2021/07/12 更新

写真a

オオモリ カズヒロ
大森 一弘
OMORI Kazuhiro
所属
岡山大学病院 講師
職名
講師

学位

  • 博士(歯学) ( 岡山大学 )

研究キーワード

  • 歯周病学

  • 歯内療法学

研究分野

  • ライフサイエンス / 保存治療系歯学

経歴

  • 岡山大学   歯科(歯周科部門)   講師

    2014年

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  • 岡山大学   歯周病態学分野   助教

    2009年 - 2014年

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所属学協会

  • 日本歯周病学会

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  • 日本歯科保存学会

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  • 岡山歯学会

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  • 国際歯科研究協会

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  • 日本歯科研究協会

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  • 日本歯科薬物療法学会

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  • Japanese Association for Dental Research

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  • Japanese Society of Oral Therapeutics and Pharmacology

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  • The Japanese Society of Periodontology

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  • The Japanese Society of Conservative Dentistry

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  • International Association for Dental Research

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▼全件表示

 

論文

  • Induction of migration of periodontal ligament cells by selective regulation of integrin subunits. 査読

    Kawamura M, Yamamoto T, Yamashiro K, Kochi S, Yoshihara-Hirata C, Ideguchi H, Aoyagi H, Omori K, Takashiba S

    Journal of cellular and molecular medicine   2018年12月

  • Fungal metabolite (+)-terrein suppresses IL-6/sIL-6R-induced CSF1 secretion by inhibiting JAK1 phosphorylation in human gingival fibroblasts. 査読 国際誌

    Satoshi Yamamoto, Kazuhiro Omori, Hiroki Mandai, Masaaki Nakayama, Saki Nakagawa, Hiroya Kobayashi, Tadashi Kunimine, Hiroshi Yoshimura, Kyosuke Sakaida, Hidefumi Sako, Soichiro Ibaragi, Tadashi Yamamoto, Hiroshi Maeda, Seiji Suga, Shogo Takashiba

    Heliyon   4 ( 11 )   e00979   2018年11月

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    記述言語:英語  

    Control of bacterial infection-induced inflammatory responses is one of the effective therapeutic approaches of periodontal diseases. Natural products such as lipid mediators and metabolites from microorganisms have been used for decreasing inflammation. We previously reported that (+)-terrein inhibited activation of STAT3 and ERK1/2 in interleukin-6 (IL-6) signaling cascade, leading to prevent vascular endothelial growth factor (VEGF) secretion in human gingival fibroblasts (HGFs). However, little is still known about the role of (+)-terrein on inflammatory responses. In this study, we provided the possibility of novel action that (+)-terrein inhibits activation of Janus-activated kinase 1 (JAK1), which has a central function in IL-6 signaling cascade, and alters expression of mRNAs and proteins induced by IL-6/soluble IL-6 receptor (sIL-6R) stimulation in HGFs. First, we performed PCR array to examine IL-6/sIL-6R-induced mRNA expression, and then expression of mRNA and protein of colony stimulating factor-1 (CSF1) and VEGF were clearly determined by quantitative RT-PCR and ELISA, respectively. Treatment with (+)-terrein suppressed expression of mRNA and protein of CSF1 and VEGF by IL-6/sIL-6R stimulation. Next, to test the effect of (+)-terrein on IL-6/sIL-6R signaling cascade, we demonstrated whether (+)-terrein affects phosphorylation of JAK1 and its downstream proteins, Akt and SHP-2. Western blotting revealed that (+)-terrein inhibited IL-6/sIL-6R-induced phosphorylation of JAK1, Akt, and SHP-2. Therefore, (+)-terrein suppresses IL-6/sIL-6R-induced expression of CSF1 and VEGF via inhibition of JAK1, Akt, and SHP-2. Based on our results, we suggest that (+)-terrein is a candidate compound for anti-inflammatory effect associated with IL-6 signaling.

    DOI: 10.1016/j.heliyon.2018.e00979

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  • IS1598 (IsPg4) distributed to abscess-forming strains of Porphyromonas gingivalis may enhance virulence through upregulation of nrdD-like gene expression 査読

    Norihiro Sonoi, Hiroshi Maeda, Toshimitsu Murauchi, Tadashi Yamamoto, Kazuhiro Omori, Susumu Kokeguchi, Koji Naruishi, Shogo Takashiba

    New Microbiologica   41 ( 1 )   52 - 60   2018年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Luigi Ponzio e figlio Editori  

    An insertion sequence, IS1598 (IsPg4) has been found in virulent strains of Porphyromonas gingivalis in a murine abscess model. The present study was performed to investigate the effects of genetic rearrangements by IS1598 on the phenotypic characteristics of the virulent strains. For this purpose, we searched for a common insertion site of IS1598 among the virulent strains. Through cloning and database search, a common insertion site was identified beside an nrdD-like gene in the virulent FDC 381, W83 and W50 strains. In this region, predicted promoters of the nrdD-like gene and IS1598 are located in tandem, and accumulation of nrdD-like gene mRNA was 5-fold higher in virulent strains (W83, W50, FDC 381) than avirulent strains (ATCC33277, SU63, SUNY1021, ESO59 without IS1598). The role of the nrdD-like gene in virulence of P. gingivalis was investigated by constructing a nrdD-deficient mutant. In the murine abscess model, the parental W83 strain produced necrotic abscesses, while the nrdD-deficient mutant had almost lost this ability. Insertion of IS1598 into the nrdD-like gene promoter region may be related to the phenotypic differences in virulence among P. gingivalis strains through upregulation of the expression of this gene.

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  • The KCNQ1 gene polymorphism as a shared genetic risk for rheumatoid arthritis and chronic periodontitis in Japanese adults: A pilot case-control study.

    Journal of Periodontology   2018年

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  • A novel, nontoxic iron chelator, super-polyphenol, effectively induces apoptosis in human cancer cell lines

    Ohara T, Tomono Y, Boyi X, Yingfu S, Omori K, Matsukawa A

    Oncotarget   2018年

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  • Assessment of pathogenesis of infective endocarditis by plasma IgG antibody titer test against periodontal bacteria. 査読

    Isoshima D, Yamashiro K, Matsunaga K, Shinobe M, Nakanishi N, Nakanishi I, Omori K, Yamamoto T, Takashiba S

    Clinical case reports   5 ( 10 )   1580 - 1586   2017年10月

  • IS1598 (IsPg4) distributed to abscess forming strains of Porphyromonas gingivalis may enhance virulence through upregulation of nrdD-like gene expression

    New microbiologica   2017年

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  • Synthetic Terrein Inhibits Progression of Head and Neck Cancer by Suppressing Angiogenin Production 査読

    Akane Shibata, Soichiro Ibaragi, Hiroki Mandai, Toki Tsumura, Koji Kishimoto, Tatsuo Okui, Nur Mohammad Monsur Hassan, Tsuyoshi Shimo, Kazuhiro Omori, Guo-Fu Hu, Shogo Takashiba, Seiji Suga, Akira Sasaki

