2022/11/29 更新

写真a

ナカジマ マユカ
中島 麻由佳
NAKAJIMA Mayuka
所属
教育研究院 医歯学系 歯学系列 助教
歯学部 歯学科 助教
医歯学総合研究科 口腔生命科学専攻 摂食環境制御学 助教
職名
助教
外部リンク

学位

  • 博士(歯学) ( 2016年3月   新潟大学 )

研究キーワード

  • ドラッグデリバリー

  • 細菌学

  • 免疫学

  • 分子生物学

  • 歯周病学

研究分野

  • ナノテク・材料 / ナノ材料科学

  • ライフサイエンス / 保存治療系歯学

経歴(researchmap)

  • 令和4年度 新潟大学 若手教員スイングバイ・プログラム 助教

    2022年4月 - 現在

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  • 日本学術振興会 海外特別研究員

    2020年4月 - 2022年3月

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  • 米国ハーバード大学ジョンA.ポールソン工学応用科学部 博士研究員

    2019年4月 - 2022年3月

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  • 新潟大学   Graduate School of Medical and Dental Sciences   日本学術振興会 特別研究員RPD

    2018年4月 - 2020年3月

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  • 新潟大学   Medical and Dental Hospital   医員

    2017年4月 - 2018年3月

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経歴

  • 新潟大学   歯学部 歯学科   助教

    2022年4月 - 現在

  • 新潟大学   医歯学総合研究科 口腔生命科学専攻 摂食環境制御学   助教

    2022年4月 - 現在

  • 新潟大学   教育研究院 医歯学系 歯学系列   助教

    2022年4月 - 現在

学歴

  • 新潟大学   医歯学総合研究科   歯周診断・再建学分野

    2012年4月 - 2016年3月

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  • 新潟大学   歯学部   歯学科

    2005年4月 - 2011年3月

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所属学協会

留学歴

  • Harvard University SEAS   Postdoctoral Fellow

    2019年4月 - 2022年3月

 

論文

  • Oral Pathobiont-Induced Changes in Gut Microbiota Aggravate the Pathology of Nonalcoholic Fatty Liver Disease in Mice 査読 国際誌

    12   766170 - 766170   2021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: 10.3389/fimmu.2021.766170

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  • Topical treatment of periodontitis using an iongel 査読 国際誌

    276   121069 - 121069   2021年9月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.biomaterials.2021.121069

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  • β2-microglobulin and neutrophil gelatinase-associated lipocalin, potential novel urine biomarkers in periodontitis: A cross-sectional study in Japanese. 査読 国際誌

    Int J Dent   2019   1394678 - 1394678   2019年

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1155/2019/1394678

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  • Oral Administration of Porphyromonas gingivalis Alters the Gut Microbiome and Serum Metabolome. 査読 国際誌

    Tamotsu Kato, Kyoko Yamazaki, Mayuka Nakajima, Yasuhiro Date, Jun Kikuchi, Koji Hase, Hiroshi Ohno, Kazuhisa Yamazaki

    mSphere   3 ( 5 )   2018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)  

    Periodontal disease induced by periodontopathic bacteria like Porphyromonas gingivalis is demonstrated to increase the risk of metabolic, inflammatory, and autoimmune disorders. Although precise mechanisms for this connection have not been elucidated, we have proposed mechanisms by which orally administered periodontopathic bacteria might induce changes in gut microbiota composition, barrier function, and immune system, resulting in an increased risk of diseases characterized by low-grade systemic inflammation. Accumulating evidence suggests a profound effect of altered gut metabolite profiles on overall host health. Therefore, it is possible that P. gingivalis can affect these metabolites. To test this, C57BL/6 mice were administered with P. gingivalis W83 orally twice a week for 5 weeks and compared with sham-inoculated mice. The gut microbial communities were analyzed by pyrosequencing the 16S rRNA genes. Inferred metagenomic analysis was used to determine the relative abundance of KEGG pathways encoded in the gut microbiota. Serum metabolites were analyzed using nuclear magnetic resonance (NMR)-based metabolomics coupled with multivariate statistical analyses. Oral administration of P. gingivalis induced a change in gut microbiota composition. The distributions of metabolic pathways differed between the two groups, including those related to amino acid metabolism and, in particular, the genes for phenylalanine, tyrosine, and tryptophan biosynthesis. Also, alanine, glutamine, histidine, tyrosine, and phenylalanine were significantly increased in the serum of P. gingivalis-administered mice. In addition to altering immune modulation and gut barrier function, oral administration of P. gingivalis affects the host's metabolic profile. This supports our hypothesis regarding a gut-mediated systemic pathology resulting from periodontal disease.IMPORTANCE Increasing evidence suggest that alterations of the gut microbiome underlie metabolic disease pathology by modulating gut metabolite profiles. We have shown that orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, alters the gut microbiome; that may be a novel mechanism by which periodontitis increases the risk of various diseases. Given the association between periodontal disease and metabolic diseases, it is possible that P. gingivalis can affect the metabolites. Metabolite profiling analysis demonstrated that several amino acids related to a risk of developing diabetes and obesity were elevated in P. gingivalis-administered mice. Our results revealed that the increased risk of various diseases by P. gingivalis might be mediated at least in part by alteration of metabolic profiles. The findings should add new insights into potential links between periodontal disease and systemic disease for investigators in periodontal disease and also for investigators in the field of other diseases, such as metabolic diseases.

