PULMONARY EMPHYSEMA AND PROTEOLYSIS - 2ND INTERNATIONAL

这项申请建议召开一次关于肺气肿的科学会议 蛋白质分解。由于α1蛋白水解酶抑制剂的关联 1963年虚证与肺气肿的临床与基础研究 肺气肿明显加重。蛋白水解酶的抗蛋白酶理论 肺气肿的演变表明患者的肺不是 通过抗蛋白水解酶防止被白细胞酶破坏 屏幕上。然而，大多数患者会患上肺气肿， 血液中存在正常水平的蛋白水解酶抑制剂。一项额外的 提出了α1蛋白水解酶抑制剂的作用机制。 可以被香烟烟雾和白色中存在的氧化剂灭活 细胞，从而潜在地造成阿尔法1蛋白酶的暂时缺陷 肺中的抑制物。这仍然不能完全解释为什么只有20%的 吸烟者继续发展为严重的呼吸道阻塞。最近， 异常抗氧化剂在疾病过程中的潜在参与 是有人建议的。提出的研讨会旨在确定我们目前的状况 了解a)肺气肿的蛋白水解酶-抗蛋白酶理论和b) 氧化剂、抗氧化剂与蛋白水解酶和抗蛋白酶的相互作用。会的 探索a)这些分子中的遗传多态和缺陷，b)其他 肺损伤理论及其与蛋白水解酶和氧化剂的关系 为生化和流行病学研究提供未来方向 包括可能的治疗方法。

This application proposes a scientific meeting on pulmonary emphysema and proteolysis. Since the association of alpha 1 protease inhibitor deficiency and emphysema in 1963, both clinical and basic studies of emphysema were greatly advanced. The protease antiprotease theory of emphysema evolved which suggested that the lungs of patients were not protected from destruction by white cell proteases by the antiprotease screen. The majority of patients develop emphysema, however, in the presence of normal blood levels of protease inhibitors. An additional mechanism was proposed which demonstrated that alpha 1 protease inhibitor could be inactivated by oxidants present in cigarette smoke and in white cells, thus potentially creating a temporary deficiency of alpha 1 protease inhibitor in the lung. This still could not fully explain why only 20% of smokers proceed to develop significant airways obstruction. Recently, the potential involvement of abnormal antioxidants in the disease process has been suggested. The symposium proposed aims to define our current status of knowledge on a) the protease antiprotease theory of emphysema and b) oxidant antioxidant interactions with proteases and antiproteases. It will explore a) genetic polymorphisms and deficits in these molecules, b) other theories of lung injury and their relation to proteases and oxidants and c) provide future direction to biochemical and epidemiological studies including possible therapeutic approaches.