    ANTICANCER RESEARCH   36 ( 5 )   2161 - 2168   2016年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:INT INST ANTICANCER RESEARCH  

    Background/Aim: Head and neck cancers are the fifth most common cancer type worldwide, affecting more than half a million patients annually. Development of effective therapeutic drugs is, therefore, required for this type of disease. This study assessed the effects of synthetic terrein on head and neck cancer. Materials and Methods: Synthetic terrein was prepared by using the modified Altenhach's procedure. The effect of synthetic terrein on cell proliferation of head and neck cancer cells and HUVECs was assessed. Angiogenin secretion and ribosome biogenesis were examined by ELISA and silver staining of the nucleolar organizer region. A mouse xenograft model was prepared by inoculating mice with suspensions of cells of the human head and neck cancer cell line OSC-19 subcutaneously into the dorsal region of each mouse. Ki-67, CD31 and angiogenin expression in xenografted tumors was examined by immunohistochemistry. Results: Synthetic terrein inhibited the growth of various head and neck cancer cells. In addition, an in vivo experiment revealed that synthetic terrein inhibited a xenograft tumor growth in athymic mice. Immunohistochemical analysis revealed that expression of Ki-67, CD31 and ANG was down-regulated in synthetic terrein-treated tumors, compared to controls. Synthetic terrein suppressed the ANG secretion and ribosome biogenesis in cancer cells, and cell proliferation in vascular endothelial cells. Conclusion: The mechanism underlying the anti-tumor effects of synthetic terrein against head and neck cancer consists of the inhibition of both tumor cell proliferation and angiogenesis via the suppression of ANG production.

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  • Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. 査読

    Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S

    Clinical case reports   2 ( 6 )   286 - 295   2014年12月

  • Synthetic (+)-terrein suppresses interleukin-6/soluble interleukin-6 receptor induced-secretion of vascular endothelial growth factor in human gingival fibroblasts

    Hiroki Mandai, Kazuhiro Omori, Daisuke Yamamoto, Toki Tsumura, Kyouta Murota, Satoshi Yamamoto, Koichi Mitsudo, Soichiro Ibaragi, Akira Sasaki, Hiroshi Maeda, Shogo Takashiba, Seiji Suga

    BIOORGANIC & MEDICINAL CHEMISTRY   22 ( 19 )   5338 - 5344   2014年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Interleukin (IL)-6 is a proinflammatory cytokine that performs a wide variety of biological functions, including important roles in the progression of chronic inflammatory diseases such as periodontal disease. (+)-Terrein, a secondary bioactive fungal metabolite isolated from Aspergillus terreus, has various biological activities; however, its anti-inflammatory effects are still unknown. The purpose of this study was to examine the effect of synthetic (+)-terrein on IL-6 signaling and related protein production in human gingival fibroblasts. To our knowledge, this study is the first to report that synthetic (+)-terrein is not cytotoxic at concentrations less than 20 mu M and suppresses IL-6/soluble IL-6 receptor (sIL-6R)-induced phosphorylation of signal transducer and activator of transcription-3, extracellular signal-regulated kinase 1/2, and c-jun N-terminal kinase 1/2-signaling proteins that are downstream of IL-6 signaling. In addition, synthetic (+)-terrein suppresses IL-6/sIL-6R-induced vascular endothelial growth factor (VEGF) secretion in a concentration-dependent manner (p < 0.01). These data suggest that synthetic (+)-terrein has potential anti-IL-6 signaling activity and suppresses VEGF-associated inflammatory disease progression. (C) 2014 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.bmc.2014.07.047

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  • Synthetic (+)-terrein suppresses interleukin-6/soluble interleukin-6 receptor induced-secretion of vascular endothelial growth factor in human gingival fibroblasts 査読

    Hiroki Mandai, Kazuhiro Omori, Daisuke Yamamoto, Toki Tsumura, Kyouta Murota, Satoshi Yamamoto, Koichi Mitsudo, Soichiro Ibaragi, Akira Sasaki, Hiroshi Maeda, Shogo Takashiba, Seiji Suga

    BIOORGANIC & MEDICINAL CHEMISTRY   22 ( 19 )   5338 - 5344   2014年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Interleukin (IL)-6 is a proinflammatory cytokine that performs a wide variety of biological functions, including important roles in the progression of chronic inflammatory diseases such as periodontal disease. (+)-Terrein, a secondary bioactive fungal metabolite isolated from Aspergillus terreus, has various biological activities; however, its anti-inflammatory effects are still unknown. The purpose of this study was to examine the effect of synthetic (+)-terrein on IL-6 signaling and related protein production in human gingival fibroblasts. To our knowledge, this study is the first to report that synthetic (+)-terrein is not cytotoxic at concentrations less than 20 mu M and suppresses IL-6/soluble IL-6 receptor (sIL-6R)-induced phosphorylation of signal transducer and activator of transcription-3, extracellular signal-regulated kinase 1/2, and c-jun N-terminal kinase 1/2-signaling proteins that are downstream of IL-6 signaling. In addition, synthetic (+)-terrein suppresses IL-6/sIL-6R-induced vascular endothelial growth factor (VEGF) secretion in a concentration-dependent manner (p < 0.01). These data suggest that synthetic (+)-terrein has potential anti-IL-6 signaling activity and suppresses VEGF-associated inflammatory disease progression. (C) 2014 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.bmc.2014.07.047

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  • Oral vitamin C supplementation prevents the recurrence of idiopathic gingival overgrowth

    Kazuhiro Omori, Yoshihisa Hanayama, Koji Naruishi, Kentaro Akiyama, Hiroshi Maeda, Fumio Otsuka, Shogo Takashiba

    Clinical Case Report   2014年

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  • Serum antibody response to group II chaperonin from Methanobrevibacter oralis and human chaperonin CCT 査読

    Kimito Hirai, Hiroshi Maeda, Kazuhiro Omori, Tadashi Yamamoto, Susumu Kokeguchi, Shogo Takashiba

    PATHOGENS AND DISEASE   68 ( 1 )   12 - 19   2013年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Both group I (HSP60) and group II (CCT) chaperonins are targets of autoantibodies. Autoimmune reactions to HSP60 have been well characterized, while immune reactions to group II chaperonin have not been clarified. Methanobrevibacter oralis is a suspected periodontal pathogen with group II chaperonin. In this study, serum responses to M.oralis chaperonin, human HSP60, and CCT subunits were examined using sera from patients with periodontitis and autoimmune diseases. In comparison with healthy controls, periodontitis patients showed significantly higher responses to CCT4 and CCT8 on dot blot analysis. Signals for CCT3 and CCT8 in autoimmune disease patients were significantly higher than in controls. Significant differences were also demonstrated by Western blotting in anti-CCT4 response in both patient groups. All subjects showed strong reactivity to M.oralis chaperonin and faint signals to human HSP60. Autoantibodies were raised against CCT rather than HSP60; and CCT3, CCT4, and CCT8 were shown to be the main targets. Host immune systems may be frequently exposed to chaperonins of Archaea in various habitats. Although further studies of the cross-reactivity between M.oralis chaperonin and human CCT are required, anti-CCT autoantibodies may be involved in the pathogenesis of periodontitis and autoimmune diseases.