    DOI: 10.1128/mSphere.00460-18

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  • Increased serum PCSK9, a potential biomarker to screen for periodontitis, and decreased total bilirubin associated with probing depth in a Japanese community survey 査読

    K. Tabeta, M. Hosojima, M. Nakajima, S. Miyauchi, H. Miyazawa, N. Takahashi, Y. Matsuda, N. Sugita, Y. Komatsu, K. Sato, T. Ishikawa, K. Akiishi, K. Yamazaki, K. Kato, A. Saito, H. Yoshie

    Journal of Periodontal Research   53 ( 3 )   446 - 456   2018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:Blackwell Munksgaard  

    Background and Objectives: Previous reports suggest that several serum biomarkers play roles in the pathogenesis, inflammatory response, and oxidative stress in periodontitis caused by bacterial infections, linking chronic periodontitis to atherosclerotic vascular disease (ASVD). The aim of this preliminary study was to investigate, in a Japanese cross-sectional community survey, potential serum biomarkers of periodontitis that are associated with ASVD and chronic periodontitis. Material and Methods: The study cohort included a total of 108 male subjects who underwent annual health examinations. Serum biomarkers (high-sensitivity C-reactive protein [hs-CRP], proprotein convertase subtilisin/kexin type 9 [PCSK9], interleukin-6, tumor necrosis factor-α, soluble CD14, myeloperoxidase, matrix metalloproteinase-3, adiponectin, total bilirubin [TBIL], and serum lipids) were analyzed to determine their association (if any) with periodontal parameters. Aortic stiffness was evaluated using the brachial-ankle aortic pulse wave velocity (PWV) index and the cardio-ankle vascular index (CAVI). Results: The concentrations of PCSK9 and hs-CRP were increased (P =.001 and.042, respectively), and the concentration of TBIL was decreased (P =.046), in subjects with periodontal disease (determined as a probing depth of ≥4 mm in at least one site) compared with periodontally healthy subjects. The ratio of low-density lipoprotein cholesterol (LDL-C) to high-density lipoprotein cholesterol and the concentrations of triglycerides, remnant-like particles-cholesterol, and oxidized LDL were elevated in subjects with periodontal disease compared with periodontally healthy subjects (P =.038,.007,.002, and.049, respectively). Multivariate regression analyses indicated that the number of sites with a pocket depth of ≥4 mm was associated with the concentration of PCSK9 and inversely associated with the concentration of TBIL independently (standardized β =.243, P =.040
    standardized β = −.443, P =.0002
    respectively). Analysis of receiver operating characteristic curves of PCSK9 indicated moderate accuracy for predicting the presence of disease sites (probing depth ≥ 4 mm) (area under the curve = 0.740). No significance in the values of PWV and CAVI was observed between subjects with periodontal disease and periodontally healthy subjects. Conclusion: In Japanese male subjects, the concentrations of serum PCSK9 and TBIL were correlated with periodontal parameters. Moreover, PCSK9 could be a candidate biomarker for diagnosing chronic periodontitis, and may also have potential to evaluate the risk for periodontitis to cause ASVD. Longitudinal studies of larger populations are necessary to confirm the exact association of periodontitis with increased serum PCSK9 and decreased TBIL.

