ライフサイエンスコーパス: asbestos

1 ressive tumors usually caused by exposure to asbestos.

2 ity to mesothelioma upon chronic exposure to asbestos.

3 usted for smoking and co-exposures including asbestos.

4 ptional alterations induced by both types of asbestos.

5 smoking and occupational exposures including asbestos.

6 tochondria are a major cytoplasmic target of asbestos.

7 e caution afforded known carcinogens such as asbestos.

8 y vehicle brake linings contained chrysotile asbestos.

9 ronchiolar epithelial cells of mice inhaling asbestos.

10 g roles in the apoptotic response induced by asbestos.

11 fecting pro- and anti-apoptotic responses to asbestos.

12 ness scores for 108 countries that ever used asbestos.

13 inflammation after inhalation of chrysotile asbestos.

14 lly associated with professional exposure to asbestos.

15 AP1 mutations were professionally exposed to asbestos.

16 is linked to fibrosis following exposure to asbestos.

17 -/-) mice challenged with LPS, bleomycin and asbestos.

18 r exposure to oxidative stress (e.g. amosite asbestos (5-25 mug/cm(2)) or H2O2 (100-250 muM)) for 24

19 We recently found that asbestos activates the nod-like receptor family member c

20 The joint effect of smoking and asbestos alone was additive (rate ratio = 14.4 [95% CI,

21 Asbestos also caused increases in IL-4, MIP-1beta, and M

22 n the lavage fluid of EC-SOD-null mice after asbestos and bleomycin exposure.

23 believed to be caused by chronic exposure to asbestos and erionite.

24 Asbestos and H2O2 diminished AEC SIRT3 protein expressio

25 present in macrophages exposed to chrysotile asbestos and if ER stress in macrophages was associated

26 % CI, 4.2-23.2) for subjects exposed to both asbestos and MW and for subjects exposed to both asbesto

27 Coexposure to either asbestos and MW or asbestos and silica seemed to increas

28 al mesothelioma for subjects exposed to both asbestos and MW or asbestos and silica.

29 ; b) relative toxicity of different forms of asbestos and other hazardous elongated mineral particles

30 and risk factors associated with toxicity of asbestos and other hazardous EMPs (e.g., nanomaterials).

31 Inhalation of asbestos and oxidant-generating pollutants causes injury

32 Both asbestos and particulates alter lung iron homeostasis, w

33 onal and environmental exposures to airborne asbestos and silica are associated with the development

34 Coexposure to either asbestos and MW or asbestos and silica seemed to increase the risk of pleur

35 stos and MW and for subjects exposed to both asbestos and silica, respectively, compared with 4.3 (95

36 subjects exposed to both asbestos and MW or asbestos and silica.

37 Coexposure to asbestos and smoke had a multiplicative effect on risk c

38 re predisposed to the tumorigenic effects of asbestos and suggest that high penetrance of mesotheliom

39 y studies, the complexity of the response to asbestos and the many unanswered questions suggested the

40 Exposure to asbestos and tobacco smoke resulted in strong risk facto

41 ased with cumulative exposure to cigarettes, asbestos, and presence of asbestosis.

42 to a profibrotic phenotype after exposure to asbestos, and the profibrotic polarization was regulated

43 he risks arising from exposure to silica and asbestos are well known, as are the means of their preve

44 Nanotubes structural aspects which resemble asbestos, as well as their ability to induce cyto and ge

45 Mesothelioma is an asbestos-associated and notoriously chemotherapy-resista

46 aling pathways leading to the development of asbestos-associated diseases are poorly understood.

47 ociated PDMM were younger than patients with asbestos-associated PDMM (median age, 45 v 64 years, res

48 lymphoma-associated PDMM were lower than in asbestos-associated PDMM (median count, 15 v 325 bodies,

49 overall survival compared with patients with asbestos-associated PDMM.

50 f malignant mesothelioma (MM), an aggressive asbestos-associated tumor.

51 s burden, and survival in this rapidly fatal asbestos-associated tumor.