    DOI: 10.1111/2049-632X.12041

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  • Serum antibody response to group Ⅱ chaperonin from Methanobrevibacter oralis and human chaperonin CCT.

    Kimito Hirai, Hiroshi Maeda, Kazuhiro Omori, Tadashi Yamamoto, Susumu Kokeguchi, Shogo Takashiba

    Pathogens and Diseases   68 ( 1 )   12 - 19   2013年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/2049-632X.12041

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  • IMMUNE RESPONSES TO PORPHYROMONAS GINGIVALIS INFECTION SUPPRESS SYSTEMIC INFLAMMATORY RESPONSE IN EXPERIMENTAL MURINE MODEL

    K. Naruishi, K. Omori, H. Maeda, N. Sonoi, K. Funakoshi, K. Hirai, M. Ishii, K. Kubo, H. Kobayashi, T. Tomiyama, D. Yamamoto, I. Tanimoto, K. Kunimatsu, S. Takashiba

    JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS   25 ( 2 )   195 - 202   2011年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOLIFE SAS  

    Periodontitis is localized infectious disease caused by periodontopathic bacteria such as Porphyromonas gingivalis (T: gingivalis), and the severity correlates to significance of immune responses. Recently, it has been reported that periodontitis is associated with the development of systemic disease such as diabetes and atherosclerosis because of increasing invasion of oral pathogens to the circulation. However, the association between local and systemic infectious responses is still unclear. In the present study, we examined the differences of biological responses in animals with or without bacterial infection. After Balb/c mice were infected subcutaneously with live P gingivalis W83, serum, skin and liver were collected according to experimental protocol. The skin and liver tissues were observed pathologically by haematoxylin-eosin staining, and serum IL-6 levels were measured using ELISA method. Throughout the experimental period, conditions of the mice were observed continuously. As expected, severe infiltration of leukocytes were observed at inflamed skin corresponding to the number of bacterial challenges. Although no inflammatory appearance of skin was observed, serum IL-6 levels were increased dramatically (P < 0.01, Student's t-test) and liver tissues were injured in the mice without bacterial challenge. Interestingly, although severe inflammatory appearance of the skin was observed, serum IL-6 levels were not increased and no inflammatory responses were observed in the liver of the 3-times bacterially challenged group. Importantly, immunoglobulin G against P gingivalis W83 was detected in the blood of mice with 3-times bacterial challenge corresponding to improvement of weight loss and survival. In conclusion, although multiple infections develop severe localized inflammation, the immune system should be sufficient to protect the systemic inflammatory responses.

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  • Diabetes-Induced Oxidative Stress Is Mediated by Ca2+-Independent Phospholipase A2 in Neutrophils 査読

    Srinivas Ayilavarapu, Alpdogan Kantarci, Gabrielle Fredman, Oya Turkoglu, Kazuhiro Omori, Hongsheng Liu, Tomoyuki Iwata, Motohiko Yagi, Hatice Hasturk, Thomas E. Van Dyke

    JOURNAL OF IMMUNOLOGY   184 ( 3 )   1507 - 1515   2010年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Neutrophils from people with poorly controlled diabetes present a primed phenotype and secrete excessive superoxide. Phospholipase A(2) (PLA(2))-derived arachidonic acid (AA) activates the assembly of NADPH oxidase to generate superoxide anion. There is a gap in the current literature regarding which PLA(2) isoform regulates NADPH oxidase activation. The aim of this study was to identify the PLA(2) isoform involved in the regulation of superoxide generation in neutrophils and investigate if PLA(2) Mediates priming in response to pathologic hyperglycemia. Neutrophils were isolated from people with diabetes mellitus and healthy controls, and HL60 neutrophil-like cells were grown in hyperglycemic conditions. Incubating neutrophils with the Ca2+-independent PLA(2) (iPLA(2)) inhibitor bromoenol lactone (BEL) completely suppressed fMLP-induced generation of superoxide. The nonspecific actions of BEL on phosphatidic acid phosphohydrolase-1, p47(phox) phosphorylation, and apoptosis were ruled out by specific assays. Small interfering RNA knockdown of iPLA(2) inhibited superoxide generation by neutrophils. Neutrophils from people with poorly controlled diabetes and in vitro incubation of neutrophils with high glucose and the receptor for advanced glycation end products ligand S100B greatly enhanced superoxide generation compared with controls, and this was significantly inhibited by BEL. A modified iPLA(2) assay, Western blotting, and PCR confirmed that there was increased iPLA(2) activity and expression in neutrophils from people with diabetes. AA (10 mu M) partly rescued the inhibition of superoxide generation mediated by BEL, confirming that NADPH oxidase activity is, in part, regulated by AA. This study provides evidence for the role of iPLA(2) in enhanced superoxide generation in neutrophils from people with diabetes mellitus and presents an alternate pathway independent of protein kinase C and phosphatidic acid phosphohydrolase-1 hydrolase signaling. The Journal of Immunology, 2010, 184: 1507-1515.

    DOI: 10.4049/jimmunol.0901219

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  • Resolvin E1 Receptor Activation Signals Phosphorylation and Phagocytosis

    Taisuke Ohira, Makoto Arita, Kazuhiro Omori, Antonio Recchiuti, Thomas E. Van Dyke, Charles N. Serhan

    JOURNAL OF BIOLOGICAL CHEMISTRY   285 ( 5 )   3451 - 3461   2010年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Resolvins are endogenous lipid mediators that actively regulate the resolution of acute inflammation. Resolvin E1 (RvE1; (5S, 12R, 18R)-trihydroxy-6Z, 8E, 10E, 14Z, 16E-eicosapentaenoic acid) is an endogenous anti-inflammatory and pro-resolving mediator derived from eicosapentaenoic acid that regulates leukocyte migration and enhances macrophage phagocytosis of apoptotic neutrophils to resolve inflammation. In the inflammatory milieu, RvE1 mediates counter-regulatory actions initiated via specific G protein-coupled receptors. Here, we have identified RvE1-specific signaling pathways initiated by the RvE1 receptor ChemR23. RvE1 stimulated phosphorylation of Akt that was both ligand-and receptor-dependent. RvE1 regulated Akt phosphorylation in a time (0-15 min)- and dose-dependent (0.01-100 nM) manner in human ChemR23-transfected Chinese hamster ovary cells. RvE1 stimulated phosphorylation of both Akt and a 30-kDa protein, a downstream target of Akt, identified using a phospho-Akt substrate antibody. The 30-kDa protein was identified as ribosomal protein S6, a translational regulator, and its phosphorylation was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin) and an ERK inhibitor (PD98059) but not by a p38-MAPK inhibitor (SB203580). Ribosomal protein S6 is a downstream target of the PI3K/Akt signaling pathway as well as the Raf/ERK pathway. In ChemR23-expressing differentiated HL60 cells, RvE1 also stimulated the phosphorylation of ribosomal protein S6. In addition, RvE1 enhanced phagocytosis of zymosanAby human macrophages, which are inhibited by PD98059 and rapamycin (mTOR inhibitor). These results indicate that RvE1 initiates direct activation of ChemR23 and signals receptor-dependent phosphorylation. These phosphorylation-signaling pathways identified for RvE1 receptor-ligand interactions underscore the importance of endogenous pro-resolving agonists in resolving acute inflammation.