    DOI: 10.1111/jre.12533

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  • Ligature-induced periodontitis in mice induces elevated levels of circulating interleukin-6 but shows only weak effects on adipose and liver tissues 査読

    Y. Matsuda, T. Kato, N. Takahashi, M. Nakajima, K. Arimatsu, T. Minagawa, K. Sato, H. Ohno, K. Yamazaki

    JOURNAL OF PERIODONTAL RESEARCH   51 ( 5 )   639 - 646   2016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:WILEY-BLACKWELL  

    Background and Objectives: Our previous study demonstrated using an oral gavage model that Porphyromonas gingivalis could induce various inflammatory changes linked to periodontitis-associated systemic diseases by altering gut microbiota. A ligature-induced periodontitis model is similar to human periodontitis in various aspects: in both cases, alveolar bone resorption depends on oral bacterial load, and gingival tissue becomes infiltrated with inflammatory cells. Therefore, this model may be suitable for the analysis of bacterial burden and gingival tissue inflammation with changes related to systemic diseases.
    Material and Methods: Periodontal tissue destruction was induced by a 2 wk ligature placement around the bilateral maxillary second molar. We analyzed the expression profile of various genes in several tissues, levels of systemic inflammatory markers and induction of insulin resistance. In addition, we studied changes in gut microbiota composition and bacterial load in the oral cavity.
    Results: Two weeks after ligature placement gingival inflammation was significantly induced with a disrupted gingival epithelial barrier and alveolar bone resorption accompanied by increased bacterial burden in the oral cavity. Gene expression analysis of the gingival tissue of ligated mice demonstrated that interleukin (Il) 1b was significantly elevated and Il6 and Il17a tended to be higher in ligated mice than in untreated mice. Although serum IL-6 was significantly elevated and serum amyloid A tended to be higher in ligated compared to untreated mice, endotoxin levels did not differ between the two groups. Among the genes whose expressions are closely related to glucose and lipid metabolisms, only phosphoenolpyruvate carboxykinase 1 (Pck1) and acetyl-coenzyme A carboxylase alpha (Acaca) showed significant changes following ligature placement in the liver, with the former upregulated and the latter downregulated. However, insulin sensitivity did not change following ligature placement. Furthermore, ligature placement weakly affected the composition of gut microbiota and gene expression in the intestines.
    Conclusion: The results suggest that increased oral commensals and gingival inflammation have limited roles in the pathological changes to adipose and liver tissues, which are important organs whose dysfunctions contribute to the development of periodontitis-related systemic diseases.

    DOI: 10.1111/jre.12344

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  • Brazilian propolis mitigates impaired glucose and lipid metabolism in experimental periodontitis in mice 査読

    Mayuka Nakajima, Kei Arimatsu, Takayoshi Minagawa, Yumi Matsuda, Keisuke Sato, Naoki Takahashi, Takako Nakajima, Kazuhisa Yamazaki

    BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE   16   2016年8月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Periodontitis has been implicated as a risk factor for metabolic disorders associated with insulin resistance. Recently, we have demonstrated that orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, induces endotoxemia via reduced gut barrier function coupled with changes in gut microbiota composition, resulting in systemic inflammation and insulin resistance. Propolis, a resinous substance collected by honeybees from leaf buds and cracks in the bark of various plants, can positively affect metabolic disorders in various experimental models. In this study, we thus aimed to clarify the effect of propolis on impaired glucose and lipid metabolism induced by P. gingivalis administration.
    Methods: Eight-week-old male C57BL/6 mice were orally administered P. gingivalis strain W83, propolis ethanol extract powder with P. gingivalis, or vehicle. We then analyzed the expression profile of glucose and lipid metabolism-related genes in the liver and adipose tissues. Serum endotoxin levels were also evaluated by a limulus amebocyte lysate test. In addition, we performed histological analysis of the liver and quantified alveolar bone loss by measuring the root surface area on the lower first molar.
    Results: Oral administration of P. gingivalis induced downregulation of genes that improve insulin sensitivity in adipose tissue (C1qtnf9, Irs1, and Sirt1), but upregulation of genes associated with lipid droplet formation and gluconeogenesis (Plin2, Acox, and G6pc). However, concomitant administration of propolis abrogated these adverse effects of P. gingivalis. Consistent with gene expression, histological analysis showed that administered propolis suppressed hepatic steatosis induced by P. gingivalis. Furthermore, propolis inhibited the elevation of serum endotoxin levels induced by P. gingivalis administration. Contrary to the systemic effects, propolis had no beneficial effect on alveolar bone loss.
    Conclusion: These results suggest that administration of propolis may be effective in suppressing periodontopathic bacteria-induced metabolic changes that increase the risk of various systemic diseases.

