Pulmonary emphysema is a disease which develops because of a localized imbalance between endogenous proteinase inhibitors and proteinases leaking from neurophils during phagocytosis at inflammatory foci within the lung. This volume not only reviews at a biochemical level what is known about the natural inhibitors and proteinases involved in connective tissue destruction within the lung, but also suggests novel methodologies for reestablishing proper enzyme-inhibitor balance, including the use of natural or synthetic inhibitors for supplementation or gene therapy.
From the Contents: Pulmonary Emphysema: What's going on.- Elastin and the Lung.- An Introduction to the Endopeptidases.- Lung Proteinase and Emphysema.- Multiple Functions of Neutrophil Proteinases and their Inhibitor Complexes.- Kinetics of the Interaction of Human Leucocyte Elastase with Protein Substrates.- Proteinase Inhibitor Candidates for Therapy of Enzyme-Inhibitor Imbalances.- Antileucoprotease (Secretory Leucocyte Proteinase Inhibitor), A Major Proteinase Inhibitor in the Human Lung.- Development and Evaluation of Antiproteases as Drugs for Preventing Emphysema.- Genetic Control of Human Alpha-1-Antitrypson and Hepatic Gene Therapy.- Neutrophils, Neutrophil Elastase and the Fragile Lung.
Inhaltsverzeichnis
From the Contents: Pulmonary Emphysema: What's going on.- Elastin and the Lung.- An Introduction to the Endopeptidases.- Lung Proteinase and Emphysema.- Multiple Functions of Neutrophil Proteinases and their Inhibitor Complexes.- Kinetics of the Interaction of Human Leucocyte Elastase with Protein Substrates.- Proteinase Inhibitor Candidates for Therapy of Enzyme-Inhibitor Imbalances.- Antileucoprotease (Secretory Leucocyte Proteinase Inhibitor), A Major Proteinase Inhibitor in the Human Lung.- Development and Evaluation of Antiproteases as Drugs for Preventing Emphysema.- Genetic Control of Human Alpha-1-Antitrypson and Hepatic Gene Therapy.- Neutrophils, Neutrophil Elastase and the Fragile Lung.
Klappentext
Pulmonary emphysema is a disease which develops because of a localized imbalance between endogenous proteinase inhibitors and proteinases leaking from neurophils during phagocytosis at inflammatory foci within the lung. This volume not only reviews at a biochemical level what is known about the natural inhibitors and proteinases involved in connective tissue destruction within the lung, but also suggests novel methodologies for reestablishing proper enzyme-inhibitor balance, including the use of natural or synthetic inhibitors for supplementation or gene therapy.
Springer Book Archives