    DOI: 10.1074/jbc.M109.044131

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  • PDK1 Regulates Chemotaxis in Human Neutrophils

    M. Yagi, A. Kantarci, T. Iwata, K. Omori, S. Ayilavarapu, K. Ito, H. Hasturk, T. E. Van Dyke

    JOURNAL OF DENTAL RESEARCH   88 ( 12 )   1119 - 1124   2009年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SAGE PUBLICATIONS INC  

    Phosphoinositide-dependent kinase (PDK1) plays a central role in signal transduction mediated by phosphatidylinositol 3-kinases (PI3K) and regulates cellular functions in neutrophils. Neutrophils from individuals diagnosed with localized aggressive periodontitis (LAP) present an in vivo phenotype with depressed chemotaxis. The aim of this study was to test the hypothesis that PDK1 regulates chemotaxis in neutrophils and is responsible for the abnormal neutrophil chemotaxis LAP. Neutrophil chemotaxis was significantly suppressed by the PDK1 inhibitor staurosporine. When cells were transfected with PDK1 siRNA, there was a significant reduction in chemotaxis, while superoxide generation was not significantly affected. In primary neutrophils from persons with LAP, PDK1 expression and activation levels were significantly reduced, and this reduction was associated with the reduced phosphorylation of Akt (Thr308) and chemotaxis. Analysis of these data demonstrates that PDK1 is essential for the chemotactic migration of neutrophils, and in the absence of PDK1, neutrophil chemotaxis is impaired.

    DOI: 10.1177/0022034509349402

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  • An endogenous regulator of inflammation, resolvin E1, modulates osteoclast differentiation and bone resorption

    B. S. Herrera, T. Ohira, L. Gao, K. Omori, R. Yang, M. Zhu, M. N. Muscara, C. N. Serhan, T. E. Van Dyke, R. Gyurko

    BRITISH JOURNAL OF PHARMACOLOGY   155 ( 8 )   1214 - 1223   2008年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Background and purpose: The inflammation-resolving lipid mediator resolvin E1 (RvE1) effectively stops inflammation-induced bone loss in vivo in experimental periodontitis. It was of interest to determine whether RvE1 has direct actions on osteoclast (OC) development and bone resorption.
    Experimental approach: Primary OC cultures derived from mouse bone marrow were treated with RvE1 and analysed for OC differentiation, cell survival and bone substrate resorption. Receptor binding was measured using radiolabelled RvE1. Nuclear factor (NF)-kappa B activation and Akt phosphorylation were determined with western blotting. Lipid mediator production was assessed with liquid chromatography tandem mass spectrometry.
    Key results: OC growth and resorption pit formation were markedly decreased in the presence of RvE1. OC differentiation was inhibited by RvE1 as demonstrated by decreased number of multinuclear OC, a delay in the time course of OC development and attenuation of receptor activator of NF-kappa B ligand-induced nuclear translocation of the p50 subunit of NF-kappa B. OC survival and apoptosis were not altered by RvE1. Messenger RNA for both receptors of RvE1, ChemR23 and BLT(1) is expressed in OC cultures. Leukotriene B(4) (LTB(4)) competed with [(3)H] RvE1 binding on OC cell membrane preparations, and the LTB(4) antagonist U75302 prevented RvE1 inhibition of OC growth, indicating that BLT(1) mediates RvE1 actions on OC. Primary OC synthesized the RvE1 precursor 18R-hydroxy-eicosapentaenoic acid and LTB(4). Co-incubation of OC with peripheral blood neutrophils resulted in transcellular RvE1 biosynthesis.
    Conclusions and implications: These results indicate that RvE1 inhibits OC growth and bone resorption by interfering with OC differentiation. The bone-sparing actions of RvE1 are in addition to inflammation resolution, a direct action in bone remodelling.

    DOI: 10.1038/bjp.2008.367

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  • Priming of neutrophil oxidative burst in diabetes requires preassembly of the NADPH oxidase

    Kazuhiro Omori, Taisuke Ohira, Yushi Uchida, Srinivas Ayilavarapu, Eraldo L. Batista, Motohiko Yagi, Tomoyuki Iwata, Hongsheng Liu, Hatice Hasturk, Alpdogan Kantarci, Thomas E. Van Dyke

    JOURNAL OF LEUKOCYTE BIOLOGY   84 ( 1 )   292 - 301   2008年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FEDERATION AMER SOC EXP BIOL  

    Hyperglycemia associated with diabetes mellitus results in the priming of neutrophils leading to oxidative stress that is, in part, responsible for diabetic complications. p47phox, a NADPH oxidase cytosolic subunit, is a key protein in the assembly of the NADPH oxidase leading to superoxide generation. Little is known about the priming mechanism of oxidative pathways in neutrophils of people with diabetes. In this study, the kinetics of p47phox activation was investigated by comparing neutrophils from diabetic and healthy subjects, and the mechanism of hyperglycemia- induced changes was studied by using neutrophil- like HL- 60 cells as a model. In resting neutrophils from diabetic subjects, p47phox prematurely translocates to the cell membrane and preassembles with p22phox, a NADPH oxidase membrane subunit. This premature p47phox translocation and preassembly with p22phox were also observed in HL- 60 cells cultured with high glucose ( HG; 25 mM) and with the specific ligand for the receptor for advanced glycation end products ( RAGE), S100B. Phosphorylation of ERK1/ 2, but not p38 MAPK, was the primary signaling pathway, as evidenced by PD98059 suppressing the translocation of p47phox in HL- 60 cells incubated with HG and S100B. HL- 60 cells cultured in HG and S100B exhibited a 1.8- fold increase in fMLP- induced superoxide generation compared with those cultured in normal glucose ( 5.5 mM). These data suggest that HG and increased AGE prime neutrophils and increase oxidative stress inducing the translocation of p47phox to the cell membrane and preassembly with p22phox by stimulating a RAGE- ERK1/ 2 pathway.