    DOI: 10.1186/s12906-016-1305-8

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    その他リンク: http://orcid.org/0000-0002-2875-2111

  • Microbiological and Clinical Effects of Sitafloxacin and Azithromycin in Periodontitis Patients Receiving Supportive Periodontal Therapy 査読

    Takako Nakajima, Takafumi Okui, Harue Ito, Mayuka Nakajima, Tomoyuki Honda, Yasuko Shimada, Koichi Tabeta, Kohei Akazawa, Kazuhisa Yamazaki

    ANTIMICROBIAL AGENTS AND CHEMOTHERAPY   60 ( 3 )   1779 - 1787   2016年3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 MICROBIOLOGY  

    Sitafloxacin (STFX) is a newly developed quinolone that has robust antimicrobial activity against periodontopathic bacteria. We previously reported that oral administration of STFX during supportive periodontal therapy was as effective as conventional mechanical debridement under local anesthesia microbiologically and clinically for 3 months. The aim of the present study was to examine the short-term and long-term microbiological and clinical effects of systemic STFX and azithromycin (AZM) on active periodontal pockets during supportive periodontal therapy. Fifty-one patients receiving supportive periodontal therapy were randomly allocated to the STFX group (200 mg/day of STFX for 5 days) or the AZM group (500 mg/day of AZM for 3 days). The microbiological and clinical parameters were examined until 12 months after the systemic administration of each drug. The concentration of each drug in periodontal pockets and the antimicrobial susceptibility of clinical isolates were also analyzed. The proportions of red complex bacteria, i.e., Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, which are the representative periodontopathic bacteria, were significantly reduced at 1 month and remained lower at 12 months than those at baseline in both the STFX and AZM groups. Clinical parameters were significantly improved over the 12-month period in both groups. An increase in the MIC of AZM against clinical isolates was observed in the AZM group. These results indicate that monotherapy with systemic STFX and AZM might be an alternative treatment during supportive periodontal therapy in patients for whom invasive mechanical treatment is inappropriate.

    DOI: 10.1128/AAC.02575-15

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    その他リンク: http://orcid.org/0000-0002-2875-2111

  • Oral Administration of P. gingivalis Induces Dysbiosis of Gut Microbiota and Impaired Barrier Function Leading to Dissemination of Enterobacteria to the Liver 査読

    Mayuka Nakajima, Kei Arimatsu, Tamotsu Kato, Yumi Matsuda, Takayoshi Minagawa, Naoki Takahashi, Hiroshi Ohno, Kazuhisa Yamazaki

    PLOS ONE   10 ( 7 )   2015年7月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Although periodontitis has been implicated as a risk factor for various systemic diseases, the precise mechanisms by which periodontitis induces systemic disease remain to be elucidated. We have previously revealed that repeated oral administration of Porphyromonas gingivalis elicits endotoxemia via changes in the gut microbiota of the ileum, and thereby induces systemic inflammation and insulin resistance. However, it is not clear to what extent a single administration of P. gingivalis could affect gut microbiota composition, gut barrier function, and subsequent influx of gut microbiota into the liver. Therefore, in the present study, C57BL/6 mice were orally administered P. gingivalis (strain W83) once and compared to sham-inoculated mice. The phylogenetic structure and diversity of microbial communities in the gut and liver were analyzed by pyrosequencing the 16S ribosomal RNA genes. Serum endotoxin activity was determined by a Limulus amebocyte lysate test. Gene expression in the intestine and expression of 16S rRNA genes in the blood and liver were examined by quantitative polymerase chain reaction. Administration of P. gingivalis significantly altered gut microbiota, with an increased proportion of phylum Bacteroidetes, a decreased proportion of phylum Firmicutes, and increased serum endotoxin levels. In the intestinal tissues, gene expression of tjp-1 and occludin, which are involved in intestinal permeability, were downregulated. Higher amounts of bacterial DNA were detected in the liver of infected mice. Importantly, changes in gut microbiota preceded systemic inflammatory changes. These results further support the idea that disturbance of the gut microbiota composition by orally derived periodontopathic bacteria may be a causal mechanism linking periodontitis and systemic disease.