52 rch findings were presented at a workshop on asbestos at the 2014 annual meeting of the Society of To

53 ns had a shorter time to adoption of a total asbestos ban (mean 8.9 [SD 6.4] years) than did countrie

54 ne were excluded because they implemented an asbestos ban before 1989.

55 governments guidelines for achieving a total asbestos ban policy, but the long-term effect of these C

56 We obtained data for year of a national asbestos ban, year of ratification of one or both intern

57 h time of implementation of a national total asbestos ban.

58 ilitates countries in moving towards a total asbestos ban.

59 ness, and implementation of a national total asbestos ban.

60 programmes and new agreements towards total asbestos bans and government commitments are needed.

61 uFTIR analyses revealed abundant proteins on asbestos bodies but not on anthracotic particles.

62 Asbestos bodies in lymphoma-associated PDMM were lower t

63 used to chemically characterize and compare asbestos bodies versus environmental particulates (anthr

64 as significantly associated with lung tissue asbestos body burden (P < 0.03), and significantly predi

65 iseased pleura from nontumor pleura and that asbestos burden and methylation profiles are independent

66 Consistent with prior work, asbestos burden was associated with an increased risk of

67 fic methylation alterations, disease status, asbestos burden, and survival in this rapidly fatal asbe

68 omprehensive review of the research field of asbestos carcinogenesis and mesothelioma, and of the pro

69 asbestos exposure, genetic predisposition to asbestos carcinogenesis and to simian virus (SV)40 infec

70 Asbestos carcinogenesis has been linked to the release o

71 uced inflammatory response that is linked to asbestos carcinogenesis, thereby increasing the risk of

72 At all time points, asbestos caused increased numbers of distal bronchiolar

73 In a murine lung epithelial cell line, asbestos caused significant increases in the phosphoryla

74 ortantly, the analyses demonstrated that the asbestos coating proteins contain high levels of beta-sh

75 onal changes in the proteic component of the asbestos coating provides new insights into long-term as

76 , the percentage change in HR for persistent asbestos consumption significantly increased by 127% (95

77 Of 108 countries with data for asbestos consumption, nine were excluded because they im

78 rt the hypothesis that community exposure to asbestos-contaminated vermiculite originating from Libby

79 tudy confirms that adoption of both the C162 Asbestos Convention and the Basel Convention facilitates

80 International Labor Organization (ILO; C162 Asbestos Convention) and the UN (Basel Convention) offer

81 1.21-4.85) after adjustment for smoking and asbestos cumulative exposure index.

82 ain time variable, adjusting for smoking and asbestos cumulative exposure index.

83 onally, other areas with naturally occurring asbestos deposits near communities in the United States

84 of mesothelial and inflammatory cells around asbestos deposits.

85 thelioma after exposure to very low doses of asbestos, doses that rarely induced mesothelioma in wild

86 te to what extent confounding by smoking and asbestos drives this association and to evaluate the rol

87 coating provides new insights into long-term asbestos effects.

88 ticulates (anthracosis) in lung tissues from asbestos exposed and control patients.

89 collected in 1981 to 1983 and for 54,243 non-asbestos-exposed blue collar male workers from Cancer Pr

90 Sham and chrysotile asbestos-exposed CC10-IkappaBalphasr Tg(+) and Tg(-) mic

91 Smoking cessation among asbestos-exposed cohorts has been little studied.

92 ase the risk of malignant mesothelioma among asbestos-exposed cohorts.

93 patients with a family history of cancer, 50 asbestos-exposed control individuals with a family histo

94 Asbestos-exposed HM activate poly(ADP-ribose) polymerase

95 EB1 and its target genes are up-regulated in asbestos-exposed human mesothelial cells through an epid

96 Because only a small fraction of asbestos-exposed individuals develop malignant mesotheli

97 HMGB1 levels in asbestos-exposed individuals were significantly higher t

98 of cancers other than mesothelioma, and 153 asbestos-exposed individuals without familial cancer.

99 audience that includes patients, millions of asbestos-exposed individuals, scientists, physicians, pu

100 ved in the initiation of oxidative stress in asbestos-exposed mammalian cells.

