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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to clarify the physiologic and clinical significances of glucocorticoid receptors in bronchoalveolar cells, we measured the glucocorticoid receptor content in bronchoalveolar cells obtained from patients with idiopathic pulmonary fibrosis (IPF), normal volunteers, control patients with localized lung cancer, and a group of patients with pulmonary manifestations associated with collagen-vascular diseases, hypersensitivity pneumonitis, pneumoconiosis, and chronic bronchitis. The contents of glucocorticoid receptors in bronchoalveolar cells from patients with IPF (5,561 +/- 3,741 sites per cell) and various pulmonary diseases (4,452 +/- 2,097 sites per cell) were lower than those in bronchoalveolar cells from normal volunteers (9,970 +/- 4,050 sites per cell) and control patients (8,354 +/- 4,367 sites per cell). Patients with IPF, who had a lower glucocorticoid receptor content in bronchoalveolar cells did not respond to glucocorticoids. On the contrary, the patients with IPF who responded well to glucocorticoids had as much glucocorticoid receptor content in bronchoalveolar cells as normal volunteers had. These results suggested that the content of glucocorticoid receptors in bronchoalveolar cells varies during disorders of the lung, and may be a useful parameter for predicting whether glucocorticoid therapy will be effective in IPF.
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PMID:Glucocorticoid receptors in bronchoalveolar cells from patients with idiopathic pulmonary fibrosis. 718 Dec 37

Based on personal clinical observations in over one hundred cases and the data in the literature, a brief general review of the clinical and biological characteristics of chronic idiopathic fibrogenous interstitial pneumopathy (diffuse idiopathic interstitial fibrosis) is presented. Chief emphasis is placed on functional characteristics (inadequacy of the ventilation/perfusion ratio and disease of the small airways and of the interstitium per se), morphologic considerations, and analysis of bronchoalveolar lavage fluid. Typically the disease runs its course within about 4 years following diagnosis, the evolution being marked by episodes of infection complicating the concurrent respiratory insufficiency. Complications stemming from pre-existing coronary insufficiency or neoplastic transformation can occur in elderly patients. Recent advances have been the result of experimental data, of a better understanding of the biochemical structure of the lung (particularly with respect to the metabolism of collagen) and of cytologic and isotopic investigations, especially iterative bronchoalveolar lavage and gallium scintigraphy. Treatment remains disappointing, however, and principally symptomatic (corticotherapy and azathioprine). In relation to acquired fibrosis (common pneumoconiosis, extrinsic allergic alveolitis, iatrogenic pneumopathy, pulmonary fibrosis secondary to systemic disease) this syndrome represents a distinct, if not unequivocal or specific entity.
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PMID:[Idiopathic fibrogenous interstitial pneumopathy]. 745 55

Serum type III procollagen peptide (PIIIP), a degradation product of the type III collagen precursor, has been put forward as an exposure marker for mineral dust. We evaluated PIIIP levels as a marker of exposure to and effects of coal dust in retired coal miners (n = 104). To this end: (a) the individual cumulative dust exposure was calculated from job-exposure matrices, and (b) in addition to routine chest radiography (CR) of all miners according to the criteria of the International Labour Organisation (ILO), a subgroup (n = 46) was screened by high-resolution computed tomography (HRCT). Profusion score (CR and HRCT) tended to increase with cumulative dust exposure, even in the absence of CR evidence for pneumoconiosis (i.e. CR < or = 0/1, n = 35). In contrast to our previous findings in active miners, PIIIP levels were not increased in miners as compared with non-dust-exposed controls (n = 29), and no differences were observed between miners without (ILO = 0/0) and miners with coal workers' pneumoconiosis (CWP; ILO > or = 0/1). No trend in PIIIP versus pneumoconiosis stage was present, either by CR or by the more sensitive HRCT score. PIIIP was also unrelated to any lung function parameter (FEV1, FVC, impedance, diffusion capacity). Age, medication, medical history and smoking habits had no significant effect on PIIIP levels. In the miners with CWP (i.e. ILO > 0/0, n = 28) a significant negative correlation was present between PIIIP values and (log) cumulative dust exposure. This decrease in serum PIIIP levels with increasing cumulative exposure may be due to chronic adaptive changes in type III collagen deposition and/or breakdown. Other relations between exposure and PIIIP were not observed. In conclusion, the present findings do not support the use of serum type III procollagen peptide as a marker of exposure to and (early) interstitial or respiratory effects of coal dust.
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PMID:Evaluation of serum type III procollagen peptide as an exposure marker in retired coal workers. 778 26

In vitro and in vivo animal studies, as well as human investigations, strongly support the role of macrophage products in the development and progression of silicosis and coal workers' pneumoconiosis. Such products include enzymes and reactive oxygen species which may cause lung damage; cytokines which recruit and/or activate polymorphonuclear leukocytes and thus result in further oxidant damage to the lung; and fibrogenic factors which induce fibroblast proliferation and collagen synthesis. This mechanistic understanding of pulmonary disease should assist in developing strategies for prevention and treatment.
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PMID:How silicosis and coal workers' pneumoconiosis develop--a cellular assessment. 838 79