    DOI: 10.1371/journal.pone.0134234

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    その他リンク: http://orcid.org/0000-0002-2875-2111

  • Oral pathobiont induces systemic inflammation and metabolic changes associated with alteration of gut microbiota 査読

    Kei Arimatsu, Hitomi Yamada, Haruna Miyazawa, Takayoshi Minagawa, Mayuka Nakajima, Mark I. Ryder, Kazuyoshi Gotoh, Daisuke Motooka, Shota Nakamura, Tetsuya Iida, Kazuhisa Yamazaki

    SCIENTIFIC REPORTS   4   2014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:NATURE PUBLISHING GROUP  

    Periodontitis has been implicated as a risk factor for metabolic disorders such as type 2 diabetes, atherosclerotic vascular diseases, and non-alcoholic fatty liver disease. Although bacteremias from dental plaque and/or elevated circulating inflammatory cytokines emanating from the inflamed gingiva are suspected mechanisms linking periodontitis and these diseases, direct evidence is lacking. We hypothesize that disturbances of the gut microbiota by swallowed bacteria induce a metabolic endotoxemia leading metabolic disorders. To investigate this hypothesis, changes in the gut microbiota, insulin and glucose intolerance, and levels of tissue inflammation were analysed in mice after oral administration of Porphyromonas gingivalis, a representative periodontopathogens. Pyrosequencing revealed that the population belonging to Bacteroidales was significantly elevated in P. gingivalis-administered mice which coincided with increases in insulin resistance and systemic inflammation. In P. gingivalis-administered mice blood endotoxin levels tended to be higher, whereas gene expression of tight junction proteins in the ileum was significantly decreased. These results provide a new paradigm for the interrelationship between periodontitis and systemic diseases.

    DOI: 10.1038/srep04828

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    その他リンク: http://orcid.org/0000-0002-2875-2111

  • Th2 cytokines efficiently stimulate periostin production in gingival fibroblasts but periostin does not induce an inflammatory response in gingival epithelial cells 査読

    Mayuka Nakajima, Tomoyuki Honda, Sayuri Miyauchi, Kazuhisa Yamazaki

    ARCHIVES OF ORAL BIOLOGY   59 ( 2 )   93 - 101   2014年2月

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    担当区分:筆頭著者   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  

    Objectives: This study aims to clarify whether gingival fibroblasts produce periostin in response to Th2 cytokines which are elevated in periodontitis lesion and, if so, whether periostin affects the inflammatory response and matrix-protein metabolism.
    Design: Human gingival fibroblasts, periodontal ligament cells and the gingival epithelial cell line epi4 were stimulated with interleukin-4 (IL-4), IL-13, tumour necrosis factor-alpha (TNF-alpha) and Porphyromonas gingivalis lipopolysaccharide (LPS). Periostin expression was analysed by real-time polymerase chain-reaction (PCR) and Western blotting. The expression of the IL-4 receptor alpha-chain was evaluated by immunocytochemistry. The effect of periostin on the production of inflammatory cytokines and the expression of matrix protein-related genes was analysed by real-time PCR and enzyme-linked immunosorbent assay (ELISA).
    Results: While IL-4 and IL-13 significantly induced periostin production in gingival fibroblasts and periodontal ligament cells, no effect was observed in epi4 cells. No stimulatory effect of TNF-alpha or P. gingivalis LPS on the production of periostin was observed. The effect of periostin on the production of inflammatory cytokines was weak in gingival fibroblasts; however, little or no effect was observed on periodontal ligament cells or epi4 cells. No significant effect of periostin on the expression of matrix protein-related genes was found.
    Conclusion: The results suggest that gingival fibroblasts may be a source of periostin in periodontitis lesions but periostin has only a limited role either in the inflammatory response or in matrix-protein metabolism. Thus, the role of periostin in the cellular interaction between epithelial and mesenchymal cells in gingiva may be distinct from that of skin. (C) 2013 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.archoralbio.2013.10.004

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    その他リンク: http://orcid.org/0000-0002-2875-2111

