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Background: Earlier studies conducted by Indian researchers have demonstrated that the elimination of tuberculosis (TB) requires proactive control of silicosis, given India's significant burden of silicosis and its common comorbidity, pulmonary TB, also known as silicotuberculosis. The TB Control Indian Health Authority saw human immunodeficiency virus infection, diabetes, and malnutrition, among others, as important risk factors for case findings, but overlooked the significance of silicosis. Silicotuberculosis control is often confronted with challenges of detecting microorganisms, uncertain treatment outcomes, a higher likelihood of mono-drug and multi-drug resistance, and increased mortality due to treatment failure.

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Silicosis represents a formidable occupational lung pathology precipitated by the pulmonary assimilation of respirable crystalline silica particulates. This condition engenders a cascade of cellular oxidative stress via the activation of bioavailable silica, culminating in the generation of reactive oxygen species (ROS). Such oxidative mechanisms lead to irrevocable pulmonary impairment.

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Pneumoconiosis is the occupational disease with the highest proportion in China. This study conducted a retrospective analysis of 5,791 deceased pneumoconiosis patients. In this study, males comprised 93.

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HMGB1 mediates epithelial-mesenchymal transition and fibrosis in silicosis via RAGE/β-catenin signaling.

Chem Biol Interact

January 2025

Hebei Key Laboratory of Organ Fibrosis, School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, China. Electronic address:

Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of silicosis. High mobility group box 1 (HMGB1) has been found to induce EMT in fibrotic diseases. Previous studies have revealed a critical role of HMGB1 in silicosis, whereas the detail mechanisms still obscure.

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Inhalation of crystalline silica particles causes silicosis, which is a severe inflammatory lung disease that is associated with granulomatous and fibrotic responses. We investigated whether silica-induced silicosis might promote airway hyperreactivity (AHR) and the role of TNF-α and thalidomide in this process. Mice received an intranasal instillation of silica particles (1.

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