Conference--Models of Emphysema: Speeding Progress

描述（由申请人提供）：肺气肿是慢性阻塞性肺疾病（COPD）的主要组成部分，是美国主要的死亡原因之一，并在全球范围内达到流行状态。尽管我们对肺气肿的发病机制有了一定的了解，但对这种疾病的治疗进展甚微，而且在大多数情况下，治疗仅仅是预防性的（戒烟或退出受污染的环境）或仅限于缓解症状。这种疾病的治疗缺乏进展的主要原因是，几十年来医学界对这种疾病的了解一直很沮丧，总的来说，研究人员对这种疾病缺乏兴趣。然而，近年来，我们对这种疾病的理解取得了很大的进步，特别是在我们开发动物模型研究这种疾病的能力方面。特别值得一提的是，最近开发的动物模型阐明了炎症和氧化应激在该疾病发病机制中的作用。关于以肺泡细胞凋亡增强和随后的基质重塑为特征的肺破坏的非炎症机制，已经提出了创新的假设。同样重要的是，在动物身上进行的基因靶向或分子操作研究，可以近距离观察特定基因（如肿瘤坏死因子或特定蛋白酶）在这种疾病发展过程中的个体贡献。但是，即使已经获得了很多知识，但对于谁将动物模型与人类疾病联系起来，仍然缺乏共识。此外，对于如何评估炎症、破坏和修复尚无共识。对于如何在动物模型和人类中进行肺气肿的形态计量学分析，也没有普遍的共识。因此，需要一个全球性的论坛，允许全球交流和讨论这些问题，并促进研究人员之间的合作。为此，一群德高望重的科学家召开了一场名为“肺气肿模型：加快进展步伐”的国际科学会议。这次会议将于2002年9月25日至26日在弗吉尼亚州沃伦顿的航空会议中心举行。该研究提案由组委会主席提出，作为寻求项目发展进一步支持的机制

DESCRIPTION (provided by applicant): Emphysema, the main component of chronic obstructive lung disease (COPD) is a major leading cause of death in the United States and is achieving epidemic status worldwide. In spite of our knowledge of the pathogenesis of emphysema little progress has been made in the treatment of this disease and for the most part treatment is merely preventive (smoking cessation or withdrawal from contaminated environments) or limited to symptom relief. The major explanation for the lack of progress in the treatment of this disease is the fact that the medical community has been frustrated for decades with the understanding of the disease and in general this disease has been looked upon with a lack of interest by the investigators. However, in recent years great advances have been achieved in our understanding of this disease and in particular in our capacity to develop animal models for the study of this disease. Particularly worth of mention are recently developed animal models clarifying the role of inflammation and oxidative stress in the pathogenesis of this disease. Innovative hypotheses have been advanced with respect to non- inflammatory mechanisms of lung destruction characterized by enhanced alveolar apoptosis and subsequent remodeling of the matrix. Equally important, studies have been conducted in which gene targeting or molecular manipulation in animals allow a close look at the individual contribution of specific genes (such as TNF or specific proteases) during the development of this disease.But if much knowledge has been gained there is still an important lack of consensus as to who to correlate the animal models with respect to the human disease. Furthermore, there is no consensus on how to assess inflammation, destruction, and repair. Nor there is universal agreement as to how to conduct the morphometric analysis of emphysema in animal models and human beings. Therefore, the need exists for a worldwide forum that allows for the global communication and discussion of these problems and promotes collaboration among investigators. To that effect, a group of highly respectable scientists have conveyed an international scientific conference entitled "Models of Emphysema: Speeding the pace of progress." This conference will take place on September 25-26, 2002 and it will be celebrated at the Airline Conference Center in Warrenton, Virginia. This research proposal then is put forward by the chairman of the organizing committee as a mechanism to look for further support for the development of the program