▶ 全件表示

MISC

  • Topical Treatment of Periodontitis Using an Iongel 査読

    Mayuka Nakajima, Samir Mitragotri

    99th General Session of the IADR   2021年7月

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  • イオンジェルを用いた局所歯周治療法の開発研究 査読

    中島麻由佳, Samir Mitragotri, 多部田康一

    プログラムおよび講演抄録集   151項   2021年6月

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  • Topical application of choline-based ionic liquid (CAGE) to the treatment of oral infectious disease. 査読

    Eden E. L. Tanner, Nao Nakajima, Kelly N. Ibsen, Samir Mitragotr

    AIChE Annual Meeting   2020年11月

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  • 腸内細菌叢の変動を介した歯周病のNAFLDへの影響

    山崎恭子, 山崎恭子, 中島麻由佳, 竹内麻衣, 原実生, 都野隆博, 都野隆博, 松岸葵, 松岸葵, 松川由実, 佐藤圭祐, 高橋直紀, 多部田康一, 坪井裕理, 菊地淳, 加藤完, 大野博司, 山崎和久

    腸内細菌学雑誌   34 ( 2 )   2020年

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  • Porphyromonas gingivalis経口投与は腸内細菌の変化を介してNAFLD病態に影響を与える

    山崎恭子, 山崎恭子, 中島麻由佳, 竹内麻衣, 原実生, 原実生, 都野隆博, 都野隆博, 松岸葵, 松岸葵, 松川由実, 佐藤圭祐, 高橋直紀, 多部田康一, 山崎和久

    新潟歯学会雑誌   50 ( 2 )   2020年

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  • Porphyromonas gingivalisがNASH病態形成に与える影響の解析

    山崎恭子, 山崎恭子, 中島麻由佳, 中島麻由佳, 竹内麻衣, 竹内麻衣, 原(山田)実生, 原(山田)実生, 都野隆博, 都野隆博, 松岸葵, 松岸葵, 松川(松田, 由美, 佐藤圭祐, 高橋直紀, 多部田康一, 山崎和久

    日本歯周病学会会誌(Web)   61 ( 春季特別 )   125 - 125   2019年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Porphyromonas gingivalisがNASH病態を進行させるメカニズムの解析

    山崎恭子, 山崎恭子, 中島麻由佳, 竹内麻衣, 原実生, 原実生, 都野隆博, 都野隆博, 松岸葵, 松岸葵, 松川由実, 佐藤圭祐, 高橋直紀, 多部田康一, 山崎和久

    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(Web)   151st   2019年

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  • Porphyromonas gingivalisが腸管上皮バリア機能へ及ぼす影響の解析

    都野隆博, 都野隆博, 高橋直紀, 竹内麻衣, 原実生, 中島麻由佳, 多部田康一, 山崎和久

    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(Web)   150th   2019年

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  • Porphyromonas gingivalis口腔投与がDSS誘導性実験的腸炎におよぼす影響の解析

    都野隆博, 都野隆博, 高橋直紀, 竹内麻衣, 原実生, 中島麻由佳, 多部田康一, 山崎和久

    日本歯周病学会会誌(Web)   61   2019年

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  • Porphyromonas gingivalis口腔投与のコラーゲン誘導性関節炎増悪メカニズムの解析

    佐藤圭祐, 高橋直紀, 中島麻由佳, 松田由実, 山田実生, 横地麻衣, 中島貴子, 山崎和久

    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(Web)   147th   56 (WEB ONLY) - 56   2017年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

    J-GLOBAL

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  • Porphyromonas gingivalis口腔投与のコラーゲン誘導性関節炎増悪メカニズムの解析

    佐藤圭祐, 佐藤圭祐, 高橋直紀, 高橋直紀, 中島麻由佳, 中島麻由佳, 松田由実, 松田由実, 山田実生, 山田実生, 横地麻衣, 横地麻衣, 多部田康一, 中島貴子, 山崎和久

    新潟歯学会雑誌   46 ( 2 )   116 - 116   2016年12月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

    J-GLOBAL

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  • Periodontopathic bacteria increases the risk of rheumatoid arthritis by affecting gut immune system