    DOI: 10.1189/jlb.1207832

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  • cAMP-response element binding protein (CREB) regulates cyclosporine-A-mediated down-regulation of cathepsin B and L synthesis

    Kazuhiro Omori, Koji Naruishi, Tomoko Yamaguchi, Shun-Ai Li, Mayumi Yamaguchi-Morimoto, Kaori Matsuura, Hideo Arai, Kohji Takei, Shogo Takashiba

    CELL AND TISSUE RESEARCH   330 ( 1 )   75 - 82   2007年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER  

    Cyclosporin A (CsA) is an immunosuppressant with severe side effects including gingival overgrowth. We have previously reported that CsA impairs the activity of the lysosomal enzymes cathepsin B and L in human gingival fibroblasts (HGFs). Here, we have examined the effects of CsA on the DNA-binding activity of the cyclic AMP response element-binding protein (CREB) and cell viability, and the effects of CREB on cathepsin B and L synthesis and activity in HGFs. We have confirmed that CsA down-regulates cathepsin B and L synthesis. Further, CsA has no effect on cell viability and dramatically impairs CREB-DNA binding activity. Importantly, the synthesis of cathepsin B and L is down-regulated, and their activity is also significantly impaired in HGFs transfected with plasmid expressing dominant-negative CREB. These results suggest that CREB is essential for the CsA-mediated down-regulation of cathepsin B and L synthesis in HGFs.

    DOI: 10.1007/s00441-007-0457-8

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  • Long term Cyclosporin A exposure suppresses Cathepsin-B and –L activity in gingival fibroblasts.

    Mayumi Yamaguchi, Koji Naruishi, Hisa Yamada-Naruishi, Kazuhiro Omori, Fusanori Nishimura, Shogo Takashiba

    Journal of Periodontal Research   39 ( 5 )   320 - 326   2004年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/j.1600-0765.2004.00746.x

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  • High glucose enhances interleukin-6-induced vascular endothelial growth factor 165 expression via activation of Gp130-mediated p44/42 MAPK-CCAAT/enhancer binding protein signaling in gingival fibroblasts

    K Omori, K Naruishi, F Nishimura, H Yamada-Naruishi, S Takashiba

    JOURNAL OF BIOLOGICAL CHEMISTRY   279 ( 8 )   6643 - 6649   2004年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Diabetic patients are susceptible to severe inflammatory periodontitis manifesting as swollen gingiva with bleeding, but the underlying mechanism is not well understood. Our purpose was to determine the effect of a high glucose (HG) condition on the interleukin-6/soluble interleukin-6 receptor (IL-6/sIL-6R)-induced activation of signaling and vascular endothelial growth factor (VEGF) expression in human gingival fibroblasts (HGFs). In this study, HGFs were cultured for at least two passages under a normal glucose (NG; 5.5 mm) condition or high glucose (25 mm) condition. Importantly, the HG condition significantly induced expression of gp130 mRNA in HGFs compared with levels in control cells. Consistent with the expression of its mRNA, the HG condition also increased the expression of gp130 protein, and phosphorylation of the tyrosine residue by gp130 was enhanced significantly by IL-6/sIL-6R stimulation. Furthermore, the HG condition enhanced the IL-6/sIL-6R-induced phosphorylation of p44/42 MAPK and led to subsequent activation of CCAAT/enhancer binding protein in nuclei. In contrast, there was no significant difference in phosphorylation of JNK between the HG and NG condition. Interestingly, HGFs increased IL-6/sIL-6R,induced VEGF165 mRNA expression and VEGF165 secretion under the HG condition compared with levels under the NG condition. In contrast, the induction of VEGF165 secretion was partially inhibited by PD98059 (selective p44/42 MAPK inhibitor) under the HG condition. In addition, the VEGF165 secretion was completely inhibited by the combination of PD98059 and SP600125 (JNK inhibitor). Our findings suggest that the HG condition indirectly increases VEGF expression via activation of gp130-mediated p44/42 MAPK-CCAAT/enhancer binding protein signaling in HGFs. Thus, elevated VEGF secretion in HGFs under the HG condition may play a role in the development of the severe periodontitis observed in diabetic patients.

    DOI: 10.1074/jbc.M311688200

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  • C-jun N-terminal kinase (JNK) interleukin SP600125, blocks interleukin (IL)-6-induced vascular endothelial growth factor (VEGF) production: Cyclosporine A partially mimics this inhibitory effect

    K Naruishi, F Nishimura, H Yamada-Naruishi, K Omori, M Yamaguchi, S Takashiba

    TRANSPLANTATION   76 ( 9 )   1380 - 1382   2003年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Angiogenesis is a common complication of organtransplant rejection. One of the primary responsible molecules for enhanced angiogenesis is vascular endothelial growth factor (VEGF). Activated protein (AP)-1 is considered to play a key role in the transcription of VEGF. c-jun N-terminal kinase (JNK), one of the MAP kinase family members, plays a critical role in AP-1 activation. Thus, we tested the effect of a novel JNK inhibitor, SP600125, on VEGF production in fibroblasts. SP600125 significantly suppressed interleukin (IL)-6-induced production of VEGF in cultured fibroblasts. Cyclosporine A (CsA), a known in vitro antiangiogenic reagent, partially mimicked this suppression. In fact, CsA suppressed IL-6-induced phosphorylation of JNK. The results indicate that although both SP600125 and CsA are anti-angiogenic by inhibiting VEGF production by way of a JNK-dependent pathway, the inhibitory effect was much stronger with the novel inhibitor of JNK than with CsA.

    DOI: 10.1097/01.TP.0000085661.52980.95

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▼全件表示

書籍等出版物

  • 成人先天性心疾患パーフェクトガイド Ⅵ. 4 口腔感染管理(共著)

    文光堂  2015年  ( ISBN:9784830619274

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  • ザ・ペリオドントロジー 第3章 検査,診断と治療 (共著)

    永末書店  2014年  ( ISBN:9784816012662

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  • 患者が求める「医療安全」「院内感染」対策 第2部 Ⅵ. 感染していることがわかった患者への対応(共著)

    株式会社ヒョーロン  2014年  ( ISBN:9784864320245

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  • 臨床歯周病学 第2版 第23章 先進的な歯周検査(共著)

    医歯薬出版  2013年  ( ISBN:9784263456620

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  • チェアーサイド歯科英会話 –分かる伝わるコミュニケーション!−

    株式会社吉備人出版  2010年 

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MISC

  • 【DH Eyes】女性特有のライフイベントを意識した広汎型侵襲性歯周炎患者に対する長期的な歯周治療支援

    日本歯科評論   123 - 131   2017年

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  • 糖尿病患者に対する医科歯科連携推進の課題

    糖尿病診療マスター   2016年

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  • 岡山県糖尿病医科・歯科連携で用いられる「歯周病セルフチェック票」の妥当性についての検討

    Diabetes Frontier   26 ( 4 )   512 - 517   2015年

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  • 基礎研究から歯科臨床へ:歯周病原細菌に対する血漿IgG抗体価検査の可能性

    日本歯周病学会会誌   2013年

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  • 海外ジャーナルWatching 糖尿病患者の血糖改善に歯周治療はどの程度貢献できるのか?

