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1 iated with matrix deposition and fibrosis in silicosis.
2 pe of inflammatory pathology in experimental silicosis.
3 omising avenue for moderating lung damage in silicosis.
4 o fabricate stone after being diagnosed with silicosis.
5 rvival and cytokine-mediated inflammation in silicosis.
6 r treating established PF, including IPF and silicosis.
7  an organ/haematological transplant, or with silicosis.
8 on, which are central to the pathogenesis of silicosis.
9 had progressive massive fibrosis, and 11 had silicosis.
10 d to play a critical role in the etiology of silicosis.
11  the development of the chronic lung disease silicosis.
12 e different pathologies of asbestosis versus silicosis.
13 of silica particles causes lung fibrosis and silicosis.
14 e in innate immunity and the pathogenesis of silicosis.
15 plate in drug discovery for the treatment of silicosis.
16 affect pathological features of experimental silicosis.
17 genesis of gouty arthritis, Alzheimer's, and silicosis.
18  alpha (TNFalpha) is a prominent mediator in silicosis.
19 ho), which included all subjects with severe silicosis.
20 nt NO-mediated apoptosis in the evolution of silicosis.
21 mediate apoptosis and inflammation in murine silicosis.
22 play an important role in the development of silicosis.
23 f Ac-Tub-alpha may be a new mechanism in rat silicosis; 2) treatment of silicotic rats with N-acetyl-
24 k of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA sta
25  of silica-containing dust particles induces silicosis, an inflammatory disease of the lungs characte
26 c exposure to crystalline silica (CS) causes silicosis, an irreversible lung inflammatory disease tha
27 ure to silica can lead to the development of silicosis, an irreversible, fibrotic pulmonary disease.
28 thological changes that strongly mimic human silicosis, an occupational lung disease marked by restri
29 the progressive pulmonary fibrotic disorders silicosis and asbestosis, respectively.
30 velopment of pneumoconiotic diseases such as silicosis and coal workers' pneumoconiosis.
31  differences between miners with less severe silicosis and controls at any loci in the TNF-alpha prom
32 f collagen/reticulin fibers was increased in silicosis and correlated with the V(v) of bFGF(+) cells
33 ing via TLR9 contributes to disease, such as silicosis and drug-induced liver injury.
34 ent of immunotherapeutic strategies to fight silicosis and lung cancer.
35 d, many of which had features of accelerated silicosis and mixed dust lesions.
36 ial sensitivity to detect active fibrosis in silicosis and other lung diseases.
37 adiological features of the various forms of silicosis and other silica-associated diseases.
38 re observed with increased radon exposure in silicosis and pulmonary fibrosis mortality and in the in
39 differential diagnosis, particularly between silicosis and sarcoidosis, are highlighted, as is the im
40 between apoptosis and inflammation in murine silicosis and support a potential role for IL-1beta-depe
41 edly increased in the lungs of patients with silicosis and that these findings associated with both h
42 e potentially involved in the progression of silicosis and the anti-fibrotic effect of Ac-SDKP.
43 sis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis.
44   The substantial morbidity and mortality of silicosis and tuberculosis among workers exposed to such
45 to address the devastating health effects of silicosis and tuberculosis in small-scale miners and the
46 wing epidemic of lung disease (predominantly silicosis and tuberculosis) among small-scale miners.
47 uce inflammatory lung reactions that lead to silicosis and/or lung cancer when the particles are biop
48 les, 70% micronodules, 45% macronodules, 15% silicosis, and 28% PMF.
49 rstanding of immune-modulatory mechanisms in silicosis, and indicates potential therapeutic targets f
50 lung diseases (coal worker's pneumoconiosis, silicosis, and mixed dust pneumoconiosis), coal miners a
51 ovided quantitative data on silica exposure, silicosis, and/or smoking.
52 ression also was found to be associated with silicosis, another granulomatous disease.
53                               Asbestosis and silicosis are incurable and may be progressive even afte
54 ant silica exposure, and silica exposure and silicosis are thought to increase risk of autoimmune dis
55 ular understanding of the immunopathology of silicosis, are highlighted.
56 l stone benchtops has led to re-emergence of silicosis around the world.
57 enesis of numerous diseases, including gout, silicosis, asbestosis, and atherosclerosis.
58  asthma, bronchiectasis, pulmonary fibrosis, silicosis, asbestosis, sarcoidosis, and tuberculosis.
59  This case series included reported cases of silicosis associated with fabrication of engineered ston
60                                              Silicosis associated with inhalation of respirable cryst
61 In this case series performed in California, silicosis associated with occupational exposure to dust
62 f human diseases, including gouty arthritis, silicosis, atherosclerosis, and type 2 diabetes.
63 , are observed in the lungs of patients with silicosis but the mechanisms mediating their formation r
64  of inflammation associated with respiratory silicosis by augmenting NLRP3 inflammasome-derived IL-1B
65  of inflammation associated with respiratory silicosis by augmenting NLRP3 inflammasome-derived IL-1b
66                    In the nodular lesions of silicosis, central hyalinized areas contained the maximu
67                                      Hepatic silicosis, cirrhosis, liver cell adenoma, and carcinomas
68                                 Among 16,648 silicosis deaths, 2,278 (13.7%) had respiratory TB liste
69 t underlie the pathogenesis of diseases like silicosis, gout, and atherosclerosis.
