Vasculitis in Kawasaki disease : the molecular and vascular biological studies

川崎病的血管炎:分子和血管生物学研究

基本信息

项目摘要

The peripheral blood mononuclear cells of Kawasaki disease (KD) patients with coronary artery lesions produced higher levels of tumor necrosis factor (TNF)-alpha in response to bacterial products. None of the polymorphisms in the 5 flanking region of the TNF-alpha gene were related to KD.These results suggest that a genetic disposition towards overproduction of TNF-alpha in response to bacterial products may be involved in the pathogenesis of KD (Kamizono S, Kato H, et al. Pediatr Int. 1999). We investigated the coronary endothelial function using intracoronary infusions of acetylcholine and isosorbide dinitrate and evaluated vascular wall morphology using intravasucular ultrasound (IVUS) imaging long-term after KD.Long-term coronary artery lesions, even after aneurysm regression, may have impaired endothelial function and abnormal vascular wall morphology (Yamakawa R, Kato H, et al. JACC, 1998, Iemura M, Kato H, et al. Heart 2000). The steroid pulse therapy migt be useful in patients with intravenous immune globulin (IVIG)-resistant Kawasaki disease who experience prolonged fever. However, transient dilatation of the coronary artery was observed during steroid pulse therapy (Hashino K, Kato H, et al. Pediatr Int, in press). We investigated the relationship between the plasma levels of soluble forms of selectin family (P-, E-, and L- selectin) and the incidence of CAL in KD patients. Alterations in plasma selectin levels are important clinical molecular markers KD patients. E-selectin molecules may have potential as a predictor of incidence of CAL in patients with KD (Furui J Kurume Med J, in press). Vascular endothelial growth factor (VEGF) was involved in the pathogenesis of KD, especially in the developing of CAL.The VEGF may have possibility to become useful predictor of CAL in patients with IVIG resistant KD (Furui J, Kato H, et al. JACC 2001, abstract).
冠状动脉病变川崎病(KD)患者外周血单个核细胞对细菌产物产生较高水平的肿瘤坏死因子(TNF)- α。tnf - α基因侧翼5个区域的多态性均与KD无关。这些结果表明,针对细菌产物产生tnf - α过量的遗传倾向可能参与了KD的发病机制(Kamizono S, Kato H, et al.)。儿科,1999)。我们通过冠状动脉内输注乙酰胆碱和硝酸异山梨酯来研究冠状动脉内皮功能,并通过血管内超声(IVUS)成像评估KD后长期血管壁形态。长期的冠状动脉病变,即使在动脉瘤消退后,也可能导致内皮功能受损和血管壁形态异常(Yamakawa R, Kato H,等)。李春华,李春华,李春华,等。心2000)。类固醇脉冲治疗可能对静脉注射免疫球蛋白(IVIG)抵抗的川崎病患者有帮助。然而,在类固醇脉冲治疗期间观察到冠状动脉的短暂扩张(Hashino K, Kato H等)。儿科,出版中)。我们研究了选择素家族可溶性形式(P-、E-和L-选择素)的血浆水平与KD患者CAL发病率之间的关系。血浆选择素水平的改变是KD患者重要的临床分子标志物。e -选择素分子可能有潜力作为KD患者CAL发病率的预测因子(Furui J Kurume Med J, in press)。血管内皮生长因子(Vascular endothelial growth factor, VEGF)参与了KD的发病机制,特别是在CAL的发展中,VEGF可能成为IVIG耐药KD患者CAL的有用预测因子(Furui J, Kato H, et al.)。JACC 2001, abstract)。

项目成果

期刊论文数量(70)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Kato H,Ishii M,Akagi T,et al.: "Interventional catheterization in Kawasaki disease." J Interven Cardiol. 11:. 355-361 (1998)
Kato H,Ishii M,Akagi T,et al.:“川崎病的介入导管插入术。”
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Akgai T, Ogawa S, Ino T, Echigo S, Tomita H, Ishii M, Kato H.: "Catheter Interventional in Kawasaki disease : a report from the Japanese pediatric interventional cardiology i investigation group."J Pediatr. Vol.137. 181-186 (2000)
Akgai T、Okawa S、Ino T、Echigo S、Tomita H、Ishii M、Kato H.:“川崎病的导管介入:日本儿科介入心脏病学调查组的报告。”J Pediatr。
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Nakamura Y,Kato H,et al.: "Cardiac sequelae of Kawasaki disease among recurrent cases." Arch Dis Child. 78:. 163-165 (1998)
Nakamura Y,Kato H,et al.:“复发病例中川崎病的心脏后遗症。”
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Iemura M, Ishii M, Kato H, et al.: "Long-term consequences of regressed voronary aneurysms after Kawasaki Disease : Vascular wall morphology and function."Heart. Vol.83. 307-311 (2000)
Iemura M、Ishii M、Kato H 等人:“川崎病后冠状动脉瘤退化的长期后果:血管壁形态和功能。”心脏。
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Nakamura Y,Kato H,et al.: "Mortality among patients with a history of Kawasaki disease:the third look" Acta Paediatr Jpn. 40. 419-423 (1998)
Nakamura Y、Kato H 等人:“有川崎病病史的患者的死亡率:第三次观察”Acta Paediatr Jpn。
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KATO Hirohisa其他文献

KATO Hirohisa的其他文献

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{{ truncateString('KATO Hirohisa', 18)}}的其他基金

Identification and characterization of biofilm regulatory autolysins
生物膜调节自溶素的鉴定和表征
  • 批准号:
    23592746
  • 财政年份:
    2011
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Development of novel drugs to control oral biofilms towards clinical application
开发控制口腔生物膜的新药并走向临床应用
  • 批准号:
    20592181
  • 财政年份:
    2008
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Gene therapy for induction of immunological tolerance in organ allografts
诱导同种异体器官移植免疫耐受的基因治疗
  • 批准号:
    13671253
  • 财政年份:
    2001
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Comparative study on Kawasaki disease between Japan and North America
日本与北美川崎病的比较研究
  • 批准号:
    09044347
  • 财政年份:
    1997
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for international Scientific Research
Development of the new transctaneous occlusion system for patent ductus arteriosus
新型经皮动脉导管未闭封堵系统的开发
  • 批准号:
    08557053
  • 财政年份:
    1996
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Study on Etiology and Pathogenesis of Kawasaki Disease
川崎病病因及发病机制研究
  • 批准号:
    07307011
  • 财政年份:
    1995
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Investigation of cause of Kawasaki disease, molecular infecto-immunolgical analysis
川崎病病因调查、分子感染免疫学分析
  • 批准号:
    06454310
  • 财政年份:
    1994
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
cDNA cloning of the recepters for the members of TGFbeta superfamily
TGFbeta超家族成员受体的cDNA克隆
  • 批准号:
    05671566
  • 财政年份:
    1993
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
Morphological and hemodynamic changes of the fetal heart : chronological evaluation from fetus to newborn
胎儿心脏的形态和血流动力学变化:从胎儿到新生儿的时间顺序评估
  • 批准号:
    04670627
  • 财政年份:
    1992
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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肿瘤坏死因子-α 对 NKCC2 亚型和血压的调节
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研究肿瘤坏死因子受体相关因子 1 在炎症性关节炎和脂多糖诱导的感染性休克动物模型中的作用
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C1q 肿瘤坏死因子相关蛋白 (CTRP) 在松弛素受体生物学中的新作用
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