    大森一弘, 高柴正悟

    Dental Diamond   2012年

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  • ヘルスケアプロバイダーとしての歯周病感染リスクマネジメントー歯周病再発のコントロール

    大森一弘, 高柴正悟

    DHstyle   2011年

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  • 歯周病と生活習慣病

    高柴正悟, 大森一弘

    岡山市医師会・疾患別検査と診断の手引き 疾患別シリーズ   2010年

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▼全件表示

講演・口頭発表等

  • 歯科治療介入が生活習慣の改善につながった糖尿病関連性歯周炎患者の一症例

    第61回日本歯周病学会  2018年 

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  • Impact of disease complexity on Hospitalization in Adult Patients with Congenital Heart Disease: retrospective cohort study

    2018年 

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  • 先天性心疾患複雑性が入院イベントに及ぼす影響 コホート研究

    日本成人先天性心疾患学会  2018年 

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  • 性別と年齢で層別した東日本大震災後の心理社会的要因と口腔内環境との関連 福島県「県民健康調査」

    第61回日本歯周病学会  2018年 

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  • 上顎中切歯の歯内-歯周病変に対して部分矯正治療と自家骨移植術を行い歯科インプラント治療を回避した一症例

    第61回日本歯周病学会  2018年 

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  • 口腔バイオフィルム感染症を制御するパウダー状の天然食品の探索

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 患者視点からの歯周組織再生療法の選択基準

    日本歯科保存学会  2017年 

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  • 歯周炎と全身疾患(糖尿病・関節リウマチ)に共通するリスク遺伝子の解析

    第60回春季日本歯周病学会学術大会  2017年 

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  • 真菌代謝産物terreinはAggregatibacter actinomycetemcomitans歯肉上皮感染時のIL-8産生を抑制する

    第60回春季日本歯周病学会学術大会  2017年 

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  • Fungal metabolite, terrein, suppresses IL-6/sIL-6R-induced CSF1 secretion in gingival fibroblasts

    95th, International Association for Dental Research  2017年 

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  • Role of Integrin Isoforms During Migration of Periodontal Ligament Cells

    95th, International Association for Dental Research  2017年 

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  • 真菌二次代謝産物(+)-terreinはRANKL誘導性破骨細胞分化におけるNFATc1の発現を抑制する

    日本歯科保存学会  2017年 

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  • インテグリンサブユニットの選択的制御による歯根膜細胞の遊走促進

    日本歯科保存学会  2017年 

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  • 循環器内科医による成人先天性心疾患診療 岡山大学ACHDセンターの試み

    日本心臓病学会学術集会  2017年 

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  • 新規除鉄剤スーパーポリフェノール(SP)を応用した口腔感染制御システムの開発

    第41回日本鉄バイオサイエンス学会学術集会  2017年 

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  • 岡山大学病院・侵襲性歯周炎センターで対応している広汎型侵襲性歯周炎患者の治療経過

    第38回岡山歯学会学術集会  2017年 

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  • 外傷性歯根破折に起因して椎前部膿瘍が生じた一症例

    第38回岡山歯学会学術集会  2017年 

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  • 多職種と連携した脳血管障害後遺症患者の管理における歯科衛生士の役割

    第60回春季日本歯周病学会学術大会  2017年 

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  • 多職種と連携した脳血管障害後遺症患者の管理における歯科衛生士の役割

    第60回春季日本歯周病学会学術大会  2017年 

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  • 初回外来化学療法患者の口腔カンジダ感染量が口腔内の疼痛やQOLに及ぼす影響

    日本歯科衛生士学会  2017年 

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  • 歯周病罹患の有無によるアテローム性動脈硬化病変部のマイクロバイオームの違い

    第60回春季日本歯周病学会学術大会  2017年 

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  • 2型糖尿病患者に対する歯周治療の効果とSPT時の課題を実感した一症例

    第60回春季日本歯周病学会学術大会  2017年 

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  • 岡山市「妊婦パートナー歯科健診」を利用した歯周病予防の取り組み

    第60回春季日本歯周病学会学術大会  2017年 

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  • 岡山市「妊婦パートナー歯科健診」を受診したある妊婦の歯周治療症例

    第60回春季日本歯周病学会学術大会  2017年 

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  • 家族性リポ蛋白リパーゼ欠損症および 2 型糖尿病に罹患した重度慢性歯周炎患者に対する非外科 的歯周治療の効果を実感した一症例

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 妊娠関連性歯周炎患者に対して禁煙支援を含めた歯周治療を行った一症例

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 人工関節置換術の周術期における早期からの口腔感染管理が奏功した慢性歯周炎患者の一症例

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 口腔細菌の特定と口腔治療が急性椎前部膿瘍の治癒に奏功した症例

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 血清 IgG 抗体価検査がスクリーニング,早期診断および管理につながった侵襲性歯周炎患者の22 年間経過症例

    第60回日本歯周病学会秋季学術大会  2017年 

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  • 歯周病罹患の有無によるアテローム性動脈硬化病変の細菌叢のメタゲノム解析

    第147回日本歯科保存学会秋季学術大会  2017年 

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  • 歯科用ユニット給水管路汚染対策用の自動注水制御シミュレータの評価

    第147回日本歯科保存学会秋季学術大会  2017年 

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  • 2型糖尿病患者に対する歯周病治療時の課題を実感した一症例

    2017年度日本糖尿病学会中四国地方会  2017年 

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  • 口腔バイオフィルム抑制用の多糖誘導体リン酸化プルランにおける歯面への付着と薬剤徐放性効果の機序解明

    第59回秋季日本歯周病学会学術大会  2016年 

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  • 抗Porphyromonas gingivalis IgG血症の診断に関わる抗原タンパク質の選定

    第23回日本歯科医学会総会  2016年 

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  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎(IE)の起炎菌推定に繋がった症例

    第23回日本歯科医学会総会  2016年 

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  • 男女・年齢別歯科関連行動と歯周病原細菌の感染度との関連

    第23回日本歯科医学会総会  2016年 

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  • 口腔細菌感染症を制御する機能性食品の探索

    第145回日本歯科保存学会秋季学術大会  2016年 

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  • インテグリン発現による歯根膜細胞の遊走制御

    第58回日本歯周病学会春季学術大会  2016年 

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  • 真菌由来代謝産物(+)-terreinはヒト歯肉線維芽細胞におけるinterleukin-6誘導性SHP2-AKTシグナル活性を抑制する

    第58回日本歯周病学会春季学術大会  2016年 

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  • 継続的な歯周支援治療が認知機能維持に及ぼす影響の検討 pilot study

    第59回秋季日本歯周病学会学術大会  2016年 

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  • 薬剤性歯肉増殖の病態に酸化ストレスが及ぼす影響

    第59回秋季日本歯周病学会学術大会  2016年 

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  • Type-I Pepsin-Solubilized Collagen From Bohadschia Bivittata Enhanced hPDLFs Cells Viability

    94th, International Association for Dental Research  2016年 

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  • 全身疾患関連性歯周炎患者の歯周治療における血液検査の必要性