    K. Sato, N. Takahashi, M. Nakajima, Y. Matsuda, M. Yamada, M. Yokoji, T. Kato, H. Ohno, K. Yamazaki

    EUROPEAN JOURNAL OF IMMUNOLOGY   46   640 - 640   2016年8月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:WILEY-BLACKWELL  

    Web of Science

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  • 結紮誘導歯周炎モデルマウスにおける全身への影響とそのメカニズムの解析

    松田由実, 松田由実, 高橋直紀, 高橋直紀, 中島麻由佳, 中島麻由佳, 佐藤圭祐, 佐藤圭祐, 多部田康一, 中島貴子, 山崎和久

    新潟歯学会雑誌   46 ( 1 )   48 - 48   2016年7月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

    J-GLOBAL

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  • Porphyromonas gingivalis口腔投与のコラーゲン誘導性関節炎増悪メカニズムの解析

    佐藤圭祐, 佐藤圭祐, 高橋直紀, 高橋直紀, 中島麻由佳, 中島麻由佳, 松田由実, 松田由実, 山田実生, 山田実生, 横地麻衣, 横地麻衣, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会会誌(Web)   58 ( 春季特別 )   116 - 116   2016年4月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • 歯周病安定期治療中の活動性歯周ポケットに対する経口抗菌療法の細菌学的,臨床的効果(第3報)

    伊藤晴江, 中島貴子, 奥井隆文, 奥井隆文, 中島麻由佳, 中島麻由佳, 本田朋之, 本田朋之, 島田靖子, 島田靖子, 多部田康一, 山崎和久

    日本歯周病学会会誌(Web)   58   2016年

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  • 歯周炎と血液・尿中バイオロジカルマーカーとの関連解析

    中島麻由佳, 中島麻由佳, 多部田康一, 宮内小百合, 杉田典子, 小松康高, 本田朋之, 高橋直紀, 宮澤春菜, 有松圭, 皆川高嘉, 松田由実, 松田由実, 佐藤圭祐, 佐藤圭祐, 山崎和久, 吉江弘正

    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(Web)   143rd   P126 (WEB ONLY) - 197   2015年11月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

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  • 歯周組織局所の炎症およびP.gingivalisによる腸内細菌叢の変動が全身に及ぼす影響とその分子機構の比較

    松田由実, 松田由実, 高橋直紀, 高橋直紀, 有松圭, 有松圭, 中島麻由佳, 中島麻由佳, 佐藤圭祐, 佐藤圭祐, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会会誌(Web)   57 ( 秋季特別 )   129 - 129   2015年8月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

    J-GLOBAL

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  • Porphyromonas gingivalis経口単回投与によるマウス腸内細菌叢の変動

    中島麻由佳, 中島麻由佳, 有松圭, 有松圭, 高橋直紀, 高橋直紀, 皆川高嘉, 皆川高嘉, 松田由実, 松田由実, 佐藤圭祐, 佐藤圭祐, 中島貴子, 多部田康一, 山崎和久

    新潟歯学会雑誌   45 ( 1 )   26 - 27   2015年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

    J-GLOBAL

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  • 歯周炎モデルマウスにおける腸内細菌叢の変動と免疫応答への影響

    高橋直紀, 有松圭, 中島麻由佳, 松田由実, 佐藤圭祐, 多部田康一, 中島貴子, 加藤完, 大野博司, 山崎和久

    腸内細菌学雑誌   29 ( 2 )   91 - 91   2015年4月

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    記述言語:日本語   出版者・発行元:(公財)日本ビフィズス菌センター  

    J-GLOBAL

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  • Porphyromonas gingivalis経口単回投与によるマウス腸内細菌叢の変動

    中島麻由佳, 有松圭, 高橋直紀, 皆川高嘉, 山田ひとみ, 松田由実, 佐藤圭祐, 多部田康一, 中島貴子, 山崎和久

    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(Web)   141st   B24 (WEB ONLY) - 62   2014年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

    J-GLOBAL

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  • 結紮誘導歯周炎モデルマウスにおける全身への影響とその分子機構の解析

    松田由実, 松田由実, 山田ひとみ, 山田ひとみ, 高橋直紀, 高橋直紀, 有松圭, 有松圭, 皆川高嘉, 皆川高嘉, 中島麻由佳, 中島麻由佳, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   57th   2014年

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  • 歯周病原細菌誘導性糖・脂質代謝変動に及ぼすPropolisの効果

