive genes was highly upregulated upon endotoxin stimulation. Among these genes, expression of the X-linked inhibitor of apoptosis (Xiap)-associated factor 1 (Xaf1) gene, which is associated with the induction of apoptosis, was specifically enhanced in β cells by endotoxin stimulation. This upregulation appeared to be mediated by macrophage-derived interferon β (IFNβ), as endotoxin-stimulated macrophages produced higher amounts of IFNβ, and exogenous addition of IFNβ into βTC6 cultures resulted in increased Xaf1 protein production and cleaved caspase 3, which accelerated β-cell apoptosis. Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNβ, which induced β-cell apoptosis by increasing the expression of Xaf1.

    DOI： 10.1055/s-0043-121467

  • Adipose tissue complement factor B promotes adipocyte maturation Reviewed

    Hiroaki Matsunaga, Misaki Iwashita, Takanori Shinjo, Akiko Yamashita, Mitsudai Tsuruta, Shoichiro Nagasaka, Ataru Taniguchi, Mitsuo Fukushima, Naoya Watanabe, Fusanori Nishimura

    Biochemical and Biophysical Research Communications   495 ( 1 )   740 - 748   2018.1

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    DOI： 10.1016/j.bbrc.2017.11.069

  • Adipose tissue complement factor B promotes adipocyte maturation. Reviewed International journal

    Matsunaga H, Iwashita M, Shinjo T, Yamashita A, Tsuruta M, Nagasaka S, Taniguchi A, Fukushima M, Watanabe N, Nishimura F.

    Biochem Biophys Res Commun.   2018.1

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  • Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance Reviewed

    Tomomi Sano, S. Nagayasu, S. Suzuki, Misaki Iwashita, Akiko Yamashita, T. Shinjo, Terukazu Sanui, A. Kushiyama, T. Kanematsu, T. Asano, Fusanori Nishimura

    Nutrition, Metabolism and Cardiovascular Diseases   27 ( 3 )   249 - 259   2017.3

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.numecd.2016.11.008

  • Serum Amyloid A3 Gene Expression in Adipocytes is an Indicator of the Interaction with Macrophages Reviewed

    Yohei Sanada, Takafumi Yamamoto, Rika Satake, Akiko Yamashita, Sumire Kanai, Norihisa Kato, Fons Aj Van De Loo, Fusanori Nishimura, Philipp E. Scherer, Noriyuki Yanaka

    Scientific Reports   6   2016.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/srep38697

  • IL-17A synergistically enhances TNFα-induced IL-6 and CCL20 production in 3T3-L1 adipocytes Reviewed

    477 ( 2 )   241 - 246   2016.8

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    Interleukin-17A (IL-17A) is known to induce inflammatory responses and to be involved in the pathogenesis of not only autoimmune diseases, but also several metabolic and infectious diseases. In this study, IL-17A is shown to induce IL-6 expression in 3T3-L1 mature adipocytes. Interestingly, we found that IL-17A synergistically amplified TNFα-induced secretion of IL-6 and upregulation of IL-17RA expression in 3T3-L1 adipocytes. Its synergistic effects on IL-6 production were inhibited by pre-treatment with inhibitors of IκBα and JNK. Furthermore, IL-17A cooperatively enhanced LPS-mediated IL-6 production in 3T3-L1 adipocytes co-cultured with RAW264.7 macrophages. In addition, IL-17A also enhanced CCL20 production in 3T3-L1 adipocytes stimulated with TNFα or co-cultured with LPS-stimulated RAW macrophages. In high-fat diet-fed mouse epididymal adipose tissues, IL-17RA and RORγt mRNA levels were significantly increased and the serum level of CCL20 was also upregulated. Taken together, these data show that, in adipose tissues, IL-17A contributes to exacerbating insulin resistance-enhancing IL-6 production and promotes the infiltration of Th17 cells in cooperation with TNFα; these findings represent a novel hypothesis for the association between IL-17A-producing cells and type 2 diabetes.

    DOI： 10.1016/j.bbrc.2016.06.049

  • Protection from diet-induced obesity and insulin resistance in mice lacking CCL19-CCR7 signaling Invited Reviewed International journal

    OBESITY   23 ( 7 )   1460 - 1471   2015.7

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1002/oby.21127

  • The inflammation-lipocalin 2 axis may contribute to the development of chronic kidney disease Reviewed International journal

    NEPHROLOGY DIALYSIS TRANSPLANTATION   29 ( 3 )   2014.3

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

    DOI： 10.1093/ndt/gft449

  • Flavonol-containing phosphorylated pullulan may attenuate pulp inflammation Reviewed

    J. Yonehiro, Y. Yoshida, Akiko Yamashita, S. Yoshizawa, K. Ohta, N. Kamata, T. Okihara, Fusanori Nishimura

    International Endodontic Journal   46 ( 2 )   119 - 127   2013.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/j.1365-2591.2012.02095.x

  • Establishment of an ex vivo pulpitis model by co-culturing immortalized dental pulp cells and macrophages Reviewed

    J. Yonehiro, Akiko Yamashita, Y. Yoshida, S. Yoshizawa, K. Ohta, N. Kamata, T. Okihara, Fusanori Nishimura

    International Endodontic Journal   45 ( 12 )   1103 - 1108   2012.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/j.1365-2591.2012.02074.x

  • [Periodontal disease]. Reviewed

    Fusanori Nishimura, Misaki Iwashita, Akiko Yamashita

    Nippon rinsho. Japanese journal of clinical medicine   70 Suppl 5   499 - 502   2012.7

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males Potential mechanism of resistance to weight loss among Japanese obese smokers Reviewed

    Shintaro Nagayasu, Shigeki Suzuki, Akiko Yamashita, Ataru Taniguchi, Mitsuo Fukushima, Yoshikatsu Nakai, Kazuko Nin, Naoya Watanabe, Shoichiro Nagasaka, Daisuke Yabe, Fusanori Nishimura

    Tobacco Induced Diseases   10 ( 1 )   2012.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1186/1617-9625-10-3

  • Adipocyte-macrophage interaction may mediate LPS-induced low-grade inflammation Potential link with metabolic complications Reviewed

