HEPATOCYTE ASIALOGLYCOPROTEIN RECEPTOR ASSAY
HEPATOCYTE ASIALOGLYCOPROTEIN RECEPTOR ASSAY
批准号:
6210347
负责人:
ERNEST V GROMAN
金额:
$10.0万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2000
资助国家:
美国
项目状态:
已结题
起止时间:
2000-09-15 至 2001-03-14
中文摘要
描述(改编自调查人员摘要):最具诊断性
预测肝功能衰竭的技术只能用大体数据来解释
肝功能,而不是特定结构的功能,如
感受器。使用以下工具获取与肝功能相关的解剖信息
放射性和磁性胶体(MRI)已被证明既昂贵又
相对来说效率不高。为了克服这些诊断限制,
研究人员计划合成并表征含半乳糖的蛋白质
以及用稳定同位素标记的纳米胶体。稳定的同位素将是
用中子活化分析进行定量。我们的非放射性、无毒
针对肝细胞去唾液酸糖蛋白受体的药物,通过
半乳糖,预计会迅速和专门从血液中去除
根据肝脏中功能性受体的数量。动力学模型的建立
血液中这些试剂的耗尽可以估计出功能的数量
肝脏中的受体。受体靶向诊断试剂与
稳定同位素标记和中子活化在技术上代表了一种
设计用于测量的代理的新的和潜在的通用方法
肝脏和其他器官中的受体功能。最重要的是,稳定
同位素标记提供了测量多种受体活性的机会
同时。
建议的商业应用:不可用
英文摘要
DESCRIPTION (Adapted from the Investigator's Abstract): Most diagnostic
techniques to predict liver failure are interpretable only in terms of gross
liver function, not in terms of the function of specific structures such as
receptors. Anatomical information related to liver function obtained by using
radioactive and magnetic colloids (MRI) has proven to be both costly and
relatively ineffective. To overcome these diagnostic limitations, the
investigators plan to synthesize and characterize galactose-containing proteins
and nanocolloids labeled with stable isotopes. Stable isotopes will be
quantitated by neutron activation analysis. Our non-radioactive, nontoxic
agents, directed to the asialoglycoprotein receptor of hepatocytes by
galactose, are expected to be rapidly and specifically removed from the blood
based upon the number of functional receptors in the liver. Kinetic modeling of
the depletion of these agents in blood can estimate the number of functioning
receptors in the liver. Receptor-targeted diagnostic agents combined with
stable isotope labeling and neutron activation represent a technologically
novel and potentially general approach to the design of agents to measure
receptor function in the liver and other organs. Most importantly, stable
isotope labeling offers an opportunity to measure multiple receptor activities
simultaneously.
PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE
期刊论文(0)
专著(0)
科研奖励(0)
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