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bronchiectasis/protease
L'enllaç es desa al porta-retalls
Pàgina 1 des de 67 resultats
Mucus hypersecretion in bronchiectasis. The role of neutrophil proteases.
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To investigate the role of neutrophil proteases in the pathogenesis of mucus hypersecretion in bronchiectasis, we collected sputum samples from seven patients with bronchiectasis and measured their secretagogue activity by examining secretion of radiolabeled macromolecules by bovine airway
[Disorders of the protease-antiprotease system of a bronchial washout in patients with bronchiectasis and the means for their correction].
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Patients with bronchiectatic disease show imbalance between the activity of proteolytic enzymes and their inhibitors contained by bronchial wash-out, manifesting in a reduction of the inhibitory potential and a rise of the activity of trypsin-like proteinases. After the standard basic treatment the
Identification of a novel SERPINA-1 mutation causing alpha-1 antitrypsin deficiency in a patient with severe bronchiectasis and pulmonary embolism.
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Deficiency in the serine protease inhibitor, alpha-1 antitrypsin (AAT), is known to cause emphysema and liver disease. Other manifestations, including airway disease or skin disorders, have also been described. A 44-year-old woman presented to our emergency department with dyspnea and respiratory
Pathogenesis of bronchiectasis.
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Non-cystic fibrosis bronchiectasis is a heterogeneous condition and its pathogenesis is still not well defined. A combination of a defect in host defense and bacterial infection allows microbial colonization of the airways resulting in chronic inflammation and lung damage. An ongoing cycle of
A New SERPINA-1 Missense Mutation Associated with Alpha-1 Antitrypsin Deficiency and Bronchiectasis.
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Alpha-1-antitrypsin deficiency (AATD) is a genetic condition caused by SERPINA1 mutations, which culminates into lower protease inhibitor activity in the serum and predisposes to emphysema. Clinical manifestations of AATD are often associated to ZZ (p.Glu342Lys) and SZ (p.Glu264Val) genotypes and
Exhaled breath condensate MMP-9 levels in children with bronchiectasis.
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Bronchiectasis (BE) is still an important cause of chronic supurative respiratory diseases in developing countries. Neutrophil-derived proteases such as neutrophil elastase and matrix metalloproteases (MMPs) are implicated in causing airway damage in chronic pulmonary disease. In this study, we
[Complex search for antiprotease-protease enzyme gene polymorphisms in patients with chronic obstructive pulmonary diseases].
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Based on the protease-antiprotease hypothesis in the pathogenesis of chronic lung diseases, we investigated the influence of Z and S mutations and TaqI-polymorphism of alpha1-antitrypsin gene (PI) and Ala - 15Thr polymorphism in signal peptide of alpha1-antichymotrypsin gene (AACT) in patients with
Pathophysiology and Genetics of Bronchiectasis Unrelated to Cystic Fibrosis.
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Bronchiectasis is characterized by deregulated inflammatory response and recurrent bacterial infection resulting in progressive lung damage and an irreversible dilatation of bronchi and bronchioles. Generally accepted model of the development of bronchiectasis is the "vicious cycle hypothesis" that
Neutrophil-mediated degradation of lung proteoglycans: stimulation by tumor necrosis factor-alpha in sputum of patients with bronchiectasis.
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Neutrophil-mediated degradation of bronchial matrix has been proposed as a pathogenetic factor in bronchiectasis. We hypothesize that neutrophils, found in abundance in the bronchial lumens of patients with bronchiectasis, are capable of degrading lung matrix proteoglycans and that proinflammatory
Human neutrophil collagenase (MMP-8), identified in bronchiectasis BAL fluid, correlates with severity of disease.
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Collagenases in bronchoalveolar lavage fluid (BALF) of patients with bronchiectasis and healthy subjects were characterized using specific functional and immunologic assays. The BAL fluid contained interstitial collagenase and collagenolytic proteinases of bacterial origin. Collagenase activities,
Inhaled hyperosmolar agents for bronchiectasis.
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BACKGROUND
Mucus retention in the lungs is a prominent feature of bronchiectasis. The stagnant mucus becomes chronically colonised with bacteria, which elicit a host neutrophilic response. This fails to eliminate the bacteria, and the large concentration of host-derived protease may contribute to
Inhaled hyperosmolar agents for bronchiectasis.
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BACKGROUND
Mucus retention in the lungs is a prominent feature of bronchiectasis. The stagnant mucus becomes chronically colonised with bacteria, which elicit a host neutrophilic response. This fails to eliminate the bacteria, and the large concentration of host-derived protease may contribute to
Inhaled hyperosmolar agents for bronchiectasis.
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BACKGROUND
Mucus retention in the lungs is a prominent feature of bronchiectasis. The stagnant mucus becomes chronically colonised with bacteria, which elicit a host neutrophilic response. This fails to eliminate the bacteria, and the large concentration of host-derived protease may contribute to
The biochemical pathogenesis of chronic obstructive pulmonary diseases: protease-antiprotease imbalance in emphysema and diseases of the airways.
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Emphysema is believed to result from destruction of elastic fibers due to an imbalance between proteases and their inhibitors in the lung. The imbalance can arise from a primary failure of secretion of the inhibitors, as occurs in hereditary alpha-1-protease inhibitor deficiency, or as the result of
Inhaled hyperosmolar agents for bronchiectasis.
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BACKGROUND
Mucus retention in the lungs is a prominent feature of bronchiectasis. The stagnant mucus becomes chronically colonised with bacteria, which elicit a host neutrophilic response. This fails to eliminate the bacteria, and the large concentration of host-derived protease may contribute to
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