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1  the development of the chronic lung disease silicosis.
2 e different pathologies of asbestosis versus silicosis.
3 of silica particles causes lung fibrosis and silicosis.
4 e in innate immunity and the pathogenesis of silicosis.
5 plate in drug discovery for the treatment of silicosis.
6 affect pathological features of experimental silicosis.
7 genesis of gouty arthritis, Alzheimer's, and silicosis.
8  alpha (TNFalpha) is a prominent mediator in silicosis.
9 ho), which included all subjects with severe silicosis.
10 nt NO-mediated apoptosis in the evolution of silicosis.
11 mediate apoptosis and inflammation in murine silicosis.
12 play an important role in the development of silicosis.
13 had progressive massive fibrosis, and 11 had silicosis.
14 iated with matrix deposition and fibrosis in silicosis.
15 d to play a critical role in the etiology of silicosis.
16 f Ac-Tub-alpha may be a new mechanism in rat silicosis; 2) treatment of silicotic rats with N-acetyl-
17 k of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA sta
18  of silica-containing dust particles induces silicosis, an inflammatory disease of the lungs characte
19 c exposure to crystalline silica (CS) causes silicosis, an irreversible lung inflammatory disease tha
20 ure to silica can lead to the development of silicosis, an irreversible, fibrotic pulmonary disease.
21 thological changes that strongly mimic human silicosis, an occupational lung disease marked by restri
22 the progressive pulmonary fibrotic disorders silicosis and asbestosis, respectively.
23  differences between miners with less severe silicosis and controls at any loci in the TNF-alpha prom
24 f collagen/reticulin fibers was increased in silicosis and correlated with the V(v) of bFGF(+) cells
25 ent of immunotherapeutic strategies to fight silicosis and lung cancer.
26 d, many of which had features of accelerated silicosis and mixed dust lesions.
27 ial sensitivity to detect active fibrosis in silicosis and other lung diseases.
28 re observed with increased radon exposure in silicosis and pulmonary fibrosis mortality and in the in
29 between apoptosis and inflammation in murine silicosis and support a potential role for IL-1beta-depe
30 e potentially involved in the progression of silicosis and the anti-fibrotic effect of Ac-SDKP.
31 sis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis.
32 les, 70% micronodules, 45% macronodules, 15% silicosis, and 28% PMF.
33 lung diseases (coal worker's pneumoconiosis, silicosis, and mixed dust pneumoconiosis), coal miners a
34 ovided quantitative data on silica exposure, silicosis, and/or smoking.
35 ression also was found to be associated with silicosis, another granulomatous disease.
36                               Asbestosis and silicosis are incurable and may be progressive even afte
37 ant silica exposure, and silica exposure and silicosis are thought to increase risk of autoimmune dis
38 enesis of numerous diseases, including gout, silicosis, asbestosis, and atherosclerosis.
39 f human diseases, including gouty arthritis, silicosis, atherosclerosis, and type 2 diabetes.
40                    In the nodular lesions of silicosis, central hyalinized areas contained the maximu
41                                      Hepatic silicosis, cirrhosis, liver cell adenoma, and carcinomas
42                                 Among 16,648 silicosis deaths, 2,278 (13.7%) had respiratory TB liste
43 t underlie the pathogenesis of diseases like silicosis, gout, and atherosclerosis.
44 al pathogenic inflammatory responses such as silicosis, graft rejection and asthma but it is also pro
45 ith a central role in the pathophysiology of silicosis, have been associated with predisposition to s
46  120 black South African gold miners without silicosis (ILO grades 0/0) in an age-frequency-matched c
47  3 nodularity, 112 patients with less severe silicosis (ILO grades 1/1 to 2/2), and 120 black South A
48       Macrophages play a fundamental role in silicosis in part by removing silica particles and produ
49 associated with severe, but not less severe, silicosis in this population.
50 ence of radiographic changes consistent with silicosis increased with: number of years worked at the
51 esence of tuberculosis (TB) in patients with silicosis increases mortality risk.
52                                              Silicosis is an interstitial lung disease caused by the
53                                              Silicosis is characterized by fibrosing nodular lesions
54                            Susceptibility to silicosis is in part genetically determined.
55 st that a crucial step in the development of silicosis is silica-induced injury of alveolar macrophag
56                                              Silicosis is the most serious occupational disease in Ch
57    Inhalation of silica, without evidence of silicosis, is believed to predispose individuals to bact
58  many inflammatory diseases, including gout, silicosis, neurodegeneration, and genetically inherited
59                               Asbestosis and silicosis occurrence is predictable among people overexp
60 ight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silic
61 se data suggest a major role for TGF-beta in silicosis, particularly in the formation of silicotic no
62      Results confirmed excess mortality from silicosis/pneumoconioses (standardized mortality ratio =
63 tein expression profiles between control and silicosis rats treated with or without Ac-SDKP.
64                         Mortality rates from silicosis remain highly elevated in the cohort.
65 lung fibrosis in the forms of asbestosis and silicosis, respectively.
66                              To characterize silicosis-respiratory TB comortality in the United State
67                   The substantial decline in silicosis-respiratory TB comortality probably reflects p
68                          The highest PMR for silicosis-respiratory TB death was associated with the "
69                                              Silicosis-respiratory TB deaths declined 99.5% during th
70                                              Silicosis-respiratory TB deaths reported from Pennsylvan
71                                           Of silicosis-respiratory TB deaths, 1,666 decedents (73.1%)
72 006 marked the first year since 1968 with no silicosis-respiratory TB deaths.
73 action as a key event in the pathogenesis of silicosis that prevents mtROS formation and reduces macr
74 p between exposure to crystalline silica and silicosis; the level of risk to current workers remains
75                                     In acute silicosis, there was marked staining of hyperplastic alv
76 related to mechanisms of the pathogenesis of silicosis underlying the anti-fibrotic effect of N-acety
77 l of suppressive ODN to prevent acute murine silicosis was examined.
78                                 Experimental silicosis was produced in rabbits by airway instillation
79  (MC) and their fibrogenic growth factors in silicosis, we performed quantitative immunohistochemistr
80                         Subjects with severe silicosis were also significantly more likely to have th
81 ith lung cancer, sarcoidosis, or anthracosis/silicosis were excluded.
82 eloping radiographic changes consistent with silicosis were increased for African Americans (odds rat
83  imaging studies, specimens with features of silicosis were significantly associated (P = 0.047) with
84 lpha promoter region, but miners with severe silicosis were significantly more likely than controls t
85 n were compared in nine patients with severe silicosis with International Labour Office (ILO) grade 3

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