BERYLLIUM RESEARCH PROGRAM, PROJECT 1

铍研究计划，项目 1

• 批准号: 7604341
• 负责人: LISA A MAIER
• 金额: $ 0.17万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604341
• 关键词: Alloys; Beryllium; Breathing; Cells; Chemicals; Chronic berylliosis; Computer Retrieval of Information on Scientific Projects Database; Cues; Cytokine Gene; Disease; Funding; Genes; Grant; Granuloma; Granulomatous; Immune; Immune System Diseases; Immune system; Individual; Institution; Lung diseases; Metals; Pathology; Process; Program Research Project Grants; Research; Research Personnel; Resources; Risk; Severity of illness; Source; Time; United States National Institutes of Health; Workplace; cytokine; particle

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. Chronic beryllium disease (CBD) is an immune system disorder caused by the inhalation of beryllium particles. Exposures and disease occur in workplaces in which beryllium metal and beryllium alloys are used, producing disease in 2-6% of workers. Currently 1 million workers in the US are exposed. Individuals become sensitized to beryllium (BeS), and in some cases progress to CBD, which is a granulomatous lung disorder. Granulomas are a form of pathology that occurs when the body's immune system "overreacts". At this time, we do not know why some individuals who are beryllium sensitized develop CBD and others do not, although there is evidence that cell chemicals called "cytokines" regulate this process. It is known that there are genes, which are associated with increased risk for BeS and CBD. Other genes may be associated with the progression of BeS to CBD and with CBD severity. The focus of this project is to examine the relationship of immune cue cytokines and the genes, which regulate those cells to the risk for BeS and CBD.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 慢性铍疾病（CBD）是由铍颗粒吸入引起的免疫系统疾病。 暴露和疾病发生在使用铍金属和铍合金的工作场所中，在2-6％的工人中产生疾病。 目前，美国有100万工人已暴露。 个体对铍（BES）敏感，在某些情况下会发展为CBD，这是一种肉芽肿性肺部疾病。 肉芽肿是一种病理形式，当人体的免疫系统“过度反应”时会发生。 目前，我们不知道为什么有些人敏化的人会发展CBD，而其他人则不知道，尽管有证据表明细胞化学物质称为“细胞因子”调节这一过程。 众所周知，存在与BES和CBD风险增加有关的基因。 其他基因可能与CBD的进展以及CBD的严重程度有关。 该项目的重点是检查免疫提示细胞因子和基因的关系，这些基因调节这些细胞对BES和CBD的风险。