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Titlebook: Biochemistry of Pulmonary Emphysema; C. Grassi,J. Travis,M. Luisetti Book 1992 Springer-Verlag London 1992 Alpha1-Proteinase Inhibitor.Lun

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31#
發(fā)表于 2025-3-26 21:42:07 | 只看該作者
32#
發(fā)表于 2025-3-27 04:10:56 | 只看該作者
33#
發(fā)表于 2025-3-27 05:33:43 | 只看該作者
Proteinases and Proteinase Inhibitors in the Pathogenesis of Pulmonary Emphysema in Humans, with the ability to digest this connective tissue and the inhibitors which protect it. This assumption forms the basis of the proteinase/antiproteinase theory of the pathogenesis of emphysema which has dominated the field of emphysema research for more than 25 years.
34#
發(fā)表于 2025-3-27 10:42:55 | 只看該作者
35#
發(fā)表于 2025-3-27 14:09:08 | 只看該作者
36#
發(fā)表于 2025-3-27 20:51:45 | 只看該作者
Begriff der Chemischen Industrieal and pathological processes. A concept that has proved helpful in this is that of splitting the enzymes into groups on the basis of (a) the type of reaction that they catalyse and (b) the chemical mechanism of catalysis that they use.
37#
發(fā)表于 2025-3-27 21:55:19 | 只看該作者
Begriff der Chemischen Industrie with the ability to digest this connective tissue and the inhibitors which protect it. This assumption forms the basis of the proteinase/antiproteinase theory of the pathogenesis of emphysema which has dominated the field of emphysema research for more than 25 years.
38#
發(fā)表于 2025-3-28 05:42:59 | 只看該作者
https://doi.org/10.1007/978-3-663-13230-1egrading foreign and damaged human proteins. As a consequence of these processes significant quantities of neutrophil proteins are released extracellularly, both through cell leakage and cell death. This places a heavy burden on normal, healthy tissues which may now become susceptible to attack by n
39#
發(fā)表于 2025-3-28 08:28:01 | 只看該作者
40#
發(fā)表于 2025-3-28 11:31:15 | 只看該作者
https://doi.org/10.1007/978-3-663-14764-0ivity in the peripheral lung due to a local imbalance between neutrophil elastase and the antineutrophil elastase screen.. This hypothesis has arisen mainly from the observation that heritable severe deficiency of α.-proteinase inhibitor (α.PI) is associated with development of the disease at a rela
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