A 63-year-old stoneworker complained of fever and a productive cough. His chest roentgenogram showed a nodular mass and a diffuse interstitial shadow in the right lung. Angiography of the pulmonary artery revealed obstruction of the right upper trunk. Open-lung biopsy was done. Histologic examination showed mixed-dust pneumoconiosis with a massive focus of mixed-dust fibrosis with silicotic nodules, and diffuse interstitial fibrosis of pattern with lymphoid infiltration. Chemical analysis revealed a high content of aluminum in lymph node, which was thought to be due to inhalation of alumina used for lettering stones. The unilateral interstitial pneumonia was thought to have developed due to deposition of free silica and aluminum dust. Although this patient had been given a diagnosis of rheumatoid arthritis and the value of rheumatoid factor was high, the interstitial pneumonia was not believed to be associated with the collagen vascular disease.
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PMID:[Unilateral mixed-dust pneumoconiosis with aluminum deposition associated with interstitial pneumonia]. 910 57

Data from autopsies for 200 coal workers were analyzed to study the significance of pleural plaque in diagnosis for pneumoconiosis. Parietal Pleural plaques were found in them. Macroscopically, pleural plaques could be divided into two types, one smooth and the other nodular. Under microscope, typical pleural plaques were composed of a basket-woven, coarse collagen fiber arrayed in parallel, and nodular plaques were collagen fiber arrayed in a folding pattern. Ferruginous bodies could be seen among collagen fiber in the histological sections of pleural plaques. It suggests that corresponding amendement to the national diagnostic criteria for pneumoconiosis is necessary.
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PMID:[Autopsies of five coal workers with pleural plaque]. 981 98

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 target cells in coal dust toxicity and related lung disorders, i.e. macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affecting these cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and related antioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins. Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role of ROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage and remodelling in the respiratory tract. It is recognised that inhaled coal dust particles are important non-cellular and cellular sources of ROS in the lung, and may be significantly involved in the damage of lung target cells as well as important macromolecules including alpha-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of important leukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor (PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-alpha (TNF alpha), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1 (ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production of various factors with potential capacity to modulate lung cells and/or extracellular matrix, including O2-., H2O2, and NO, fibroblast chemoattractants (e.g. Transforming Growth Factor-beta (TGF beta), PDGF, and fibronectin) and a number of factors that have been shown to stimulate and/or inhibit fibroblast growth or collagen production such as (TNF alpha, TGF beta, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact of these factors.
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PMID:Mechanisms and mediators in coal dust induced toxicity: a review. 1002 91

By measuring the activity of telomerase in a silica-instilled rat lung, the study found a significant increase in telomerase activity compared to that of the control. Pneumoconiosis displays the characteristics of fibroblast-proliferation and accumulation of collagen, which finally causes the pathologic changes of irreversible and progressive fibrosis of the lung. On the basis of the hypothesis that cellular proliferation may trigger telomerase-activity, the experiment was carried out with telomerase-activation in silicosis. Silica-instilled rat lungs showed increased activity of telomerase, which was measured by TRAP (telomeric repeat amplification protocol) assay, at the time of the 1st, 5th and 8th week after intratracheal instillation of silica in vivo. However, no activity was shown in silica-co-cultured fibroblast in vitro. By summarizing these results, the activity of telomerase is thought to be a very sensitive marker for the evaluation of pathogenicity, showing cellular immortalization in an experimental silicosis model.
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PMID:Activation of telomerase by silica in rat lung. 1064 71

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 pathophysiological mechanisms remain unclear, it has been established that the lung responds to silica by massive enrollment of alveolar macrophages, triggering an inflammatory cascade of reactions. An imbalance in the expression of lung proteases and their inhibitors is implicated in extracellular matrix remodelling and basement membrane disruption. Moreover, exposure to silica can initiate apoptotic cell death of macrophages. This review summarises the current knowledge on cysteine cathepsins that have been ignored so far during silicosis and outlines the recent progress on cellular pathways leading to silica-induced caspase activation, which have been partly delineated.
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PMID:Cysteine cathepsins and caspases in silicosis. 1691 35

Silicosis is a kind of pneumoconiosis caused by inhalation of silica dust, which is characterized by lung fibrosis. The biologically active form of transforming growth factor-beta1 (TGF-beta1) plays a key role in the development of lung fibrosis. CD36 is involved in the transformation of latent TGF-beta1 (L-TGF-beta1) to active TGF-beta1. The antagonistic effect of the synthetic peptide was analyzed by the administration of CD36 (93-110) synthetic peptide to the silicosis model of mice. The hydroxyproline content of the silica + CD36 (93-110) synthetic peptide group was significantly lower than that of the other experimental groups [silica and silica + CD36 (208-225) synthetic peptide groups] (p < .05). Inflammation, fibrotic degree and distribution of collagen fibers in silicotic nodules of the silica + CD36 (93-110) synthetic peptide group were less than those of the other experimental groups. The expressions of collagen I and III of the silica + CD36 (93-110) synthetic peptide group were significantly lower than those of the other experimental groups (p < .05). CD36 (93-110) synthetic peptide reduced the tissue fibrotic pathologies and collagen accumulation in the silicosis model of mice, resulting in the decreased severity of silica-induced lung fibrosis.
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PMID:A CD36 synthetic peptide inhibits silica-induced lung fibrosis in the mice. 2005 42


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