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Página 1 a partir de 22 resultados
[Changes in serum protease and cytokine in patients with silicosis, tuberculosis, and lung cancer].
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OBJECTIVE
To investigate the changes in serum protease and cytokine in patients with silicosis, tuberculosis, and lung cancer.
METHODS
Serum samples of patients with silicosis, tuberculosis, and lung cancer were collected. The variation trends of the expression of granzyme A, cathepsin G,
An attempt to evaluate lung aggression in monkey silicosis: hydrolases, peroxidase and antiproteases activities in serial bronchoalveolar lavages.
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Exposure to silica can induce fibrosis and/or emphysema. Various factors such as proteases, other hydrolases and oxidants may be involved in the destruction of lung parenchyma. On the other hand, antiproteases play an important role in the protection of lung parenchyma against the action of
[Status of the protease inhibitor system in patients with dust-induced lung diseases].
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Investigation of protease inhibitors in the blood of silicosis and dust bronchitis patients revealed disbalance in the silicosis cases which manifested itself in growing elastase activity against normal protease inhibitors content--alpha 1 antitrypsin and alpha 2 macroglobuline. Meanwhile the
Application of protein chip combined with SELDI-TOF-MS detection to investigate serum protein expression in patients with silicosis fibrosis.
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The present study aimed to observe the identification of biomarkers of silicosis based on the differentially expressed serum proteins between normal healthy individuals and patients with silicosis fibrosis. A total number of 20 patients with clinically diagnosed silicosis were screened, which were
[Discovery of novel protein biomarkers in early silicosis by proteomics and identification of alpha B-crystallin].
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OBJECTIVE
To establish 2-dimensional gel electrophoresis (2-DE) image for the early lung injury rats induced by silica dioxide and to identify differentially expressed protein biomarkers during the early stage of silicosis.
METHODS
The animal models of silicosis were established and morphology
Comparison of hydrolases, peroxidase and protease inhibitors in bronchoalveolar fluid from Macacus cynomolgus and human controls.
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1. Serial bronchoalveolar lavages were performed on a subhuman primate (Macacus cynomolgus) in order to give an experimental model for silicosis. 2. We have measured glycosidases, proteases, peroxidase and antiproteases of the BAL fluids from seven normal monkeys. 3. The results obtained were
Involvement of the ICE family of proteases in silica-induced apoptosis in human alveolar macrophages.
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Exposure to silica dust can result in lung inflammation that may progress to fibrosis for which there is no effective clinical treatment. The mechanisms involved in the development of pulmonary silicosis have not been well defined; however, most current evidence implicates a central role for
Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.
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Previous study strongly suggests that silicotic fibrosis is mediated by macrophages and their soluble mediators. The biochemical properties of the mediators involved in silicotic fibrosis, however, are as yet ill defined. The current study, therefore, determined whether human monocyte-macrophages
Transforming growth factor-beta (TGF-beta) in silicosis.
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Silicosis is characterized by fibrosing nodular lesions that may eventually develop into progressive massive fibrosis (PMF). Cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha] and growth factors insulin-like growth factor-1 [IGF-1] platelet-derived growth factor [PDGF])
Proteomic profiling change during the early development of silicosis disease.
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BACKGROUND
Silicosis is one of several severe occupational diseases for which effective diagnostic tools during early development are currently unavailable. In this study we focused on proteomic profiling during the early stages of silicosis to investigate the pathophysiology and identify the
Cysteine cathepsins and caspases in silicosis.
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Silicosis is an occupational pneumoconiosis caused by inhalation of crystalline silica. It leads to the formation of fibrohyalin nodes that result in progressive fibrosis. Alternatively, emphysema may occur, with abnormal destruction of collagen fibres in the advanced stages. Although the
Silicosis and coal workers' pneumoconiosis.
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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by
Suppressive effects of Stephania tetrandra on the neutrophil function in patients with rheumatoid arthritis.
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Crude preparations of Stephania tetrandra (ST), a traditional herbal medicine, have been used safely for arthritis and silicosis in China. The concentration of granulocyte elastase - alpha 1 protease inhibitor complex in plasma is enhanced in inflammatory processes, e.g. in septicaemia and
The specific chymase inhibitor TY-51469 suppresses the accumulation of neutrophils in the lung and reduces silica-induced pulmonary fibrosis in mice.
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Chymase is a chymotrypsin-like serine protease that is present in mast cells. Its activities include various effects associated with inflammatory responses. But little is known about the effects of chymase in pulmonary fibrosis. The mouse silicosis model was induced by intratracheal injection of 10
Dose-response thresholds for progressive diseases.
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Many diseases, including cancers, heart diseases, and lung diseases, can usefully be viewed as arising from disruption of feedback control systems that normally maintain homeostasis of tissues and cell populations. Excessive exposure can destabilize feedback control loops, leading to sustained
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