PULMONARY EMPHYSEMA AND PROTEOLYSIS - 2ND INTERNATIONAL

本申请提出了一个关于肺气肿的科学会议， 蛋白水解 由于α 1蛋白酶抑制剂 缺乏和肺气肿在1963年，临床和基础研究， 肺气肿已经严重恶化。 蛋白酶抗蛋白酶理论 肺气肿的发展，这表明病人的肺不是 通过抗蛋白酶保护免受白色细胞蛋白酶的破坏 屏幕 大多数患者发展为肺气肿，然而， 血液中蛋白酶抑制剂水平正常。 额外 提出了α 1蛋白酶抑制剂 可以被香烟烟雾中的氧化剂和白色 细胞，从而可能造成暂时缺乏α 1蛋白酶 肺中的抑制剂。 这仍然不能完全解释为什么只有20%的 吸烟者继续发展严重的气道阻塞。 近日 异常抗氧化剂在疾病过程中的潜在参与， 被建议。 研讨会的目的是确定我们目前的地位 关于a）肺气肿的蛋白酶抗蛋白酶理论和B） 氧化剂抗氧化剂与蛋白酶和抗蛋白酶的相互作用。 它将 探索a）这些分子的遗传多态性和缺陷，B）其他 肺损伤理论及其与蛋白酶和氧化剂的关系，以及c） 为生物化学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.