    Hideo Nakarai, Akiko Yamashita, Shintaro Nagayasu, Misaki Iwashita, Sonoko Kumamoto, Hideki Ohyama, Masaki Hata, Yoshihiko Soga, Akifumi Kushiyama, Tomoichiro Asano, Yoshimitsu Abiko, Fusanori Nishimura

    Innate Immunity   18 ( 1 )   164 - 170   2012.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1177/1753425910393370

  • Periodontal disease and chronic low-grade inflammation Reviewed

    Fusanori Nishimura, Misaki Iwashita, Akiko Yamashita

    Journal of the Japan Diabetes Society   54 ( 7 )   490 - 492   2011.7

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Periodontal disease and hypertriglyceridemia in Japanese subjects Potential association with enhanced lipolysis Reviewed

    Hideo Nakarai, Akiko Yamashita, Mikimasa Takagi, Masataka Adachi, Masaharu Sugiyama, Haruhiko Noda, Masafumi Katano, Ryuji Yamakawa, Keiji Nakayama, Hitomi Takumiya, Yoshikatsu Nakai, Ataru Taniguchi, Fusanori Nishimura

    Metabolism: Clinical and Experimental   60 ( 6 )   823 - 829   2011.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.metabol.2010.07.034

  • DNA microarray analyses of genes expressed differentially in 3T3-L1 adipocytes co-cultured with murine macrophage cell line RAW264.7 in the presence of the toll-like receptor 4 ligand bacterial endotoxin Reviewed

    Akiko Yamashita, Y. Soga, Y. Iwamoto, T. Asano, Y. Li, Y. Abiko, Fusanori Nishimura

    International Journal of Obesity   32 ( 11 )   1725 - 1729   2008.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/ijo.2008.153

  • Macrophage-adipocyte interaction Marked interleukin-6 production by lipopolysaccharide Reviewed

    Akiko Yamashita, Yoshihiko Soga, Yoshihiro Iwamoto, Sayuri Yoshizawa, Hirotaka Iwata, Susumu Kokeguchi, Shogo Takashiba, Fusanori Nishimura

    Obesity   15 ( 11 )   2549 - 2552   2007.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/oby.2007.305

  • High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1 Reviewed

    Hirotaka Iwata, Yoshihiko Soga, Michio Meguro, Sayuri Yoshizawa, Yuka Okada, Yoshihiro Iwamoto, Akiko Yamashita, Shogo Takashiba, Fusanori Nishimura

    Innate Immunity   13 ( 4 )   227 - 234   2007.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1177/0968051907082608

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Books

  • 日本歯周病学会編　糖尿病患者に対する歯周治療ガイドライン改定第3版

    西村英紀, 青山典生, 稲垣幸司, 梅﨑陽二朗, 讃井彰一, 白方良典, 鈴木茂樹, 高橋慶壮, 富田幸代, 内藤徹, 中川種昭, 長澤敏行, 中島貴子, 二宮雅美, 沼部幸博, 林丈一朗, 水谷幸嗣, 水野智仁, 三辺正人, 山下明子, 山本直史.（ Role： Joint author）

    医歯薬出版株式会社  2023.5 

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    Language：Japanese   Book type：Scholarly book

  • 臨床歯周病学　第3版第3刷　6章ペリオドンタルメディシン

    山下明子、西村英紀（ Role： Joint author）

    医歯薬出版株式会社  2023.4 

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    Responsible for pages：50-62   Language：Japanese   Book type：Scholarly book

  • ザ・ペリオドントロジー　第4版　第3章　ペリオドンタルメディシン　2．歯周病と糖尿病

    山下明子、西村英紀（ Role： Joint author）

    永末書店  2023.4 

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    Responsible for pages：56-59   Language：Japanese   Book type：Scholarly book

  • 第3版　臨床歯周病学

    山下明子、西村英紀（ Role： Joint author）

    医歯薬出版株式会社  2020.2 

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    Language：Japanese   Book type：Scholarly book

  • 歯科衛生士のための糖尿病予防指導マニュアル

    @山下明子, @西村英紀（ Role： Joint author）

    医歯薬出版株式会社  2019.12 

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    Responsible for pages：総論第3章 糖尿病と歯周病の関係 総論第4章 糖尿病患者における歯周治療の流れと歯科衛生士の役割   Language：Japanese   Book type：Scholarly book

  • 歯科衛生士講座　第4版　歯周病学

    山下明子、西村英紀（ Role： Joint author）

    永末書店  2019.3 

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    Language：Japanese   Book type：Scholarly book

  • ザ・ペリオドントロジー第３版　第３章　ペリオドンタルメディシン　２．歯周病と糖尿病

    山下明子、西村英紀（ Role： Joint author）

    永末書店 

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    Responsible for pages：62-64   Language：Japanese   Book type：Scholarly book

  • 臨床歯周病学第３版　６章　ペリオドンタルメディシン

    山下明子、西村英紀（ Role： Joint author）

    医歯薬出版株式会社 

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    Responsible for pages：50-62   Language：Japanese   Book type：Scholarly book

  • 臨床歯周病学第３版 ６章 ペリオドンタルメディシン

    山下明子, 西村英紀（ Role： Joint author）

    医歯薬出版株式会社 

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    Language：Japanese   Book type：Scholarly book

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  • ザ・ペリオドントロジー第３版 第３章 ペリオドンタルメディシン ２．歯周病と糖尿病

    山下明子, 西村英紀（ Role： Joint author）

    永末書店 

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    Language：Japanese   Book type：Scholarly book

