Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Badger lungs contain dark granular foci (0.2 to 2.0 mm) comprising aggregates of enlarged macrophages containing birefringent crystalline particles. Particles were examined from the lungs of three badgers; many were silicates and a significant number were pure silica (SiO2). The particles and the accompanying pathology resembled mixed dust fibrosis and silicosis in humans, diseases associated with increased susceptibility to tuberculosis.
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PMID:Environmental silica in badger lungs: a possible association with susceptibility to Mycobacterium bovis infection. 298 23

Aims of our study were: to evaluate small airway function of subjects with past or present silica dust exposure and normal spirometric values; to investigate whether small airway disease is related to radiographic signs of silicosis, to cumulative dust exposure (ES) and to cigarette smoking. Maximal expiratory flow at 50% (MEF50) and 25% (MEF25) of forced expired vital capacity were measured in 112 subjects, 69 with radiographic signs of silicosis, group I, and the remaining 43 with normal chest X-rays. Even if age and ES were significantly higher in group I, no significant difference in respiratory function tests and in prevalence of small airway disease was found between the two groups. In both groups small airway function was significantly negatively related to smoking habits, while it was independent of the other variables considered. Multiple regression analysis with MEF50 and MEF25 as dependent variables did not show any significant relationship. We conclude that small airway disease due to encroachment of bronchiolar walls by SiO2 deposition is masqued by the damage produced by cigarette smoking, even in the presence of radiographic signs of silicosis.
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PMID:[Functional compromise of the small airways in subjects exposed to SiO2]. 302 80

The retrospective evaluation of 472 judgements of professional disease in persons exposed to dusts showed that all observed restrictions of cardio-pulmonary function (obstructive lung disease, increase of residual volume, respiratory failure, pulmonary hypertension) occurred almost independently from the presence and stage of silicosis, but correlated first of all with the duration of exposure. Frequency and degree of functional disorders in exposed persons without radiologically demonstrable silicosis indicate that the fraction of nonspecific dusts, which is by far larger than the SiO2-fraction, produces chronic obstructive lung disease and its sequelae (emphysema, pulmonary hypertension). The term "pneumoconiosis" should therefore be used in a much broader sense than hitherto. This leads to considerations of the present practice of judgement on silicosis which are presented and discussed in detail.
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PMID:[Interpretation of pneumoconiosis--results of cardiopulmonary function tests in dust-exposed patients with and without silicosis]. 401 1

Antiserum against the fibrogenesis controlling macrophage RNase was produced in rabbits. It caused an inhibition of 57% in the RNase activity in vitro. A distinct dose-response relationship was observed in the inhibiting effect of the antiserum on RNase-induced 3H-thymidine incorporation into cultured granulation-tissue fibroblasts. The antifibrogenic properties of the antiserum were also tested in vivo. Rat lungs were made silicotic by intratracheal administration of SiO2. This treatment clearly increased the following parameters: wet weight, DNA, RNA, nitrogen and hydroxyproline content of the lung tissue, and protein concentration, RNase activity, and cell count of the lung lavage fluid. Also, the RNase activity of the lavage fluid cells was increased. Periodical intratracheal administration of the anti-RNase antiserum, optimally at 1:1,000 dilution, decreased the DNA, RNA, and hydroxyproline content of the lung tissue, each by about 30%. The RNase activity of lavage fluid cells was decreased by about 60%. In conclusion the antiserum had no effect on the normal lungs, but it significantly suppressed the development of silicosis.
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PMID:Antifibrogenic effects of antiserum against the macrophage RNase. 683 34

Sterile saline was instilled into and aspirated from the lung of dust-exposed rabbits in imitation of clinical method of the whole-lung lavage. The changes of the biochemical and cellular components in alveolar fluid were observed before and after lavage with a view to providing evidence for the applicability of the method in the treatment of silicosis. The results showed that the number of cells, the protein content and the activities of both LDH and AKP were significantly lower than those of control group, except the total phospholipid and dipalmityl phosphatidyl choline (DPPC) in alveolar fluid after lavage. A certain amount of dust was also removed from lung with lavage. The wash-out of SiO2 from the first lavage was higher than that of the second lavage. It is suggested that lavage might delay the development of silicosis and be more effective in early stages of silicosis.
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PMID:[Experimental studies on the therapeutic effects of lung lavage with large volume of saline on silicosis]. 1032 5