70 al pathogenic inflammatory responses such as silicosis, graft rejection and asthma but it is also pro
71 ension alters the dispersion and severity of silicosis has not been adequately investigated.
72 ith a central role in the pathophysiology of silicosis, have been associated with predisposition to s
73  120 black South African gold miners without silicosis (ILO grades 0/0) in an age-frequency-matched c
74  3 nodularity, 112 patients with less severe silicosis (ILO grades 1/1 to 2/2), and 120 black South A
75 greater alveolar inflammation typical of the silicosis in human disease.
76       Macrophages play a fundamental role in silicosis in part by removing silica particles and produ
77  instillation led to a greater penetrance of silicosis in the genetically heterogeneous Diversity Out
78 associated with severe, but not less severe, silicosis in this population.
79 ence of radiographic changes consistent with silicosis increased with: number of years worked at the
80 esence of tuberculosis (TB) in patients with silicosis increases mortality risk.
81                                              Silicosis is a common occupational disease and represent
82                                        While silicosis is a completely preventable disease, unfortuna
83                                              Silicosis is a global threat, and more than 2.2 million
84                                              Silicosis is a lethal pneumoconiosis for which no therap
85                                  Respiratory silicosis is a preventable occupational disease that dev
86                                  Respiratory silicosis is a preventable occupational disease that dev
87                                              Silicosis is an ancient and potentially fatal pneumoconi
88                                              Silicosis is an interstitial lung disease caused by the
89                                              Silicosis is characterized by fibrosing nodular lesions
90                                              Silicosis is historically a disease of miners; however,
91                            Susceptibility to silicosis is in part genetically determined.
92                       The pathophysiology of silicosis is poorly understood, limiting development of
93 st that a crucial step in the development of silicosis is silica-induced injury of alveolar macrophag
94                                              Silicosis is the most serious occupational disease in Ch
95    Inhalation of silica, without evidence of silicosis, is believed to predispose individuals to bact
96  can cause life-threatening diseases such as silicosis, lung cancer, and chronic obstructive pulmonar
97  many inflammatory diseases, including gout, silicosis, neurodegeneration, and genetically inherited
98                               Asbestosis and silicosis occurrence is predictable among people overexp
99 ight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silic
100 se data suggest a major role for TGF-beta in silicosis, particularly in the formation of silicotic no
101      Results confirmed excess mortality from silicosis/pneumoconioses (standardized mortality ratio =
102 ors of ILC2-ILC1 conversion, associated with silicosis progression via the Notch3-IL-18 signaling axi
103 ) conversion to ILC1s is closely involved in silicosis progression, which is mediated by activated fi
104 tein expression profiles between control and silicosis rats treated with or without Ac-SDKP.
105                         Mortality rates from silicosis remain highly elevated in the cohort.
106 ease, while their immune-modulatory roles in silicosis remain unclear.
107 lung fibrosis in the forms of asbestosis and silicosis, respectively.
108                              To characterize silicosis-respiratory TB comortality in the United State
109                   The substantial decline in silicosis-respiratory TB comortality probably reflects p
110                          The highest PMR for silicosis-respiratory TB death was associated with the "
111                                              Silicosis-respiratory TB deaths declined 99.5% during th
112                                              Silicosis-respiratory TB deaths reported from Pennsylvan
113                                           Of silicosis-respiratory TB deaths, 1,666 decedents (73.1%)
114 006 marked the first year since 1968 with no silicosis-respiratory TB deaths.
115 jury and ILD, including bleomycin treatment, silicosis, sarcoidosis, chronic hypersensitivity pneumon
116 as robust and present regardless of smoking, silicosis status, and cancer subtype.
117 action as a key event in the pathogenesis of silicosis that prevents mtROS formation and reduces macr
118 p between exposure to crystalline silica and silicosis; the level of risk to current workers remains
119                                     In acute silicosis, there was marked staining of hyperplastic alv
120 related to mechanisms of the pathogenesis of silicosis underlying the anti-fibrotic effect of N-acety
121  silica and in a longitudinal mouse model of silicosis using multiple modalities including whole-lung
122 ution and greatest incidence and severity of silicosis was determined in inbred and outbred mice.
123     Here, the requirement for cathepsin Z in silicosis was determined using WT mice and mice deficien
124 l of suppressive ODN to prevent acute murine silicosis was examined.
125                                 Experimental silicosis was produced in rabbits by airway instillation
126  (MC) and their fibrogenic growth factors in silicosis, we performed quantitative immunohistochemistr
127                         Subjects with severe silicosis were also significantly more likely to have th
128 ith lung cancer, sarcoidosis, or anthracosis/silicosis were excluded.
129 eloping radiographic changes consistent with silicosis were increased for African Americans (odds rat
130  imaging studies, specimens with features of silicosis were significantly associated (P = 0.047) with
131 lpha promoter region, but miners with severe silicosis were significantly more likely than controls t
132 lline silica (CS) particle exposure leads to silicosis which is characterized as progressive fibrosis
133 n were compared in nine patients with severe silicosis with International Labour Office (ILO) grade 3
134  variation in methods to induce experimental silicosis with the effects of dose and route of exposure

 
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