    日本歯周病学会・第8回中国地区臨床研修会  2016年 

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  • 妊娠性歯周炎患者に対して細菌検査を併用しながら積極的な歯周治療を行った一症例

    日本歯周病学会・第8回中国地区臨床研修会  2016年 

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  • 産科併設歯科における母子歯科保健システムを活用した歯周病予防の取り組み

    日本歯周病学会・第8回中国地区臨床研修会  2016年 

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  • 多血小板血漿を併用した自家骨移植が奏功した重度慢性歯周炎患者症例の考察

    第58回日本歯周病学会春季学術大会  2016年 

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  • 先天性ネフローゼ症候群患者の薬物性歯肉増殖症への対応

    第58回日本歯周病学会春季学術大会  2016年 

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  • 歯根・歯槽骨が吸収した下顎第二大臼歯に対する智歯移植前の根管処置症例の考察

    第143回日本歯科保存学会春季学術大会  2016年 

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  • 海藻由来レクチンを用いた口腔バイオフィルム感染症の制御

    第143回日本歯科保存学会春季学術大会  2016年 

     詳細を見る

  • Natural Products for Prevention of Oral Biofilm: Effects of Abietic Acid

    63rd Annual Meeting of Japanese Association for Dental Research  2015年 

     詳細を見る

  • IL-6/sIL-6R enhances cathepsin-B secretion via caveolin-1-mediated ERK 1/2 in gingival fibroblasts

    93rd, International Association for Dental Research  2015年 

     詳細を見る

  • 真菌由来代謝産物(+)-terrein誘導体がIL-6誘導性VEGFおよびCSF-1の産生に及ぼす影響の検討

    第58回日本歯周病学会春季学術大会  2015年 

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  • 生体の反応を確認しつつ歯周—矯正-補綴治療を行った広汎型侵襲性歯周炎の一症例

    第58回日本歯周病学会春季学術大会  2015年 

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  • ROCK阻害剤は歯根膜細胞の遊走を促進する

    第142回日本歯科保存学会春季学術大会  2015年 

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  • 院内腫瘍センターにおける初回外来がん化学療法患者の“口内炎症状”調査

    日本歯科衛生誌学会学術大会  2015年 

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  • 真菌由来代謝産物(+)-terreinはRANKL誘導性破骨細胞分化を抑制する

    第143回日本歯科保存学会秋季学術大会  2015年 

     詳細を見る

  • 新たな糖尿病合併症に迫る 〜糖尿病患者にとっての歯周病治療を再考する〜

    第29回日本糖尿病合併症学会学術大会  2015年 

     詳細を見る

  • 歯周病原細菌に対する指尖血漿IgG抗体価検査が感染性心内膜炎の起炎菌推定に繋がった一症例

    第57回日本歯周病学会秋季学術大会  2015年 

     詳細を見る

  • 骨格性下顎前突症を伴う広汎型重度慢性歯周炎患者に対し外科的矯正治療を併用した包括的歯周治療を行った一症例

    第57回日本歯周病学会秋季学術大会  2015年 

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  • 女性のライフイベントを意識した広汎型侵襲性歯周炎患者に対する歯周治療の支援

    第57回日本歯周病学会秋季学術大会  2015年 

     詳細を見る

  • IL-6/sIL-6Rは歯肉線維芽細胞から活性を有するリソソーム酵素カテプシンB,Lの分泌を亢進する

    第57回日本歯周病学会秋季学術大会  2014年 

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  • 血清中ビタミンCの欠乏が原因の一つと考える歯肉増殖症患者の歯周治療経過

    第30回岡山歯学会総会・学術集会  2014年 

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  • 真菌由来代謝産物(+)-terreinはinterleukin-6誘導生colony stimulating factor-1の遺伝子発現を抑制する

    第135回日本歯科保存学会秋季学術大会  2014年 

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  • 脆弱な歯肉を有する侵襲性歯周炎患者の治療例とリスク因子の考察

    日本歯周病学会  2014年 

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  • 血清中ビタミンCの欠乏が惹起したと考える特発性歯肉増殖症患者の歯周治療経過

    第57回日本歯周病学会春季学術大会  2014年 

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  • レクチンを応用した口腔感染リスクへの検査薬としての可能性

    第7回口腔検査学会総会  2014年 

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  • 血管新生阻害物質terrein がヒト歯肉線維芽細胞におけるIL-6/sIL-6R誘導性angiogeninおよびVEGFの産生に及ぼす影響

    第56回日本歯周病学会春季学術大会  2013年 

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  • 産科併設歯科における”母子歯科保健システム“を活用した歯周病予防の取り組み

    第56回日本歯周病学会春季学術大会  2013年 

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  • 妊娠性歯周炎患者に対して細菌検査を併用しながら積極的な歯周治療を行った一症例

    第56回日本歯周病学会春季学術大会  2013年 

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  • 歯周病患者および自己面疾患患者におけるシャペロニンタンパクCCTに対する自己免疫応答の解析

    第56回日本歯周病学会春季学術大会  2013年 

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  • Caveolin-1 is required for IL-6/sIL-6R-induced cathepsin secretion in gingival fibroblasts.

    91st, International Association for Dental Research  2013年 

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  • Possible mechanisms of periapical healing by IL-1alpha in osteoblastic MC3T3-E1

    90th International Adssoication for Dental Research  2012年 

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  • Activated MMP-3 enhances sIL-6R production in macrophage like differentiated THP-1 cells

    90th International Adssoication for Dental Research  2012年 

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  • 岡山大学病院糖尿病センターにおける医科歯科連携パス運営の課題

    第27回日本糖尿病合併症学会  2012年 

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  • 上顎側切歯にみられた歯内歯の治療評価における歯科用CT画像検査の有用性

    第135回日本歯科保存学会春季学術大会  2012年 

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  • ヒト歯肉線維芽細胞におけるカベオリン-1を標的としたIL-6誘導性のリソソーム酵素カテプシンBとL分泌の抑制制御

    第135回日本歯科保存学会春季学術大会  2012年 

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  • 特発性歯肉増殖の発症因子を追求している一症例

    日本歯周病学会 第7回中国地区臨床研修会  2012年 

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  • 天然多糖プルランリン酸化合物と塩化セチルピリジニウム混合液が細胞と生体および口腔内細菌の変化に与える影響

    第55回日本歯周病学会秋季学術大会  2012年 

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  • Safety evaluation of phosphorylated-pullulan mixed with/without CPC

    98th American Academy of Periodontology  2012年 

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  • ヒト歯肉線維芽細胞におけるIL-6/sIL-R誘導性Angiogenin産生に血管新生阻害薬Terreinが及ぼす影響

    第55回日本歯周病学会春季学術大会  2012年 

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  • IL-6sIL6RはRAW264.7細胞におけるRANKL誘導性の破骨細胞分化を抑制し,IL-8の産生を亢進する

