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Abbreviations: AM = alveolar macrophage; AP-1 = activator protein-1; IFN = interferon; IL = interleukin; iNOS = inducible nitric oxide synthase; MCP = monocyte chemotactic protein; NF-[Kappa]B = nuclear factor-[Kappa]B; PMA = phorbol myristate acetate; RPA = ribonuclease protection assay; (CHEST 2001; 120:24S-25S)

Exposure to silica or asbestos elicits a striking inflammatory response that is characterized by the influx of inflammatory cells, increased expression of inflammatory cytokines, cell injury, and compensatory cell proliferation.[1] The regulation of these events may be dependent on the activation of transcription factors such as nuclear factor-[Kappa]B (NF-[Kappa]B) and/or activator protein-1 (AP-1) since the promoter regions of many genes involved in inflammation, proliferation, and/or apoptosis are known to contain binding sites for these transcription factors.[2,3] Previous work from this laboratory has demonstrated increased AP-1 binding to DNA and AP-1-dependent gene transcription in mesothelial cells and tracheal epithelial cells after exposure to asbestos in vitro.[4,5] We and others[6,7] also have shown that asbestos causes NF-[Kappa]B activation in these cell types in vitro and in an inhalation model of asbestosis. However, whether silica causes transcriptional activation of NF-[Kappa]B and AP-1-dependent gene expression in the lung after exposures in vivo is unclear.

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