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pulmonary edema/protease
Veza se sprema u međuspremnik
Stranica 1 iz 60 rezultatima
Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.
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Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different
Use of a protease inhibitor, ulinastatin, for reexpansion pulmonary edema following evacuation of bilateral pleural effusion.
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A study on the protective effect of bromelain, crude pineapple proteases, against adrenaline-induced pulmonary edema in rats.
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HIV protease inhibitors that block GLUT4 precipitate acute, decompensated heart failure in a mouse model of dilated cardiomyopathy.
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The clinical use of HIV protease inhibitors is associated with insulin resistance and other metabolic changes that increase long-term cardiovascular risk. Since the failing heart has increased reliance on glucose, the influence of drug exposure on glucose homeostasis, myocardial glucose uptake,
High-altitude pulmonary edema. Characteristics of lung lavage fluid.
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To evaluate the cellular and biochemical composition of bronchoalveolar fluid in high-altitude pulmonary edema (HAPE), we performed bronchoalveolar lavage in three climbers with HAPE in a research facility at 4400 m on Mount McKinley. Three healthy climbers were used as controls. The HAPE fluids
Importance of serratia protease in the pathogenesis of experimental Serratia marcescens pneumonia.
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The results of studies to evaluate the possible importance of serratia proteases in the development of experimental Serratia marcescens pneumonia revealed the following. (i) Administration of a highly purified serratia protease to the lungs of guinea pigs and mice resulted in extensive pulmonary
Lung injury produced by pancreatic proteases in dogs.
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With an isolated, blood-perfused canine lung-lobe preparation, the potential role of reactive oxygen metabolites and neutrophils in pancreatic protease (alpha-chymotrypsin)-induced acute lung injury was studied. Administration of alpha-chymotrypsin caused a low-pressure pulmonary edema (mean lung
Acute pulmonary edema associated with transfusion of packed red blood cells.
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We experienced a patient who suffered noncardiogenic acute pulmonary edema after transfusion of packed red blood cells which contained antigranulocyte antibodies. The data suggested that complement activation and the release of polymorphonuclear protease were involved in the pathogenesis of the
Selected contribution: limiting Na(+) transport rate in airway epithelia from alpha-ENaC transgenic mice: a model for pulmonary edema.
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The amiloride-sensitive epithelial Na(+) channel (ENaC) is essential for fluid clearance from the airways. An experimental animal model with a reduced expression of ENaC, the alpha-ENaC transgenic rescue mouse, is prone to develop edema under hypoxia exposure. This strongly suggests an involvement
Changes in factor VII-activating protease in a bleomycin-induced lung injury rat model and its influence on human pulmonary fibroblasts in vitro.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by non-cardiogenic pulmonary edema, respiratory distress and hypoxemia. Factor VII-activating protease (FSAP) is a plasma-derived protease which inhibits the proliferation and migration of hepatic stellate cells
[Usefulness of a protease inhibitor (urinastatin) in ARDS with infectious diseases].
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The usefulness of urinastatin (UST) for adult respiratory distress syndrome (ARDS) induced by gram-negative sepsis was evaluated in clinical and experimental studies. Twelve cases of clinical septic ARDS were treated with combination therapy of UST and methylprednisolone (M-PSL). Ten out of 12
Protease-activated receptor-2 activation induces acute lung inflammation by neuropeptide-dependent mechanisms.
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Protease-activated receptors (PARs) and tachykinin-immunoreactive fibers are located in the lung as sentries to respond to a variety of pathological stimuli. The effects of PAR activation on the lung have not been adequately studied. We report on the effects of instilling PAR-activating peptides
Raised protein levels and altered cellular expression of factor VII activating protease (FSAP) in the lungs of patients with acute respiratory distress syndrome (ARDS).
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BACKGROUND
The acute respiratory distress syndrome (ARDS) is characterised by inflammation of the lung parenchyma and changes in alveolar haemostasis with extravascular fibrin deposition. Factor VII activating protease (FSAP) is a recently described serine protease in plasma and tissues known to be
[Non-cardiac pulmonary edema: an enigma today].
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Pulmonary oedema is caused by an excessive accumulation of interstitial fluid in the lungs: in the case of left ventricular failure, oedema arises due to an increase in capillary hydrostatic pressure. Non-cardiac oedema, on the other hand, is brought about by a change in alveolar capillary membrane
Contribution of vasopressor and plasma kininogen changes towards acute adrenaline pulmonary edema in the rat.
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Acute pulmonary edema, evidenced by increased lung/body weight ratios, was evoked in rats within 5 min following the intravenous injection of 16-40 mug/kg of adrenaline. This change was accompanied by a decrease of 40% of circulatory kininogen not due to generalized plasma protein loss. Rats treated
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