    第54回日本歯周病学会春季学術大会  2011年 

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  • 出産前後の口腔内状態とオーラルケアに関する調査(2)-妊婦のつわりの実態について

    第54回日本歯周病学会春季学術大会  2011年 

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  • 活性型MMP-3がマクロファージ様THP-1細胞の膜型IL-6受容体の発現に及ぼす影響

    第133回日本歯科保存学会春季学術大会  2011年 

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  • 宿主感受性が高いと判断した侵襲製歯周炎患者の治療に血清IgG抗体価検査を指標として用いた症例

    第55回日本歯周病学会秋季学術大会  2011年 

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  • Activated MMP-3 enhances sIL-6R production in macrophage like differentiated THP-1 cells

    59th Japanese Association for Dental Research  2011年 

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  • nrdD様遺伝子の存在は血中移行したPorphyromonas gingivalisの病原性を決定する

    第53回日本歯周病学会秋季学術大会  2010年 

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  • 出産前後の口腔内状態とオーラルケアに関する調査(1)-妊婦の実態について

    第53回日本歯周病学会秋季学術大会  2010年 

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  • 歯周病原細菌の感染による全身性炎症性反応に抗する免疫応答の意義

    第133回日本歯科保存学会秋季学術大会  2010年 

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  • IL-1raによるマウス骨芽細胞様細胞MC3T3-E1におけるIL-1誘導性OPGおよびIL-6産生制御

    第53回日本歯周病学会春季学術大会  2010年 

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  • MMP-3によるヒト単球系細胞株THP-1からの可溶型IL-6受容体の産生亢進

    第132回日本歯科保存学会春季学術大会  2010年 

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  • Inhibition of IL-6/sIL-6R-induced VEGF production by sgp130 in gingival fibroblasts

    88th International Association for Dental Research  2010年 

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  • 歯肉線維芽細胞におけるカベオリン-1および可溶性gp130を標的としたIL-6誘導性VEGF産生の抑制制御

    第130回日本歯科保存学会春季学術大会  2009年 

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  • Mail medicine using fingertip plasma for screening and monitoring periodontitis

    95th Annual Meeting of American Academy of Periodontology  2009年 

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  • 歯周病治療を通じて,Ⅱ型糖尿病患者の行動変容を促した一症例

    第24回日本糖尿病合併症学会  2009年 

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  • cAMP-response element binding protein (CREB) regulates cyclosporine A-mediated down-regulation of cathepsin B and L synthesis

    第30回岡山歯学会総会・学術集会  2009年 

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  • RvE1 receptor activation signals phosphorylation and phagocytosis in macrophages

    87th International Association for Dental Research  2009年 

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  • Chronic periodontitis and severe hyperglycemia increase iPLA2 expression in neutrophils

    87th International Association for Dental Research  2009年 

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  • 糖尿病患者の歯周病治療を通して患者の行動が変容した症例

    第52回日本歯周病学会春季学術大会  2009年 

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  • cAMP-response element binding protein (CREB) regulates cyclosporine A-mediated down-regulation of cathepsin B and L synthesis

    2009年 

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  • Role of PAK2 in localized aggressive periodontitis neutrophils

    87th International Association for Dental Research  2009年 

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  • α3β1 integrin-mediated MC3T3-E1 osteoblasts adherence induced by Interleukin-1α

    56th Japanese Association for Dental Research  2008年 

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  • Hypoxia-induced factor 1α expression and activity in LAP PMN

    86th International Association for Dental Research  2008年 

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  • The expression of PDK1 is decreased in neutrophils from LAP subjects

    86th International Association for Dental Research  2008年 

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  • Hyperglycemia-mediated PMN priming occurs through iPLA2 activation

    86th International Association for Dental Research  2008年 

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  • 急性骨髄性白血病の歯周病治療における歯周病細菌の血清IgG抗体価および細菌DNA検査の応用例

    第1回口腔検査学会  2008年 

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  • The reduction of caspase-3 expression delays apoptosis in LAP PMN

    86th International Association for Dental Research  2008年 

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  • PAK2 in superoxide generation by LAP neutrophils

    86th International Association for Dental Research  2008年 

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  • Resolvin E1 on PKC activity in neutrophils from LAP subjects

    37th American Association for Dental Research  2008年 

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  • Hyperglycemia suppress diacylglycerol kinase-α expression in human neutrophils

    37th American Association for Dental Research  2008年 

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  • IL-1αおよびIL-1βによるマウス骨芽細胞様細胞MC3T3-E1の動態におけるMAPK系の関与

    第129回日本歯科保存学会秋季学術大会  2008年 

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  • p47phox is pre-assembled in neutrophils from diabetic subjects

    85th International Association for Dental Research  2007年 

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  • ATLa and RevE1 suppress NADPH oxidase activity in human neutrophils

    85th International Association for Dental Research  2007年 

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  • iPLA2 activates superoxide generation in neutrophils from diabetic subjects

    85th International Association for Dental Research  2007年 

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  • Mechanism of RAGE expression on neutrophils in response to hyperglycemia

    85th International Association for Dental Research  2007年 

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  • Lipopolysaccharide (LPS) downregulates resolvin E1 receptor ChemR23 in human monocytes/macrophages

    85th International Association for Dental Research  2007年 

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  • ATLa and RevE1 suppress NADPH oxidase activity in human neutrophils

    85th International Association for Dental Research  2007年 

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  • Hyperglycemia primes neutrophil-like HL-60 cells through p47phox and pleckstrin phosphorylation

    35th American Association for Dental Research  2006年 

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  • Expression of RAGE on neutrophils in response to hyperglycemia

    35th American Association for Dental Research  2006年 

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  • High glucose-mediated enhancement of IL-6-induced VEGF165 production via p44/42 MAPK-C/EBP signaling

    82nd International Association for Dental Research  2003年 

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  • サイクロスポリンの抗 angiogenic 効果はJNKの活性低下を介したVEGFの産生抑制による

    第46回日本歯周病学会秋季学術大会  2003年 

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  • 高グルコース状態がヒト歯肉線維芽細胞のIL-6刺激伝達系に及ぼす影響 : gp130下流シグナル伝達経路の解明

    第46回日本歯周病学会秋季学術大会  2003年 

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  • 高グルコース状態は IL-6/sIL-6R 刺激によるヒト歯肉線維芽細胞の VEGF 産生を促進する

    第117回日本歯科保存学会秋季学術大会  2002年 

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  • Supportive Periodontal Treatmentの効果を左右する因子に関する研究

    第44回日本歯周病学会秋季学術大会  2001年 

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受賞

  • 岡山歯学会奨励論文賞

    2008年  

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    受賞国:日本国

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  • 日本歯科保存学会奨励論文賞

    2005年  

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    受賞国:日本国

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  • 歯髄・歯内病変治療専門学(講義・演習) (2021年度) 特別  - その他

  • 口腔感染・炎症制御学(実習(臨床実習)) (2020年度) 特別  - その他

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