The authors verify whether in silicosis the accumulation of silicon dioxide (SiO2) particles in the lung can induce changes of the activated T lymphocytes in the peripheral blood. The lymphoblastic transformation of lymphocytes stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), Mycobacterium tuberculosis (Mt) and purified protein derivative (PPD) was studied using the classical methods. It was observed that in patients exposed to SiO2 lymphocyte reactivity to the above stimulants decreases. Significant differences between patients and controls were observed only in the response to PHA (p < 0.001).
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PMID:Value of the lymphoblastic transformation in patients with silicosis. 1066 Sep 71

This work presents the concentrations dynamics of dust in a cast iron foundry, in parallel with the frequency and gravity dynamics of the getting sick of silicosis. The knowing of the real risk of exposure to silicotic dust was possible through the data processing concerning the dusting degree (the average of working place), the content of silicon free-crystalline dioxide (SiO2 l.c.) for the calculation of the maximum admitted concentration (C.M.A.) and the dispersion degree of dust in a cast iron and steel foundry for the studied period (1982-1996). New cases of silicosis appeared in this period were studied and they were colligated with the age at declaration, the average length of service and the profession. The values of the dusting degree outrun the C.M.A. up to 168 times, especially at the preparation of mixture and grinding with a prevalence of particles under 3 micron (40-70%) and the Si02 l.c. content varies between 35.2% and 64.5%. From those 98 new cases of silicosis appeared in 15 years, 82.65% were traced out in the incipient phases of the disease. The average age in service and the average age increase (43.1 respective 19.8 years). The coefficients of correlation and regress (+0.286 respective +0.383) show a good correlation between the silicosis number and the age in service. The advanced stages of silicosis and age in service under 10 years were found at the foundry-workers and formators, occupations which imply a high silicotic risk. The foretelling calculations for the next 20 years show an increase of the silicosis incidence for foundry-workers.
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PMID:[The dynamics of exposure to silicotic dusts and silicosis in a foundry]. 1075 97

Long-term exposure to silica (SiO2) may induce silicosis as well as extrapulmonary diseases such as scleroderma. Infiltration of mononuclear cells and release of proinflammatory cytokines from these cells have been suggested to play a role in the development of inflammatory and immunological events typical of scleroderma as well as of silica-induced scleroderma. We showed that silica is able to directly activate cytokine expression in blood monocytes, collagenase expression in cultured dermal fibroblasts and ICAM-1 expression in human dermal microvascular endothelial cells. In the study reported here we found that silica and TNFalpha induce mRNA and protein of the chemokines RANTES and MCP-1 in endothelial cells. In addition, we demonstrated that culture supernatants of silica-treated endothelial cells are chemotactic for mononuclear cells from peripheral blood, suggesting that activation of endothelial cells may contribute to the chemotactic gradient necessary for extravasation of inflammatory blood cells into the surrounding tissue found in early scleroderma. However, a polyclonal anti-RANTES antibody failed to block chemotaxis suggesting that other proteins are involved in this phenomenon. We also studied the expression of RANTES in situ in the skin of systemic sclerosis patients and of healthy individuals. We found abundant RANTES mRNA expression in the skin of SSc patients, whereas in control skin no expression was found. From our data we conclude that RANTES and MCP-1 induction by silica may be an initiating event in inflammatory infiltration, whereas TNFalpha-mediated inflammation may propagate the disease more efficiently.
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PMID:Chemokine release from activated human dermal microvascular endothelial cells--implications for the pathophysiology of scleroderma? 1096 58

The 'Sendzimir' Steel Mill, Cracow, Poland, gives employment to approximately 17,000 workers. During the years 1994-98, 1396 compensation claims for diseases related to occupational hazards were registered. After a scrupulous investigation, 851 cases were certified as occupation-related diseases. Of this number, 481 cases (56.5%) were diagnosed as pulmonary diseases, including silicosis (n = 225, 46.7%); chronic bronchitis (n = 138, 28.7%); lung carcinoma (n = 59, 12.3%); epithelial cancer (n = 42); adenocarcinoma (n = 12); microcellular carcinoma (n = 5); asthma, 12 atopic and 24 non-atopic (n = 36, 7.5%); and asbestosis (n = 23, 4.8%). Chronic bronchitis was diagnosed in patients exposed to industrial dusts, containing SiO2, NOx, and SO2. Asthma occurred most frequently among those exposed mainly to Cr+6, Co and Ni containing dusts, and lung carcinoma in those exposed to policyclic aromatic hydrocarbons, including benz(a)pyren, asbestos, chromium, vapours of oils and lubricants. In 1994-96, chronic bronchitis and silicosis, and in 1997-98, lung carcinoma and asthma were most frequently diagnosed in the workers under study. It is likely that the diminishing frequency of chronic bronchitis and silicosis was the consequence of technological progress, and greater concern for hygiene standards. Increasing incidence of lung cancer reflects long latency characteristic of this illness.
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PMID:Occurrence of pulmonary diseases in steel mill workers. 1096 40

