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Development of periodontal disease-diagnosis kit by nanotechnology and the application for information on health network

纳米技术牙周病诊断试剂盒的研制及健康网信息应用

基本信息

批准号：
20390531
负责人：
NISHIHARA Tatsuji
金额：
$ 12.15万
依托单位：
Kyushu Dental College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2008
资助国家：
日本
起止时间：
2008 至 2010
项目状态：
已结题

项目摘要

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 … More 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

我们利用奈米科技研发出牙周疾病诊断工具，并发现它将是一个有用的工具，以检视牙周疾病与系统功能障碍之间的关系。我们还建立了通过微通道芯片的开发，在流体系统中的巨噬细胞的体外斑块形成的评价方法。在微通道中，LPS刺激后RAW264.7细胞的空斑形成显著增加。目前的研究试图阐明粘附分子在斑块形成中的作用。最初，证实了LPS刺激的RAW 264.7细胞中噬斑形成的时间依赖性增加。流式细胞术和Western blotting检测RAW264.7细胞表面粘附分子的表达。LPS刺激后0 h细胞ICAM-1的表达水平很低。然而，这些水平显着升高，在LPS刺激的细胞在6和12小时的刺激。LFA-1和LFA-2的表达水平 ...更多信息 d在刺激0 h时，L-选择素在未刺激和LPS刺激的细胞中为中等。LPS刺激12 h后，LFA-1表达水平显著升高。然而，在LPS刺激的细胞中L-选择素水平没有增加。Western blot检测LPS刺激2 h后RAW264.7细胞ICAM-1的表达。这些结果表明，LPS增加了RAW264.7细胞中的斑块形成，并上调了ICAM-1和LFA-1的表达，但不上调L-选择素的表达，这与先前报道的单核细胞粘附分子如LFA-1、Mac-1和ICAM-1的表达增加的结果雅阁。总之，这项研究证实了在我们的微通道芯片上流动的液体流中巨噬细胞形成的斑块。目前的研究表明，ICAM-1和LFA-1在LPS刺激的巨噬细胞的细胞聚集中起重要作用。我们的微通道芯片是一个合适的工具，在体外评价动脉粥样硬化的病因，包括牙周炎。少

项目成果

期刊论文数量（0）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Heparin inhibits osteoclast differentiation and function

肝素抑制破骨细胞分化和功能

DOI：
发表时间：
2008
期刊：
J Cell Biochem 103(6)
影响因子：
0
作者：
Ariyoshi W;Takahashi T;Kanno T; Ichimiya H;Shinnmyouzu K;Takano H;Koseki T;Nishihara T.
通讯作者：
Nishihara T.

Ozonated Water Improves Lipopolysaccharide -Induced Responses of Odontoblast-like Cell Line.

臭氧水改善脂多糖诱导的成牙本质细胞样细胞系的反应。