BERYLLIUM RESEARCH PROGRAM, PROJECT 1

铍研究计划，项目 1

• 批准号: 7719386
• 负责人: LISA A MAIER
• 金额: $ 0.02万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7719386
• 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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 慢性铍病（CBD）是一种由吸入铍颗粒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，使2-6%的工人患病。 目前，美国有100万工人受到感染。 个体对铍（BeS）敏感，在某些情况下进展为CBD，这是一种肉芽肿性肺病。 肉芽肿是一种病理形式，发生时，身体的免疫系统“反应过度”。 在这个时候，我们不知道为什么有些人谁是铍致敏开发CBD和其他人不，虽然有证据表明，细胞化学物质称为“细胞因子”调节这一过程。 据了解，有一些基因与BeS和CBD的风险增加有关。 其他基因可能与BeS向CBD的进展以及CBD的严重程度有关。 该项目的重点是研究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。