| Project/Area Number |
20390531
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
NISHIHARA Tatsuji Kyushu Dental College, 歯学部, 教授 (80192251)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJISAWA Toshiyuki 九州歯科大学, 歯学部, 准教授 (60265006)
ISODA Takaaki 北九州市立大学, 国際環境工学部, 准教授 (70284544)
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| Co-Investigator(Renkei-kenkyūsha) |
AKIFUSA Sumio 九州大学, 歯学部, 准教授 (40295861)
YAMASHITA Yoshihisa 九州大学, 歯学部, 教授 (20192403)
KIYOHARA Yutaka 九州大学, 医学部, 教授 (80161602)
IIDA Mitsuo 九州大学, 医学部, 教授 (00127961)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2010: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2009: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2008: ¥9,230,000 (Direct Cost: ¥7,100,000、Indirect Cost: ¥2,130,000)
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| Keywords | 健康増進 / 歯周病 / 歯周病細菌 / バイオセンサ / 診断キット / バイオセンサー / 診断機器 / ナノテクノロジー / 歯周病原因子 / 炎症性サイトカイン / 炎症性メディエーター / 抗原抗体反応 / 歯周病診断 / 歯周医学 / 心筋梗塞 |
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| Research Abstract |
We developed the periodontal disease-diagnosis kit by nanotechnology and found that it would be useful tool to examine the relationship between the periodontal diseases and systemic dysfunctions. We also established the method involving the evaluation of in vitro plaque formation by macrophage cells in a fluid system via development of the micro-channel chip. In the micro-channel, plaque formation by RAW264.7 cells increased significantly following LPS stimulation. The current study attempted to elucidate the role of adhesion molecules in plaque formation. Initially, the time-dependent increase in plaque formation in LPS-stimulated RAW264.7 cells was confirmed. Expression of adhesion molecules on RAW264.7 cells was examined with flow cytometry and Western blotting analysis. Expression levels of ICAM-1 were very low in LPS-stimulated cells at 0h of stimulation. However, these levels were elevated markedly in LPS-stimulated cells at 6 and 12h of stimulation. Expression levels of LFA-1 an
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d L-selectin were medium in un-stimulated and LPS-stimulated cells at 0h of stimulation. Levels of LFA-1 were elevated significantly in LPS-stimulated cells at 12h of stimulation. However, L-selectin levels did not increase in LPS-stimulated cells. Western blot analysis detected ICAM-1 in RAW264.7 cells stimulated with LPS for 2h. These finding indicated that LPS increases plaque formation and up-regulates expression of ICAM-1 and LFA-1, but not that of L-selectin, in RAW264.7 cells, which are accord with the results of the previous report showing the increased expression of monocyte adhesion molecules, such as LFA-1, Mac-1 and ICAM-1. Taken together, this study confirmed plaque formation by macrophages in a flowing liquid stream on our micro-channel chip. The current investigation indicated that ICAM-1 and LFA-1 play an important role in cell aggregation of LPS-stimulated macrophages. Our micro-channel chip is a suitable tool for the in vitro evaluation of etiological factors of atherosclerosis including periodontitis. Less
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