    中島麻由佳, 中島麻由佳, 有松圭, 有松圭, 高橋直紀, 高橋直紀, 山田ひとみ, 山田ひとみ, 皆川高嘉, 皆川高嘉, 松田由実, 松田由実, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   57th   2014年

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  • Porphyromonas gingivalis経口投与はマウス腸内細菌叢を変動させインスリン抵抗性を誘導する

    有松圭, 有松圭, 山田ひとみ, 山田ひとみ, 宮内小百合, 宮沢春菜, 中島麻由佳, 中島麻由佳, 多部田康一, 中島貴子, 山崎和久

    新潟歯学会雑誌   44 ( 2 )   2014年

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  • Porphyromonas gingivalis経口投与によるマウス腸内細菌叢の変動と内毒素血症の関連

    有松圭, 有松圭, 山田ひとみ, 山田ひとみ, 宮内小百合, 宮澤春菜, 宮澤春菜, 中島麻由佳, 中島麻由佳, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   57th   2014年

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  • 歯周病安定期治療中の活動性歯周ポケットに対する経口抗菌療法の細菌学的効果(第2報)

    中島貴子, 伊藤晴江, 奥井隆文, 中島麻由佳, 中島麻由佳, 宮下博考, 宮下博考, 多部田康一, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   56th   2013年

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  • 歯周ポケットからの臨床分離株に対する抗菌薬の有効性,耐性の検討

    中島貴子, 奥井隆文, 伊藤晴江, 中島麻由佳, 中島麻由佳, 多部田康一, 山崎和久

    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(Web)   139th   2013年

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  • Porphyromonas gingivalis口腔感染マウスモデルで誘導されるインスリン抵抗性は脂肪組織及び肝臓における炎症反応と関連する

    有松圭, 有松圭, 土門久哲, 土門久哲, 山田ひとみ, 山田ひとみ, 宮内小百合, 宮内小百合, 宮沢春菜, 宮沢春菜, 皆川高嘉, 皆川高嘉, 中島麻由佳, 中島麻由佳, 中島貴子, 多部田康一, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   56th   2013年

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  • Porphyromonas gingivalis口腔感染はマウス腸内細菌叢を変動サせインスリン抵抗性を誘導する

    山崎和久, 有松圭, 有松圭, 土門久哲, 土門久哲, 山田ひとみ, 山田ひとみ, 宮内小百合, 宮内小百合, 宮澤春菜, 宮澤春菜, 皆川高嘉, 皆川高嘉, 中島麻由佳, 中島麻由佳, 中島貴子, 多部田康一

    日本歯周病学会学術大会プログラムおよび講演抄録集   56th   2013年

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▶ 全件表示

講演・口頭発表等

  • イオンジェルを⽤いた経粘膜局所感染制御法の開発

    中島 麻由佳, 多部田康一

    第65回春季⽇本⻭周病学会学術⼤会  2022年6月 

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    会議種別:口頭発表(一般)  

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受賞

  • Flash Talk Audience Award in The 5th Japan-US Science Forum

    2020年12月   JSPS Washington Office, Consulate-General of Japan in Boston, UJA  

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  • 新潟歯学会賞

    2016年4月   新潟歯学会  

    中島 麻由佳

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  • IADR/Unilever Hatton Divisional Award

    2015年3月   93rd International Association for Dental Research  

    中島 麻由佳

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共同研究・競争的資金等の研究

  • 唾液腺への特異的なIgA産生細胞の誘導メカニズムの解明

    研究課題/領域番号:19K18993  2022年4月 - 2025年3月

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    中島 麻由佳

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    配分額:4290000円 ( 直接経費:3300000円 、 間接経費:990000円 )

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  • 腸内細菌叢の変動を介した歯周炎とNASHの関連メカニズムの解明

    2018年4月 - 2021年3月

    新潟大学  特別研究員奨励費 

    中島 麻由佳

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    担当区分:研究代表者  資金種別:競争的資金

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  • 腸内細菌叢の変動を介した歯周炎とNASHの関連メカニズムの解明

    2017年8月 - 2018年3月

    新潟大学  研究活動スタート支援 

    中島 麻由佳

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    担当区分:研究代表者  資金種別:競争的資金

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担当経験のある授業科目

  • 歯周病学

    2022年
    -
    現在
    機関名:新潟大学