Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inhalation treatment of silicosis with polyvinyl-pyridine-oxide of molecule weight about 90,000 under the name Kexiping is the most perspective method at the moment for etiological effect of the silicotic fibrosis. The authors performed two 6-week inhalation course with interval of 6 months with 38 ill with silicosis. The daily dose 10 ml of 4% solution of Kexiping "Bayer". The first results alone and in comparison with the control group of 50 patients are very encouraging. The tolerance to the preparation is excellent, with no side effects or unfavourable deviations in the paraclinical indices. Further extensive, therapeutic applications and inhalation prophylaxis with healthy persons subject to high dust risk are completely justified. For final evaluation of the long-term effect a continuous observation of both treated and controls is necessary.
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PMID:[Inhalation treatment of silicosis with Kexiping]. 263 9

Effects of silica, diamond dust, and carrageenan on mouse macrophages were studied by phase-contrast cine-micrography, electron microscopy, histochemical techniques for lysosomal enzymes and measurements of the release of lysosomal enzymes into the culture medium. All added materials were rapidly taken up into phagosomes, to which lysosomes became attached. In all cases lysosomal enzymes were discharged into the phagosomes to form secondary lysosomes. Within 24 hr most of the silica particles and enzyme had escaped from the secondary lysosomes and lysosomal enzymes were found in the culture media. Most macrophages were killed by this time. With nontoxic particles (diamond dust, aluminium-coated silica, or silica in the presence of the protective agent polyvinyl-pyridine-N-oxide, PVPNO) ingested particles and lysosomal enzymes were retained within the secondary lysosomes for a much longer time, and cytotoxic effects were considerably delayed or absent altogether. It is concluded that silica particles are toxic because they are efficiently taken up by macrophages and can then react relatively rapidly with the membranes surrounding the secondary lysosomes. The particles and lytic enzymes can then escape into the cytoplasm, producing general damage, and thence into the culture medium. It is suggested that hydrogen bonding of silicic acid with lipid and protein constituents of the membrane accounts for the induced permeability. Protective agents such as PVPNO are retamed in lysosomes and preferentially form hydrogen bonds with silicic acid. Carrageenan is demonstrable within macrophages by its metachromatic reaction. It brings about release of enzymes from secondary lysosomes, but much more slowly than does silica. Silica released from killed macrophages is as cytotoxic as the original preparation. It is suggested that repeated cycles of macrophage killing in vivo leads to the mobilization of fibroblasts and fibrogenesis characterizing the disease silicosis.
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PMID:An examination of the cytotoxic effects of silica on macrophages. 428 9

Silica-induced lung injury and the development of silicosis is one of the major occupational diseases. Accumulation and deposition of respirable dust containing silica mineral particles in the lung produces chronic lung disease characterized by granulomatous and fibrotic lesions. Knowledge of precise mechanisms, which induce this process is still limited, hence problems faced in the treatment of silicosis, especially the casual one. This article describes various trials of casual silicosis treatment with tetrandrine (Tet), isolated from the root of Stephania tetrandra, tumor necrosis factor (TNF) antagonists, polyvinyl-pyridine-N-oxide (PVNO), aluminum compounds, corticosteroids or bronchoalveolar lavage (BAL). The existing methods are not sufficient, which warrants further investigations. At present, prevention of the disease and treatment of its complications are most important.
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PMID:[Trials of casual treatment of silicosis]. 1712 34