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11 resultats
Low levels of functional of alpha 1-proteinase inhibitor in the promotion of C3-cleavage by granulocyte-neutral proteases in pleural empyema.
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It has been suggested that C3 breakdown by granulocyte-neutral proteases in pleural empyemas may be related to a decreased inhibitor potential for these enzymes. In the present study it was shown that in 17 infected pleural effusions, high proteolytic activity on 125I-labeled C3 (16.3% +/- 4.4%)
Cleavage of C3 by neutral proteases from granulocytes in pleural empyema.
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The possibility of direct inactivation of C3 by granular enzymes from polymorphonuclear leukocytes (PMNLs) in pleural empyema was examined. As a group, pleural empyema from 10 patients with purulent effusions and a positive bacteriologic culture cleaved significantly more 125I-labeled C3 bound to
Alveolar epithelial injury and pleural empyema in acute P. aeruginosa pneumonia in anesthetized rabbits.
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We developed an experimental model of acute Pseudomonas aeruginosa pneumonia in anesthetized ventilated rabbits to determine whether bacterial-induced injury to the alveolar epithelium would occur and the effect of the injury on the pleural space. Dose-response studies established that 10(9)
Clinical implications and characterization of Group A Streptoccoccus infections in adults with cystic fibrosis.
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BACKGROUND
Persistent airway infection is a hallmark feature of cystic fibrosis (CF). However, increasingly it has been observed that non-classical pathogens may transiently infect CF lower airways. Streptococcus pyogenes (Group A Streptococcus; (GAS)) is an uncommon but potentially dangerous cause
Proteomic Analyses of Chlorhexidine Tolerance Mechanisms in Delftia acidovorans Biofilms.
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Protein expression and fatty acid profiles of biofilm cells of chlorhexidine-tolerant Delftia acidovorans (MIC = 15 µg/ml) and its chlorhexidine-susceptible mutant (MIC = 1 µg/ml) were investigated. The chlorhexidine-susceptible mutant (MT51) was derived from the parental strain (WT15) using Tn5
Extensive heterogeneity of human urokinase, as detected by two-dimensional mapping.
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Urokinase (uPA, urinary plasminogen activator) is a serine protease belonging to the peptidase S1 family. Specifically, uPA cleaves the zymogen plasminogen into the active form (plasmin), which then degrades the fibrin clots. It is widely used as a fibrinolytic agent in thrombolytic therapy and it
The thoracic surgeon's role in the management of patients with HIV infection and AIDS.
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The advent of improved medical therapy with multidrug HIV medicines including protease inhibitors has prolonged life expectation of patients with HIV infection. The risk of perinatal transmission has also decreased with education and antiviral medications. Education of all groups about precautions
The contribution of factor V to the coagulant property of pleural fluid.
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Intrapleural fibrin deposition commonly accompanies pleural injury and may contribute to the organization of exudative pleural effusions, which leads to lung entrapment. Previous investigators have observed an increase in procoagulant proteins in pleural effusions but very little thrombin formation.
Pathophysiology of pleural space infections.
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The pleura responds to the presence of infecting organisms with a vigorous inflammatory response associated with an exudation of white blood cells and proteins. Changes in pleural permeability lead to formation of an exudative pleural effusion. The pleural mesothelial cell is the primary cell lining
Mesomesenchymal transition of pleural mesothelial cells is PI3K and NF-κB dependent.
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Pleural organization follows acute injury and is characterized by pleural fibrosis, which may involve the visceral and parietal pleural surfaces. This process affects patients with complicated parapneumonic pleural effusions, empyema, and other pleural diseases prone to pleural fibrosis and
Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease
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Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution
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