asbestosis/phosphatase

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[Pathological observation of experimental asbestosis treated by hydroxy piperquin phosphate in dogs].

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The paper presents experimental asbestosis treated with hydroxy piperquin phosphate (HPQP) in dogs. Results showed that the total cell number of bronchoalveolar lavage fluid, the viability of alveolar macrophages and the enzyme activities of lactate dehydrogenase, acid phosphatase and

Inhibition of lung injury, inflammation, and interstitial pulmonary fibrosis by polyethylene glycol-conjugated catalase in a rapid inhalation model of asbestosis.

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Several in vitro studies suggest the involvement of active oxygen metabolites in cell damage caused by asbestos. To determine if lung injury, inflammation, and asbestosis could be inhibited in vivo in a rapid-onset, inhalation model of disease, a novel method of chronic administration of antioxidant

Development and characterization of a rapid-onset rodent inhalation model of asbestosis for disease prevention.

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A short-term inhalation model of asbestosis was developed in rodents to examine possible preventive approaches to lung disease. Fischer 344 (F344) rats were exposed for 10 and 20 days to National Institute of Environmental Health Sciences (NIEHS) crocidolite asbestos while sham controls were exposed

Enzyme activities of lung lavage in asbestosis.

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We analyzed lung lavage supernatant for amylase, lactate dehydrogenase (LD), alkaline phosphatase (ALP), beta-glucuronidase (beta G), and albumin, and a differential count was made of the cellular component of lung lavage in 18 normal controls and 36 long-term asbestos workers of the mines and mills

Asbestos-induced MKP-3 expression augments TNF-alpha gene expression in human monocytes.

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TNF-alpha is associated with the development of interstitial fibrosis. We have demonstrated that the p38 mitogen-activated protein (MAP) kinase regulates TNF-alpha expression in monocytes exposed to asbestos. In this report, we asked if extracellular signal-regulated kinase (ERK) was also involved

Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways.

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Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is

Biochemical mechanisms in asbestos toxicity.

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The alarming hazardous nature of asbestos makes it the foremost among toxic fugitive dusts. The biochemical mechanisms responsible for the diverse biological effects of asbestos, such as fibrosis, asbestos bodies, pleural plaques, respiratory difficulty, cancer, and cytotoxicity, are being studied

Approaches to prevention of asbestos-induced lung disease using polyethylene glycol (PEG)-conjugated catalase.

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Asbestos-associated damage to cells of the respiratory tract in vitro can be prevented by the simultaneous addition of scavengers of active oxygen species to cultures. To determine if administration of scavenger enzymes to animals and humans is a plausible approach to the prevention of

Soluble mesothelin-related protein in malignant pleural mesothelioma.

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OBJECTIVE Building-up evidence suggests that soluble mesothelinrelated protein (SMRP) carries a diagnostic and a prognostic value in malignant pleural mesothelioma (MPM). Egypt suffers endemic asbestosis and thus this study was conducted to evaluate the sensitivity and specificity of SMRP in

Functional inactivation of NF2/merlin in human mesothelioma.

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The tumor suppressor merlin is encoded by the neurofibromatosis type 2 gene (NF2) which is located on chromosome 22q12 and mutations in this gene have been found in 40% of mesothelioma. Mutations including deletions and insertions lead to truncated and inactivated merlin. Experimental animal models

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