Molecular Basis of Bioelectronic Medicine
生物电子医学的分子基础
基本信息
- 批准号:9071799
- 负责人:
- 金额:$ 51.42万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2016
- 资助国家:美国
- 起止时间:2016-05-01 至 2021-04-30
- 项目状态:已结题
- 来源:
- 关键词:Anti-Inflammatory AgentsAnti-inflammatoryAutoimmune DiseasesBiologyCytokine GeneDataDevicesDiseaseElectronicsEtiologyFundingFutureGene ExpressionImmune responseInfectionInflammationInflammation MediatorsInflammatoryInjuryLaboratoriesMapsMediatingMedicineModalityMolecularMolecular TargetNational Institute of General Medical SciencesNeurotransmittersPreventionReflex actionRegulationReperfusion InjuryResearch PersonnelResearch SupportSepsisShockSterilityTherapeuticWorkbasecytokineneural circuitpublic health relevancetherapy development
项目摘要
DESCRIPTION (provided by applicant): Inflammation, mediated by the immune response to infection and sterile injury, is a major underlying cause of disease. Advances in understanding the molecular mechanisms of inflammation hold promise for developing future therapies for severe sepsis, shock, ischemia reperfusion injury, autoimmune diseases, and other debilitating diseases of national importance. Research supported by the NIGMS in the principle investigator's lab has revealed mechanisms to control inflammation by identifying and targeting specific cytokines, and by mapping and targeting specific neural circuits that control their activity. This work has now progressed to launching a new field, termed "bioelectronic medicine," which holds promise as strategy to develop therapies using electronic devices to target anti-inflammatory neural circuits. The present proposal seeks to understand unanswered questions about the molecular mechanisms controlling inflammation as derived from three existing RO1 funded projects in the PI's laboratory. The first is to understand the identity and mechanisms of the reflex neural circuits that control immune responses. The second is to understand the biology of cytokine mediators of inflammation that are necessary and sufficient for disease causation. And the third is to understand the molecular mechanisms that regulate cytokine release under the influence of neurotransmitters, including regulation of cytokine gene expression and inflammasome activity. The successful completion of this work will provide significant new data necessary to develop therapeutic modalities for the prevention and treatment of inflammation using bioelectronic devices.
描述(由申请人提供):由对感染和无菌性损伤的免疫反应介导的炎症是疾病的主要根本原因,对炎症分子机制的了解的进展为未来开发治疗严重脓毒症、休克、缺血再灌注的疗法带来了希望。 NIGMS 在研究者实验室支持的研究揭示了通过识别和靶向特定细胞因子以及绘制和靶向控制炎症的机制。这项工作现已发展到启动一个新领域,称为“生物电子医学”,该领域有望成为利用电子设备开发针对抗炎神经回路的疗法的策略。关于控制炎症的分子机制的未解答问题来自 PI 实验室的三个现有 RO1 资助的项目,第一个是了解控制免疫反应的反射神经回路的身份和机制,第二个是了解细胞因子介质的生物学。的第三是了解在神经递质影响下调节细胞因子释放的分子机制,包括细胞因子基因表达和炎症小体活性的调节,这项工作的成功完成将提供重要的新数据。有必要开发使用生物电子设备预防和治疗炎症的治疗方式。
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)
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Kevin J Tracey其他文献
From mouse to man: or what have we learned about cytokine-based anti-inflammatory therapies?
从小鼠到人类:或者我们对基于细胞因子的抗炎疗法了解了什么?
- DOI:
- 发表时间:
1999 - 期刊:
- 影响因子:3.1
- 作者:
Kevin J Tracey;Edward Abraham - 通讯作者:
Edward Abraham
Tumor necrosis factor in the malnutrition (cachexia) of infection and cancer.
感染和癌症营养不良(恶病质)中的肿瘤坏死因子。
- DOI:
- 发表时间:
1992 - 期刊:
- 影响因子:3.3
- 作者:
Kevin J Tracey;A. Cerami - 通讯作者:
A. Cerami
Kevin J Tracey的其他文献
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{{ truncateString('Kevin J Tracey', 18)}}的其他基金
PKR mediated inflammasome activation and pyroptosis in sepsis
脓毒症中 PKR 介导的炎症小体激活和细胞焦亡
- 批准号:
8496322 - 财政年份:2014
- 资助金额:
$ 51.42万 - 项目类别:
Macrophage Inactivation in Sepsis after Shock or Trauma
休克或创伤后脓毒症中巨噬细胞失活
- 批准号:
7933295 - 财政年份:2009
- 资助金额:
$ 51.42万 - 项目类别:
VAGUS NERVE STIMULATION IN RHEUMATOID ARTHRITIS (VANSRA)
迷走神经刺激治疗类风湿性关节炎 (VANSRA)
- 批准号:
7951920 - 财政年份:2009
- 资助金额:
$ 51.42万 - 项目类别:
CHOLINERGIC MODULATION OF CYTOKINE SYNTHESIS IN SEPSIS SURVIVORS
脓毒症幸存者细胞因子合成的胆碱能调节
- 批准号:
7719247 - 财政年份:2008
- 资助金额:
$ 51.42万 - 项目类别:
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