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Presentations

  • 血管内皮細胞におけるインスリン抵抗性は実験的歯周炎を増悪させる

    瀬々起朗、新城尊徳、西村優輝、佐藤晃平、今川澪、陳爽、Al-Kafee Ahmed, 梁尚陽、岩下未咲、山下明子、西村英紀

    令和５年度日本歯周病学会九州五大学日本臨床歯周病学会九州支部合同研修会  2023.11 

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    Event date： 2023.11

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：福岡市   Country：Japan  

  • 実験的歯周炎を惹起したKK-Ayマウスでは、糸球体中のHPGDS発現上昇を介して腎症が増悪する

    佐藤晃平、新城尊徳、瀬々起朗、今川澪、梁尚陽、陳爽、Al-Kafee Ahmed、大塚穂佳、西村優輝、岩下未咲、山下明子、西村英紀

    令和５年度日本歯周病学会九州五大学日本臨床歯周病学会九州支部合同研修会  2023.11 

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    Event date： 2023.11

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：福岡市   Country：Japan  

  • SPOCK1はシクロスポリンによる薬物性歯肉増殖症において歯周炎を介した歯肉肥厚と歯槽骨吸収を増大する

    今川澪、新城尊徳、佐藤晃平、川上賢太郎、瀬々起朗、西村優輝、岩下未咲、山下明子、西村英紀

    第１５９回日本歯科保存学会秋季学術大会  2023.11 

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    Event date： 2023.11

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：浜松市   Country：Japan  

  • 掌蹠膿疱症の増悪因子として口腔内の感染病巣が疑われた慢性歯周炎患者の一症例

    山下明子、新城尊徳、西村英紀

    第６６回秋季日本雌雄病学会学術大会  2023.10 

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    Event date： 2023.10

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：長崎市   Country：Japan  

  • 血管内皮細胞におけるインスリン抵抗性は糖尿病関連歯周炎を増悪させる

    瀬々起朗、新城尊徳、西村優輝、佐藤晃平、今川澪、陳爽、梁尚陽、岩下未咲、山下明子、西村英紀

    日本歯科保存学会２０２３年度春季学術大会（第１５３回）  2023.6 

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    Event date： 2023.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：松江市   Country：Japan  

  • miR-582-5p, that targets Skp1 and suppresses NF-kB signaling-mediated inflammation, is down-regulated in periodontitis and obesity.

    Li Rongzhi, Tomomi Sano, Takao Fukuda, Takanori Shinjo, Misaki Iwashita, Akiko Yamashita, Terukazu Sanui, Fusanori Nishimura

    2023.6 

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    Event date： 2023.6

    Language：English  

    Country：Japan  

  • Endothelial insulin resistance contributes to the pathogenesis of diabetes-related periodontitis. International conference

    2022 IADR/APR General Session  2022.5 

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    Event date： 2023.6

    Language：English  

    Country：Japan  

  • Endothelial insulin resistance contributes to the pathogenesis of diabetes-related periodontitis. International conference

    Tatsuo Zeze, Takanori Shinjo, Kohei Sato, Mio Imagawa, Yuki Nishimura, Misaki Iwashita, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura

    2022 IADR/APR General Session  2022.5 

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    Event date： 2023.6

    Language：English  

    Country：Japan  

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  • 実験的歯周炎を惹起したKK-Ayマウスでは、糸球体中HPGDS発現上昇を介して腎症が増悪する

    佐藤晃平、新城尊徳、瀬々起朗、今川澪、梁尚陽、陳爽、西村優輝、岩下未咲、山下明子、西村英紀

    第６６回日本歯周病学会春季学術大会  2023.5 

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    Event date： 2023.5

    Language：Japanese  

    Venue：高松市   Country：Japan  

  • 血管内皮細胞におけるインスリン抵抗性は、インスリン作用によるPI3K-Akt－FoxO１経路を介した炎症誘導性VCAM－１発現を破綻させることで歯周炎の増悪に寄与する

    ＠瀬々起朗、＠新城尊徳、＠西村優輝、＃佐藤晃平、＃今川澪、＃陳爽、＃梁尚陽、＠岩下未咲、＠山下明子、＠西村英紀

    第６６回日本歯周病学会春季学術大会  2023.5 

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    Event date： 2023.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：高松市   Country：Japan  

  • 実験的歯周炎によって２型糖尿病モデルKK-Ayマウスにおける腎症は増悪する

    @新城尊徳、#佐藤晃平、@横溝久、@瀬々起朗、@今川澪、@岩下未咲、@山下明子、@西村英紀

    第６６回日本糖尿病学会年次学術集会  2023.5 

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    Event date： 2023.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：鹿児島市   Country：Japan  

  • XAF１の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    ＠西村優輝、＠岩下未咲、＠新城尊徳、＠瀬々起朗、＠佐野朋美、＠山下明子、＠西村英紀

    第157回日本歯科保存学会2022年度秋季学術大会  2022.11 

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    Event date： 2022.11

    Language：Japanese  

    Country：Japan  

  • XAF１の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    西村優輝, 岩下未咲, 新城尊徳, 瀬々起朗, 佐野朋美, 山下明子, 西村英紀

    第157回日本歯科保存学会2022年度秋季学術大会  2022.11 

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    Event date： 2022.11

    Language：Japanese  

    Country：Japan  

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  • 実験的歯周炎により2型糖尿病モデルKK-Aｙマウスの糖尿病性腎臓病は増悪する

    ＃佐藤晃平、＠新城尊徳、＃瀬々起朗、＃今川澪、＠西村優輝、＠岩下未咲、＠山下明子、＠西村英紀

    令和4年度日本歯周病学会九州五大学日本臨床歯周病学会九州支部合同研修会  2022.11 

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    Event date： 2022.11

    Language：Japanese  

    Country：Japan  

  • 実験的歯周炎により2型糖尿病モデルKK-Aｙマウスの糖尿病性腎臓病は増悪する

    佐藤晃平, 新城尊徳, 瀬々起朗, 今川澪, 西村優輝, 岩下未咲, 山下明子, 西村英紀

    令和4年度日本歯周病学会九州五大学日本臨床歯周病学会九州支部合同研修会  2022.11 

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    Event date： 2022.11

    Language：Japanese  

    Country：Japan  

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  • SPOCK1はシクロスポリンによる薬剤性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    ＃今川澪、＠新城尊徳、＠山下明子、＃佐藤晃平、＃瀬々起朗、＠西村優輝、＃川上賢太郎、＠岩下未咲、＠西村英紀

    第65回秋季日本歯周病学会学術大会  2022.9 

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    Event date： 2022.9

    Language：Japanese  

    Country：Japan  

  • SPOCK1はシクロスポリンによる薬剤性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    今川澪, 新城尊徳, 山下明子, 佐藤晃平, 瀬々起朗, 西村優輝, 川上賢太郎, 岩下未咲, 西村英紀

