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Pneumoconiosis that pursues a chronic course may result from repeated injury and repair caused by dust particles that remain in the lungs, leading to fibrosis. We will introduce in vivo studies concerning these processes using animals exposed to man-made mineral fibers and asbestos. We will report on whether there are developmental changes with the mineral fiber and animal model in proinflammatory cytokine, chemokine, free radicals, proteinase and other genes that lead to injury, as well as in genes that effect repair such as growth factor, and we will also report on the effects of surfactant protein and clara cell secretory protein on fibrosis.
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Morimoto et al. (2001) studied this question.
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