pneumoconiosis/protease

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[Pneumoconiosis and protease inhibitors (author's transl)].

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[Impaired balance of the lung proteolytic system in patients with pneumoconiosis and chronic dust-induced bronchitis].

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The activity of neutrophilic elastase and the level of its major inhibitor--an alpha 1-inhibitor of proteinases were studied to evaluate the protease-antiprotease system in the bronchoalveolar lavage fluid (BALF) of patients with chronic dust-induced bronchitis (CDB) and pneumoconiosis (PC). It was

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

[Evaluation of matrix metalloproteinases (pro-MMP-1, MMP-2,8) and their inhibitor (TIMP-1) contents in patients with occupational lung diseases].

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Studies of matrix metalloproteinases in patients with occupational bronchopulmonary diseases and in individuals exposed to asbestos dust revealed hyperactivated protease system--lower level of MMP-1 proenzyme and increased production of TIMP-1 (metalloproteinases inhibitor)--in all the examinees

From Coal Mine Dust To Quartz: Mechanisms of Pulmonary Pathogenicity.

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Exposure to coal mine dust or crystalline silica can result in the initiation and progression of interstitial lung disease. Pathogenesis is the consequence of damage to lung cells and resulting lung scarring associated with activation of fibrotic processes. This review presents the radiologic and

[Clinical and pathogenetic features of exposure of workers to antimonate ore].

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A total of 100 miners exposed to antimonate dust concentrations considerably exceeding the MAC were examined, and 16% of the subjects appeared to have chronic bronchitis. No pneumoconioses were diagnosed. The chronic bronchitis was characterized by mild slow course with I degree of ventilation

[Occupational dust exposure and chronic obstructive bronchopulmonary disease. Etiopathogenic approach to the problem of compensation in the mining environment].

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In order to support the hypothesis of a causal relationship between exposure to respirable coal mine dusts and chronic obstructive pulmonary disease (COPD), investigations were performed to assess the biological disorders affecting the distal air spaces in coal workers with pneumoconiosis. Broncho

The pathobiology and epidemiology of human emphysema.

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Emphysema is defined in anatomical terms as enlargement of the gas-exchanging part of the lung (the acinus) accompanied by destruction of respiratory tissue. Emphysema is classified by the way that the acinus is dominantly involved. In proximal acinar emphysema, the proximal part of the

Particles causing lung disease.

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The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of

Why is damage limited to the mucosa in ulcerative colitis but transmural in Crohn's disease?

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It has been a big puzzle as why the inflammation of ulcerative colitis (UC) is limited to the mucosa, while in Crohn's disease (CD) the inflammation is transmural and can be seen in all layers of the gut. Here, I give a tentative explanation extended from the unified hypothesis I proposed on 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

Mechanisms and mediators in coal dust induced toxicity: a review.

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Chronic inhalation of coal dust can cause several lung disorders, including simple coal workers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lung function loss, and emphysema. This review focuses on the cellular actions and interactions of key inflammatory cells and

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