    第65回秋季日本歯周病学会学術大会  2022.9 

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    Event date： 2022.9

    Language：Japanese  

    Country：Japan  

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  • SPOCK1はシクロスポリンによる薬剤性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    ＃今川澪、＠新城尊徳、＠山下明子、＃佐藤晃平、＠瀬々起朗、＠西村優輝、＃川上賢太郎、＠岩下未咲、＠西村英紀

    第156回日本歯科保存学会2022年春季学術大会  2022.6 

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    Event date： 2022.6 - 2022.7

    Language：Japanese  

    Country：Japan  

  • SPOCK1はシクロスポリンによる薬剤性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    今川澪, 新城尊徳, 山下明子, 佐藤晃平, 瀬々起朗, 西村優輝, 川上賢太郎, 岩下未咲, 西村英紀

    第156回日本歯科保存学会2022年春季学術大会  2022.6 

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    Event date： 2022.6 - 2022.7

    Language：Japanese  

    Country：Japan  

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  • Insulin resistance in vascular endothelial cells contributes to the exacerbation of periodontitis via dysregulation of inflammation-induced VCAM-1expression. International conference

    Zeze T, Shinjo T, Nishimura Y, Sato K, Imagawa M, Yamashita A, Nishimura F

    JADR 69th annual meeting.  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Country：Japan  

  • 血管内皮細胞におけるインスリン抵抗性は炎症誘導性VCAM-1発現制御が破綻することで歯周炎増悪に寄与する

    #瀬々起朗、@新城尊徳、#西村優輝、#佐藤晃平,#今川澪、@岩下未咲、@山下明子、@西村英紀

    第64回秋季日本歯周病学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 実験的歯周炎により2型糖尿病モデルKK-Ayマウスの糖尿病性腎臓病は増悪する

    #佐藤晃平、@新城尊徳、#西村優輝、#瀬々起朗、#今川澪、@岩下未咲、@山下明子、@西村英紀

    第64回秋季日本歯周病学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • SPOCK1は歯周炎における歯槽骨吸収と歯肉肥厚に関与する

    #今川澪、@新城尊徳、@山下明子、#西村優輝、#瀬々起朗、#佐藤晃平、@岩下未咲、@西村英紀

    2021年度日本歯科保存学会秋季学術大会（第154回）  2021.10 

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    Event date： 2021.10

    Language：Japanese  

    Country：Japan  

  • High-fat diet-induced XAF1exacerbates diabetes by promoting pancreatic β-cell apoptosis. International conference

    2021.10 

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    Event date： 2021.10

    Language：English  

    Country：Japan  

  • 膵β細胞Xaf１が膵島機能および糖尿病発症に及ぼす影響

    ＃西村優輝、＠岩下未咲、＠林大翔、＠新城尊徳、＃瀬々起朗、＠佐野朋美、＠山下明子、＠西村英紀

    2021年度日本歯科保存学会春季学術大会（第154回）  2021.6 

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    Event date： 2021.6

    Language：Japanese  

    Country：Japan  

  • 脂肪細胞CCL19が脂肪組織炎症および脂質代謝に及ぼす影響

    ＃林大翔、＠岩下未咲、＃西村優輝、＠新城尊徳、＃瀬々起朗、＠佐野朋美、＠山下明子、＠西村英紀

    第63回春季歯周病学会学術大会  2020.7 

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    Event date： 2020.7

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 膵β細胞Xaf1が膵島機能および糖尿病発症に及ぼす影響

    ＃西村優輝、＠岩下未咲、＠林大翔、＠新城尊徳、＠佐野朋美、＠山下明子、＠西村英紀

    第152回日本歯科保存学会春季学術大会  2020.5 

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    Event date： 2020.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues International conference

    @Tomomi Sano, #Taiki Sanada, #Alshargabi Yahya Rehab,@ Akiko Yamashita, @Hiroaki Matsunaga, @Misaki Iwashita, @Fusanori Nishimura

    the 59th general Session of Korean Acdemy of Periodontology  2019.11 

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    Event date： 2019.11

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Country：Japan  

  • Identification of microRNAs involved in adipose tissue inflammation International conference

    Sano T, Sanada T, Rehab A, Shinjo T, Li R, Iwashita M, Yamashita A, Nishimura F

    Taiwan Academy of Periodontology Annual Meeting and International Symposium  2019.11 

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    Event date： 2019.11

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Country：Taiwan, Province of China  

  • SPOCK-1 is a novel epithelial mesenchymal transition (EMT) inducer in drug induced gingival overgrowth. International conference

    #Alshargabi Yahya Rehab, @Tomomi Sano,@ Akiko Yamashita, #Taiki Sanada,@Takao Fukuda,@Misaki Iwashita,@Terukazu Sanui, @Fusanori Nishimura

    the 59th general Session of Korean Acdemy of Periodontology  2019.11 

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    Event date： 2019.11

    Language：English   Presentation type：Symposium, workshop panel (public)  

    Country：Korea, Republic of  

  • 脂肪細胞で高発現するCCL19が脂肪組織炎症および脂質代謝に及ぼす影響

    #林大翔、@岩下未咲、#西村優輝、@佐野朋美、@新城尊徳、@山下明子、@西村英紀

    第62回秋季日本歯周病学会学術大会  2019.10 

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    Event date： 2019.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：北九州国際会議場   Country：Japan  

  • 脂肪細胞に発現するCCL19が脂肪組織炎症および代謝制御に及ぼす影響

    ＃林大翔、＠岩下未咲、＃西村優輝、＠佐野朋美、＠山下明子、＠西村英紀

    第150回日本歯科保存学会  2019.6 

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    Event date： 2019.6

    Language：Japanese  

    Country：Japan  

  • SPOCK-1　upreguratetion is a novel epithelial mesenchymal transition (EMT) inducer in calcium channel blocker-induced gingival overgrowth

    第62回春季日本歯周病学会学術  2019.5 

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    Event date： 2019.6

    Language：English   Presentation type：Oral presentation (general)  

