AUTOIMMUNE MECHANISMS IN DIABETIC NEUROPATHY

糖尿病神经病的自身免疫机制

基本信息

  • 批准号:
    7376616
  • 负责人:
  • 金额:
    $ 0.1万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2006
  • 资助国家:
    美国
  • 起止时间:
    2006-04-05 至 2007-02-28
  • 项目状态:
    已结题

项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The causes of long-term complications associated with type 2 diabetes mellitus are poorly understood. Previous studies suggest that patients with type 2 diabetes can develop autoimmune immunoglobulins (autoantibodies directed against their own tissues) during the course of their illness. We will examine the hypothesis that a significant percentage of patients with type 2 diabetes will slowly develop autoantibodies during the course of their illness and that these autoantibodies contribute to the injury and loss of cells in the nervous system, a well-known complication in long-term diabetic patients. Two groups of type 2 diabetic patients will be enrolled in this study. Group 1 will have the diabetes for three to four years at the time of enrollment. Group 2 will have had diabetes for seven to eight years at the time of enrollment. Both groups will undergo a thorough examination of their nervous system function and have blood drawn to screen for the presence of autoantibodies. All participants will undergo re-evaluation between three to four years after the initial testing. These studies will help to determine the significance of autoimmune mechanisms in the natural history of nerve injury that occurs in type 2 diabetes mellitus
本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者(PI)可能已经从另一个NIH来源获得了主要资金,因此可以在其他CRISP条目中表示。列出的机构是中心的,不一定是研究者的机构。与2型糖尿病相关的长期并发症的原因尚不清楚。先前的研究表明,2型糖尿病患者在发病过程中可产生自身免疫球蛋白(针对自身组织的自身抗体)。我们将检验一种假设,即很大比例的2型糖尿病患者在发病过程中会缓慢地产生自身抗体,这些自身抗体会导致神经系统细胞的损伤和损失,这是长期糖尿病患者的一种众所周知的并发症。本研究将纳入两组2型糖尿病患者。第一组在入组时患有糖尿病3 - 4年。第二组在入组时已经患有糖尿病7 - 8年。两组患者都将接受神经系统功能的全面检查,并抽血检查自身抗体的存在。所有参与者将在初始测试后的三到四年之间接受重新评估。这些研究将有助于确定自身免疫机制在2型糖尿病发生的神经损伤的自然史中的重要性

项目成果

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JOHN W WILEY其他文献

JOHN W WILEY的其他文献

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{{ truncateString('JOHN W WILEY', 18)}}的其他基金

Actions of Resolvins on Intestinal Inflammation and Pain
Resolvins 对肠道炎症和疼痛的作用
  • 批准号:
    10370415
  • 财政年份:
    2020
  • 资助金额:
    $ 0.1万
  • 项目类别:
Actions of Resolvins on Intestinal Inflammation and Pain
Resolvins 对肠道炎症和疼痛的作用
  • 批准号:
    10597042
  • 财政年份:
    2020
  • 资助金额:
    $ 0.1万
  • 项目类别:
Chronic Stress and Abdominal Pain: Novel Mechanisms
慢性压力和腹痛:新机制
  • 批准号:
    8478935
  • 财政年份:
    2013
  • 资助金额:
    $ 0.1万
  • 项目类别:
Chronic Stress and Abdominal Pain: Novel Mechanisms
慢性压力和腹痛:新机制
  • 批准号:
    8815954
  • 财政年份:
    2013
  • 资助金额:
    $ 0.1万
  • 项目类别:
Chronic Stress and Abdominal Pain: Novel Mechanisms
慢性压力和腹痛:新机制
  • 批准号:
    8626396
  • 财政年份:
    2013
  • 资助金额:
    $ 0.1万
  • 项目类别:
Chronic Stress and Abdominal Pain: Novel Mechanisms
慢性压力和腹痛:新机制
  • 批准号:
    9020949
  • 财政年份:
    2013
  • 资助金额:
    $ 0.1万
  • 项目类别:
Stress and Visceral Hyperalgesia: Epigenetic Mechanisms
压力和内脏痛觉过敏:表观遗传机制
  • 批准号:
    8541353
  • 财政年份:
    2012
  • 资助金额:
    $ 0.1万
  • 项目类别:
Autoimmune Mechanisms of Diabetic Neuropathy
糖尿病神经病变的自身免疫机制
  • 批准号:
    7919084
  • 财政年份:
    2009
  • 资助金额:
    $ 0.1万
  • 项目类别:
AUTOIMMUNE MECHANISMS IN DIABETIC NEUROPATHY
糖尿病神经病的自身免疫机制
  • 批准号:
    7603776
  • 财政年份:
    2007
  • 资助金额:
    $ 0.1万
  • 项目类别:
AUTOIMMUNE MECHANISMS IN DIABETIC NEUROPATHY
糖尿病神经病的自身免疫机制
  • 批准号:
    7603703
  • 财政年份:
    2007
  • 资助金额:
    $ 0.1万
  • 项目类别:

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