Effects of poly-2-vinylpyridine-N-oxide (PVNO) were investigated in numerous in vivo and in vitro studies published in the nineteen sixties and seventies. These studies showed that PVNO inhibited development of fibrosis from quartz dust and improved lung clearance of quartz after inhalation exposure. Ameliorating effects of PVNO were observed also for pulmonary damage from colloidal SiO2 and organic substances, and the fibrogenic inflammation caused by carrageenan. Although it is not proven that silicosis is a precondition for quartz-induced lung tumours, we investigated the hypothesis that PVNO could reduce the lung tumour risk from quartz in rats. A carcinogenicity study was therefore started in rats with the main focus on the quantitative relationships among pulmonary inflammation, fibrosis and neoplasia caused by intratracheal instillation of 3 mg quartz DQ 12 with or without additional subcutaneous PVNO treatment. Other study groups were treated with multiple dust instillations, i.e. 30 instillations of 0.5 mg amorphous SiO2 at intervals of 2 weeks, 10 instillations of 0.5 mg of ultrafine carbon black or 1 mg coal at weekly intervals. The analyses of the bronchoalveolar lavage fluid (BALF) 9 months after start of the life-time study showed that the aim of producing similar levels of increased enzyme concentrations in the four groups treated with quartz/PVNO, amorphous SiO2, carbon black and coal was achieved. A 2.5- to 7.7-fold increase for lactate dehydrogenase (LDH), total protein, alkaline phosphatase and gamma-glutamyl transferase (gamma-GT) was found in these groups as compared to the control. In contrast, quartz treatment without PVNO increased the LDH level up to 24-fold and of total protein to 13-fold. However, the cell counts in the BALF were not so much different in all five groups, i.e. quartz without PVNO (leukocytes: 480.000, PMN: 190.000), quartz with PVNO (leukocytes: 300.000, PMN: 100.000), amorphous SiO2 (leukocytes: 570.000, PMN: 315.000), carbon black (leukocytes: 390.000, PMN: 150.000) and coal (leukocytes: 200.000, PMN: 65.000). Histopathological investigations after four weeks and three months revealed that the used PVNO sample was active in the quartz and amorphous SiO2 groups and markedly reduced the incidences or severity of several pulmonary changes such as macrophage accumulation, inflammatory cell infiltration, interstitial fibrosis, bronchiolo-alveolar hyperplasia, alveolar lipoproteinosis and amorphous SiO2 -induced granulomatous alveolitis/interstitial fibrotic granulomas. Also in the lung-associated lymph nodes (LALN), PVNO treatment significantly reduced the incidence and severity of inflammation in both quartz and amorphous SiO2 groups as evidenced by the presence of well-circumscribed aggregates of intact particle-laden macrophages without signs of degeneration and accompanying granulocytic infiltration and fibrosis. Immunological investigations at the 9 months timepoint on the in vitro production of reactive nitrogen (RNI) or oxygen (ROI) intermediates and tumour necrosis factor (TNF-alpha) from BALF-derived cells indicated a diminished responsiveness to LPS in all particle treatment groups. A diminished production of ROI was also found in the quartz, carbon black, and coal dust groups, respectively, as compared to the values seen in the quartz/PVNO- and amorphous SiO2 treated groups. Treatment with quartz plus PVNO restored the capability of the cells to respond to LPS as compared to the treatment with quartz alone. TNF-alpha production was diminished in the groups treated with quartz, carbon black, and coal dust alone whereas in the quartz/PVNO- and amorphous SiO2-treated groups an elevated TNF-alpha production was seen. These results led to the conclusion that only amorphous SiO2 did not affect the "normal" ability of the cells to respond to LPS and that PVNO protected the cells from a toxic effect of the quartz particles.
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PMID:Pulmonary inflammation in rats after intratracheal instillation of quartz, amorphous SiO2, carbon black, and coal dust and the influence of poly-2-vinylpyridine-N-oxide (PVNO). 1221 32


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