    Venue：神奈川県民ホール   Country：Japan  

  • CCR7欠損マウスにおける脂肪および歯周組織炎症抑制機序の考察

    佐野朋美、眞田大樹、武村翼、Alshargabi　Rehab、岩下未咲、山下明子、藤田剛、栗原英見、西村英紀

    第61回秋季日本歯周病学会学術大会  2018.10 

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    Event date： 2019.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：リーガロイヤルホテル大阪   Country：Japan  

  • 脂肪・歯周組織で発現誘導されるmiRNAによる抗炎症効果の検討

    眞田大樹、佐野朋美、松永紘明、岩下未咲、山下明子、Rehab Alshargabi,兼松隆、西村英紀

    第62回春季日本歯周病学会学術大会  2019.5 

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    Event date： 2019.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：神奈川県民ホール   Country：Japan  

  • エピカテキンは歯肉線維芽細胞─マクロファージ相互作用による過剰な炎症反応を抑制する

    眞田大樹,佐野朋美,山下明子

    日本歯周病学会60周年記念京都大会  2018.6 

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    Event date： 2018.6

    Language：Japanese  

    Country：Japan  

  • the role of proteoglycans in the pathogenesis of drug induced gingival overgrowth (DIGO)

    Rehab Alshargabi, Akiko Yamashita, Misaki Iwashita, Takao Fukuda, Terukazu Sanui, Fusanori Nishimura

    2018.6 

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    Event date： 2018.5 - 2018.6

    Language：Japanese  

    Country：Japan  

  • 脂肪細胞complement factorB は脂肪細胞の成熟および肥満を促進する

    松永紘明、岩下未咲、山下明子、新城尊徳、鶴田満大、西村英紀

    第61回春季日本歯周病学会学術大会  2018.6 

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    Event date： 2018.5 - 2018.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：京王プラザホテル   Country：Japan  

  • 膵島に浸潤した活性化マクロファージはIFBβーXaf１経路を介した膵β細胞のアポトーシスを促進する

    鶴田満大、岩下未咲、新城尊徳、松永紘明、山下明子、西村英紀

    第61回春季日本歯周病学会学術  2018.6 

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    Event date： 2018.5 - 2018.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 薬剤性歯肉増殖症におけるspock-1の役割

    Rehab Alshargabi, 山下明子

    平成29年度日本歯周病学会60周年記念京都大会  2017.12 

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    Event date： 2017.12

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：京都国際会議場   Country：Japan  

  • CCR7欠損マウスにおけるエネルギー消費亢進機序についての検討

    佐野朋美、山下明子　他

    2017.10 

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    Event date： 2017.10

    Language：Japanese  

    Venue：盛岡市   Country：Japan  

  • Study on the mechanism of increased energy expenditure of CCR7 deficient mouse

    Sano T. Yamashita Y

    he 65th Annual Meeting of Japanese Association for Dental Research.  2017.10 

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    Event date： 2017.10

    Language：Japanese  

    Country：Japan  

  • the effect of cathepsin-B deficiency on gingival overgrowth in mice International conference

    Akiko Yamashita, Alshargabi Rehab Yahya Fara Sallam, Shinjo Takanori, Misaki Iwashita, Hiroaki Matsunaga, Mitsudai Tsuruta, Hashimoto Yoko, Fusanori NISHIMURA

    94th IADR general session  2016.6 

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    Event date： 2017.6

    Language：English   Presentation type：Symposium, workshop panel (public)  

    Country：Korea, Republic of  

  • the effect of cathepsin-B deficiency on gingival overgrowth in mice

    2016.5 

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    Event date： 2017.6

    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • epicatechin down-regulates inflammatory genes in adipocytes co-cultured with endotoxin-activated macrophages. International conference

    Akiko Yamashita, Tomomi Sano, Shintaro Ngayasu, Misaki Iwashita, Shinjo Takanori, Fusanori NISHIMURA

    95th IADR general session  2017.3 

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    Event date： 2017.3 - 2017.6

    Language：English   Presentation type：Symposium, workshop panel (public)  

    Country：United States  

  • マクロファージと共存する脂肪細胞はLPS刺激によってcomplement factor Bを強発現し，血中complement factor Bはインスリン抵抗性と相関する

    山下 明子, 新城 尊徳, 鶴田　満大, 松永　紘明, 箸方　厚之, 谷口　中, 福島　光夫, 中井　義勝, 長坂　昌一郎, 西村 英紀

    第58回日本糖尿病学会年次学術集会  2015.5 

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    Event date： 2016.5

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：海峡メッセ、下関市民会館、（下関市）   Country：Japan  

  • 脂肪組織complemnt factorBが炎症および代謝制御に及ぼす影響

    松永紘明、山下明子、岩下未咲、新城尊徳、鶴田満大、西村英紀

    第59回春季日本歯周病学会学術大会  2016.5 

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    Event date： 2016.5

    Language：Japanese  

    Venue：かごしま県民交流センター   Country：Japan  

  • CCL19-CCR7経路がエネルギー消費に及ぼす影響に関する検討

    佐野　朋美, 岩下 未咲, 山下 明子, 新城 尊徳, 箸方厚之, 永安慎太郎, 西村 英紀

    第58回春季日本歯周病学会　学術大会  2015.5 

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    Event date： 2016.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：幕張メッセ　（千葉市）   Country：Japan  

  • マクロファージと共存する脂肪細胞はLPS刺激によって補体B因子を強発現し、血中補体B因子はインスリン抵抗性と相関する

    鶴田　満大, 山下 明子, 新城 尊徳, 松永　紘明, 西村 英紀

    第５８回春季日本歯周病学会学術大会  2015.5 

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    Event date： 2015.5

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：幕張メッセ（千葉市）   Country：Japan  

  • DPP4阻害薬anagliptinは、活性化マクロファージおよびマクロファージ共培養下脂肪細胞の炎症反応を抑制する

    山下 明子, 新城尊徳, 岩下未咲, 鈴木茂樹, 西村 英紀

    第57回日本歯周病学会春季学術大会  2014.5 

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    Event date： 2014.5

    Language：Japanese  

    Venue：岐阜   Country：Japan  

  • 血管内皮細胞におけるインスリン抵抗性は糖尿病関連歯周炎を増悪させる

    瀬々 起朗, 新城 尊徳, 西村 優輝, 佐藤 晃平, 今川 澪, 陳 爽, 梁 尚陽, 岩下 未咲, 山下 明子, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2023.5  (NPO)日本歯科保存学会

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  • ヒロシマスタディの別角度からの解析～炎症マーカーとヘモグロビンA1cの相関解析でわかること～

    山下 明子, 宗永泰一, 土井伸浩, 中村茂夫, 西村 英紀

    第57回秋季日本歯周病学会　学術大会  2014.10 

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    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

    Venue：神戸国際会議場、神戸市   Country：Japan  

  • 血管内皮細胞におけるインスリン抵抗性は,インスリン作用によるPI3K-Akt-FoxO1経路を介した炎症誘導性VCAM-1発現を破綻させることで歯周炎の増悪に寄与する

    瀬々 起朗, 新城 尊徳, 西村 優輝, 佐藤 晃平, 今川 澪, 陳 爽, 梁 尚陽, 岩下 美咲, 山下 明子, 西村 英紀

    日本歯周病学会会誌  2023.4  (NPO)日本歯周病学会

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  • Skp1を標的としNF-κBシグナルを介した炎症を抑制するmiR-582-5pは歯周炎と肥満において抑制されている(miR-582-5p, that targets Skpl and suppresses NF-κB signaling-mediated inflammation, is down-regulated in periodontitis and obesity)

    Li Rongzhi, Sano Tomomi, Fukuda Takao, Shinjo Takanori, Iwashita Misaki, Yamashita Akiko, Sanui Terukazu, Nishimura Fusanori

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2023.5  (NPO)日本歯科保存学会

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    Language：English  

  • SPOCK1はシクロスポリンによる薬物性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    今川 澪, 新城 尊徳, 山下 明子, 佐藤 晃平, 瀬々 起朗, 西村 優輝, 川上 賢太郎, 岩下 未咲, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2022.5  (NPO)日本歯科保存学会

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    Language：Japanese  

  • SPOCK1はシクロスポリンによる薬物性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    今川 澪, 新城 尊徳, 山下 明子, 佐藤 晃平, 瀬々 起朗, 西村 優輝, 川上 賢太郎, 岩下 未咲, 西村 英紀

    日本歯周病学会会誌  2022.8  (NPO)日本歯周病学会

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  • SPOCK1はシクロスポリンによる薬物性歯肉増殖症において歯周炎症を介した歯肉肥厚と歯槽骨吸収を増大する

    今川 澪, 新城 尊徳, 佐藤 晃平, 川上 賢太郎, 瀬々 起朗, 西村 優輝, 岩下 未咲, 山下 明子, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2023.10  (NPO)日本歯科保存学会

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  • XAF1の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    西村 優輝, 岩下 未咲, 新城 尊徳, 瀬々 起朗, 佐野 朋美, 山下 明子, 西村 英紀

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集  2022.10  (NPO)日本歯科保存学会

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  • XAF1の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    西村 優輝, 岩下 未咲, 新城 尊徳, 瀬々 起朗, 佐野 朋美, 山下 明子, 西村 英紀

    糖尿病  2024.4  (一社)日本糖尿病学会

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  • 全身性疾患への影響を考慮した新たな歯周病重症度検査項目の策定　学会主導型多施設臨床研究

    松田 真司, 菅谷 勉, 加藤 幸紀, 根本 英二, 竹内 康雄, 喜田 大智, 沼部 幸博, 西田 哲也, 小方 頼昌, 申 基哲, 長野 孝俊, 両角 俊哉, 小松 康高, 出分 菜々衣, 神谷 洋介, 北村 正博, 田口 洋一郎, 高柴 正悟, 湯本 浩通, 山下 明子, 吉永 泰周, 吉村 篤利, 河口 浩之

    日本歯周病学会会誌  2022.8  (NPO)日本歯周病学会

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  • 全身性疾患への影響を考慮した新たな歯周病重症度検査項目の策定　学会主導型多施設臨床研究(第二報)

    松田 真司, 菅谷 勉, 加藤 幸紀, 根本 英二, 竹内 康雄, 山下 慶子, 沼部 幸博, 西田 哲也, 小方 頼昌, 申 基哲, 長野 孝俊, 両角 俊哉, 小松 康高, 出分 菜々衣, 後藤 亮真, 北村 正博, 田口 洋一郎, 高柴 正悟, 湯本 浩通, 山下 明子, 吉永 泰周, 吉村 篤利, 河口 浩之

    日本歯周病学会会誌  2023.4  (NPO)日本歯周病学会

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  • 学会主導型多施設共同研究　全身性疾患への影響を考慮した新たな歯周病重症度検査項目の策定　口腔内検査データ解析

    松田 真司, 湯本 浩通, 小松 康高, 出分 菜々衣, 岩田 隆紀, 長野 孝俊, 両角 俊哉, 後藤 亮真, 加藤 幸紀, 山下 元三, 林 丈一朗, 関野 愉, 山下 明子, 山下 慶子, 吉村 篤利, 菅谷 勉, 高柴 正悟, 田口 洋一郎, 根本 英二, 沼部 幸博, 河口 浩之

    日本歯周病学会会誌  2024.4  (NPO)日本歯周病学会

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  • 実験的歯周炎によって2型糖尿病モデルKK-Ayマウスにおける腎症は増悪する

    新城 尊徳, 佐藤 晃平, 横溝 久, 瀬々 起朗, 今川 澪, 岩下 未咲, 山下 明子, 西村 英紀

    糖尿病  2023.4  (一社)日本糖尿病学会

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  • 実験的歯周炎に応答し発現が上昇した糸球体PGD2はKK-Ayマウスにおける糖尿病性腎症の増悪に寄与する

    佐藤 晃平, 新城 尊徳, 瀬々 起朗, 今川 澪, 梁 尚陽, 陳 爽, Ahmed Alkafee, 大塚 穂佳, 西村 優輝, 岩下 未咲, 山下 明子, 西村 英紀

    日本歯周病学会会誌  2024.4  (NPO)日本歯周病学会

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  • 実験的歯周炎を惹起したKK-Ayマウスでは,糸球体中のHPGDS発現上昇を介して腎症が増悪する

    佐藤 晃平, 新城 尊徳, 瀬々 起朗, 今川 澪, 梁 尚陽, 陳 爽, 西村 優輝, 岩下 未咲, 山下 明子, 西村 英紀

    日本歯周病学会会誌  2023.4  (NPO)日本歯周病学会

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  • 掌蹠膿疱症の増悪因子として口腔内の感染病巣が疑われた慢性歯周炎患者の一症例

    山下 明子, 新城 尊徳, 西村 英紀

    日本歯周病学会会誌  2023.10  (NPO)日本歯周病学会

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  • XAF1の過剰発現は膵β細胞のアポトーシスを促進することで糖尿病を悪化させる

    西村 優輝, 岩下 未咲, 新城 尊徳, 瀬々 起朗, 佐野 朋美, 山下 明子, 西村 英紀

    糖尿病  2024.4  (一社)日本糖尿病学会

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    Language：Japanese  

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Professional Memberships

  • 日本歯科保存学会

  • 日本歯周病学会

  • 日本歯周病学会

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  • 日本歯科保存学会

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Committee Memberships

  • 日本歯周病学会   運営委員  

    2021.4 - 2023.3   

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  • Steering committee member   Domestic

    2021.4 - 2023.3   

  • 日本歯周病学会   ペリオドンタルメディシン委員   Domestic

    2021.4 - 2023.3   

  • 九州大学   口腔検査センター委員会委員  

    2018.4 - 2024.4   

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    Committee type：Other

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  • 九州大学   保険診療適正化推進委員会歯科部門委員会  

    2018.4 - 2024.3   

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    Committee type：Other

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  • 九州大学   口腔検査センター委員会委員  

    2018.4 - 2023.3   

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    Committee type：Other

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  • 九州大学   保険診療適正化推進委員会歯科部門委員会  

    2018.4 - 2023.3   

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    Committee type：Other

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  • 九州大学   一斉技能試験WG  

    2018.1 - 2024.3   

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    Committee type：Other

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  • 九州大学   一斉技能試験WG  

    2018.1 - 2023.3   

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    Committee type：Other

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Academic Activities

  • 日本歯周病学会

    2021.4 - 2023.3

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    Type：Academic society, research group, etc. 

  • 日本歯周病学会

    Role(s)： Review, evaluation

    2021.4 - 2023.3

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    Type：Peer review 

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Research Projects

  • miRNAを標的とした薬剤性歯肉増殖症新規治療薬の開発

    Grant number：24K12947  2024 - 2026

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    山下 明子, 佐野 朋美, 西村 英紀

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    Authorship：Principal investigator  Grant type：Scientific research funding

    薬物性歯肉増殖症(DIGO)は、歯周病を難治性にする。申請者らは、SPOCK1がDIGOの病因に関与すること、SPOCK1過剰発現マウスにサイクロスポリン(CysA)を投与すると、DIGOの病態悪化することを解明した。CysAはカルシニューリン(CN)/NFATシグナルを抑制することで、線維化に関わるコラーゲン発現を亢進させるため、CysA誘導性DIGOの悪化には本経路が関与すると考えられる。本研究では歯肉組織においてNFAT発現抑制時に発現亢進するmiRNAを特定し、そのmiRNA阻害剤の歯肉線維化抑制効果を検証し、DIGOとNFAT抑制による難治性歯周病への治療効果を実証することを目指す。

    CiNii Research

  • 歯肉増殖症や肥満に関わる新規分子SPOCK1のシグナリング経路の探索

    2021 - 2023

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯肉増殖症や肥満に関わる新規分子SPOCK1のシグナリング経路の探索

    Grant number：21K09897  2021 - 2023

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    山下 明子, 佐野 朋美, 西村 英紀

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    Authorship：Principal investigator  Grant type：Scientific research funding

    本研究ではSPOCK1の受容体候補の結合タンパクを探索し、次いでSPOCK1のシグナル伝達経路を検討する。これらの結果を基盤として、SPOCK1過剰発現マウスへ受容体候補分子やシグナリングに関わる分子群の抗体や阻害剤を投与し、歯肉増殖症や肥満の発現への効果を検証することを目指す。本研究成果は、歯肉増殖症のみならず肥満やメタボリックシンドロームの発症に関わるSPOCK1の作用機序を解明するという学術的意義に加えて、歯肉増殖症や肥満の新たな治療標的を見出せる可能性がある。更に将来的には癌の転移の研究や治療法の開発にも繋がる可能性を秘めている。

    CiNii Research

  • 歯肉増殖症の病態解明～spock1による蓄積と分解抑制のシナジー効果の観点から

    2018 - 2021

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯肉増殖症の病態解明～spock1による蓄積と分解抑制のシナジー効果の観点から

    Grant number：18K09578  2018 - 2020

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    山下 明子, 西村 英紀, 岩下 未咲

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    Authorship：Principal investigator  Grant type：Scientific research funding

    本研究は，歯肉増殖症の発生・進展の機序を明らかにし，将来的な発症予防や治療法確立へ繋げることを目指すものであり，研究期間中に以下を明らかにした。カルシウム拮抗薬によって誘発された歯肉増殖症におけるSPOCK1、TGF-β1、およびMMP-9の発現が、非増殖組織における発現よりも高いことを明らかにした。Spock1を過剰発現するトランスジェニックマウスは、明らかな歯肉増殖症と線維症の表現型を発症し、EMTの変化と正の相関があることを示した。さらにin vitroデータによってSPOCK1、TGF-β1、およびMMP-9間の三方向の相互作用が歯肉増殖を引き起こすことを明らかにした。

    CiNii Research

  • 歯肉増殖症におけるカテプシンの役割の解明～多様なカテプシンKOマウスを用いた検討

    Grant number：15K11393  2015 - 2017

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯肉増殖症におけるカテプシンの役割の解明～多様なカテプシンKOマウスを用いた検討

    Grant number：15K11393  2015 - 2017

    日本学術振興会  科学研究費助成事業  基盤研究(C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

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Class subject

  • 歯周病学１

    2024.10 - 2025.3   Second semester

  • 口腔機能修復学特論

    2024.4 - 2025.3   Full year

  • 歯科臨床実習

    2024.4 - 2025.3   Full year

  • 歯周病学２

    2024.4 - 2024.9   First semester

  • 歯周病学１

    2023.10 - 2024.3   Second semester

  • 歯科臨床実習

    2023.4 - 2024.3   Full year

  • 口腔機能修復学特論

    2023.4 - 2024.3   Full year

  • 歯周病学２

    2023.4 - 2023.9   First semester

  • 歯周病学１

    2022.10 - 2023.3   Second semester

  • 口腔機能修復学特論

    2022.4 - 2023.3   Full year

  • 歯科臨床実習

    2022.4 - 2023.3   Full year

  • 歯周病学２

    2022.4 - 2022.9   First semester

  • 歯周病学１

    2021.10 - 2022.3   Second semester

  • 歯科臨床実習

    2021.4 - 2022.3   Full year

  • 口腔機能修復学特論

    2021.4 - 2022.3   Full year

  • 歯周病学２

    2021.4 - 2021.9   First semester

  • 歯周病学１

    2020.10 - 2021.3   Second semester

  • 口腔機能修復学特論

    2020.4 - 2021.3   Full year

  • 歯科臨床実習

    2020.4 - 2021.3   Full year

  • 歯周病学１

    2019.10 - 2020.3   Second semester

  • 歯科臨床実習

    2019.4 - 2020.3   Full year

  • 歯周病学２

    2019.4 - 2019.9   First semester

  • 口腔機能修復学特論

    2019.4 - 2019.9   First semester

  • 口腔機能修復学特論

    2019.4 - 2019.9   First semester

  • 歯周病学１

    2018.10 - 2019.3   Second semester

  • 歯科臨床実習

    2018.4 - 2019.3   Full year

  • 歯周病学Ⅱ

    2018.4 - 2018.9   First semester

  • 歯周病学

    2018.4 - 2018.9   First semester

  • 口腔機能修復学特論

    2018.4 - 2018.9   First semester

  • 歯周病学Ⅰ

    2017.10 - 2018.3   Second semester

  • 歯科臨床実習

    2017.4 - 2018.3   Full year

  • 歯周病学基礎実習

    2017.4 - 2017.9   First semester

  • 歯周病学

    2017.4 - 2017.9   First semester

  • 口腔機能修復学特論

    2017.4 - 2017.9   First semester

  • 口腔機能修復学特論

    2016.4 - 2017.3   Full year

  • 歯科臨床実習

    2016.4 - 2017.3   Full year

  • 歯周病学

    2016.4 - 2016.9   First semester

  • 歯周病学基礎実習

    2016.4 - 2016.9   First semester

  • 歯周病学Ⅰ　講義（3年生　後期）

    2015.10 - 2016.3   Second semester

  • 臨床基礎演習

    2015.4 - 2016.3   Full year

  • 歯科臨床実習

    2015.4 - 2016.3   Full year

  • 歯周病学

    2015.4 - 2016.3   Full year

  • 口腔機能修復学特論

    2015.4 - 2016.3   Full year

  • 歯周病学基礎実習

    2015.4 - 2015.9   First semester

  • 歯周病学Ⅰ　講義（3年生　後期）

    2014.10 - 2015.3   Second semester

  • 歯科臨床実習

    2014.4 - 2015.3   Full year

  • 歯周病学基礎実習

    2014.4 - 2014.9   First semester

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FD Participation

  • 2023.8   Role：Participation   Title：令和５年度４部局合同男女共同参画ＦＤ

    Organizer：University-wide

  • 2023.5   Role：Participation   Title：「科学研究費補助金採択率向上に向けた工夫」等について

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2022.7   Role：Participation   Title：科研費申請書ー採択に近づく書き方のコツ

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2022.4   Role：Participation   Title：2022年度CPXの概要と昨年度からの変更点について

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2020.6   Role：Participation   Title：ジャーナルをめぐる現状と論文の投稿・入手について

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2019.5   Role：Participation   Title：一斉技能試験トライアル教員ＦＤ

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2019.3   Role：Participation   Title：2019年度臨床実地試験トライアル説明会（FD）

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.5   Role：Participation   Title：臨床実習後臨床能力試験トライアルの実施に向けて

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2018.3   Role：Participation   Title：東京医歯大における国家試験対策の実践

    Organizer：[Undergraduate school/graduate school/graduate faculty]

  • 2017.11   Role：Participation   Title：ARO次世代医療センターの活用方法

    Organizer：[Undergraduate school/graduate school/graduate faculty]

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Media Coverage

  • 歯周疾患の管理 Newspaper, magazine

    糖尿病マスター  2016.4

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    歯周疾患の管理

  • 歯科受診スマートサポート Newspaper, magazine

    糖尿病ケア（メディカ出版）  2015.10

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    歯科受診スマートサポート

  • 特集：患者さんにそのまま見せたい！イラスト＆写真でわかる糖尿病合併症 歯周病 歯周病のケア Newspaper, magazine

    糖尿病ケア  2014.11

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    特集：患者さんにそのまま見せたい！イラスト＆写真でわかる糖尿病合併症
    歯周病
    歯周病のケア

  • 特集：糖尿病診療と感染症－全身をめぐる諸連関―　歯周病 Newspaper, magazine

    プラクティス  2014.11

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    特集：糖尿病診療と感染症－全身をめぐる諸連関―　歯周病

Specialized clinical area

  • Biology / Medicine, Dentistry and Pharmacy / Dentistry / Periodontal Dentistry

Clinician qualification

  • Certifying physician

    日本歯周病学会

  • Specialist

    日本歯周病学会

Year of medical license acquisition

  • 2005

Notable Clinical Activities

  • 歯学部5年生、6年生の臨床実習生の教育に従事している。 また、歯科衛生士、歯科技工士などの外部専門学校からの臨床実習生の指導も行っている。