101 Asbestos-exposed mice harboring a conditional deletion o

102 To evaluate ER stress in vivo, asbestos-exposed mice showed fibrosis development, and a

103 in bronchoalveolar lavage fluid (BALF) from asbestos-exposed mice, but to a lesser extent (p < or =

104 Microarrays performed on lung tissues from asbestos-exposed OPN(+/+) and OPN(-/-) mice showed that

105 and eotaxin) also were significantly less in asbestos-exposed OPN(-/-) mice.

106 e curve of 0.87 for plasma specimens from 96 asbestos-exposed persons as compared with 48 patients wi

107 lung cancer among male cigarette smokers or asbestos-exposed persons taking beta-carotene-a surprisi

108 sma (from 92 patients with mesothelioma, 136 asbestos-exposed persons without cancer, 93 patients wit

109 r milliliter in the New York cohort) than in asbestos-exposed persons without mesothelioma (14+/-1 ng

110 patients with early-stage mesothelioma with asbestos-exposed persons, the sensitivity was 100% and t

111 ically relevant Bap1 mutations compared with asbestos-exposed wild-type littermates.

112 pendent risk factor for lung cancer death in asbestos-exposed workers and could be used as an additio

113 s study was designed to examine this link in asbestos-exposed workers.

114 We estimated cumulative asbestos exposure (fibers per cubic centimeters x months

115 between tobacco smoke and both occupational asbestos exposure (OR, 12.04 [CI, 4.32 to 38.28]) and ex

116 4 [CI, 4.32 to 38.28]) and extraoccupational asbestos exposure (OR, 8.42 [CI, 2.77 to 30.58]).

117 [95% CI, 4.0-13.7]), and by smoking without asbestos exposure (rate ratio = 10.3 [95% CI, 8.8-12.2])

118 Lung cancer mortality was increased by asbestos exposure alone among nonsmokers (rate ratio = 3

119 with 4.3 (95% CI, 1.9-9.8) for occupational asbestos exposure alone.

120 Analyses of associations between cumulative asbestos exposure and lung cancer mortality among textil

121 e a large number of pulmonary diseases, with asbestos exposure being the most risky.

122 Asbestos exposure has been proposed as a risk factor for

123 100 fiber-years per milliliter of cumulative asbestos exposure in a cohort study of textile workers i

124 Lack of information on asbestos exposure in the LLPC limited the ability to val

125 Asbestos exposure increased mitochondrial Ca(2+) influx

126 Additional studies revealed that asbestos exposure induced a highly significant increase

127 Rationale: Asbestos exposure is associated with a dose-dependent ri

128 Asbestos exposure is one important environmental cause o

129 ormation of membrane "pores"; the effects of asbestos exposure may therefore consist of multiple (not

130 s with rounded atelectasis have a history of asbestos exposure or pleural effusion due to various cau

131 ccupational Safety and Health Administration asbestos exposure standard of <0.1 fibers/mL, we estimat

132 A further reduction in asbestos exposure to a standard of <0.05 fibers/mL was e

133 ers) when interpreting asbestos toxicity; d) asbestos exposure to susceptible populations; and e) usi

134 sociations between pleural abnormalities and asbestos exposure using multiple logistic regression to

135 mortality by age 90 years under the observed asbestos exposure was 9.44%.

136 A history of asbestos exposure was associated with idiopathic RPF (od

137 Chrysotile asbestos exposure was measured in fiber-years per millil

138 Asbestos exposure was most specifically associated with

139 justed for age, birth date, and occupational asbestos exposure were used to estimate odds ratios (OR)

140 elopment of mesothelioma is linked mainly to asbestos exposure, but the combined contributions of gen

141 In addition to asbestos exposure, genetic predisposition to asbestos ca

142 In comparison with observed asbestos exposure, if the facility had operated under th

143 not vary according to age, sex, duration of asbestos exposure, or degree of radiographic changes and

144 ng cancer incidence by sex, tobacco smoking, asbestos exposure, presence of asbestosis, and pleural p

145 shed between malignant mesothelioma (MM) and asbestos exposure, the exact mechanism by which asbestos

146 on a specific membrane effect of crocidolite asbestos exposure, which deserves to be tested also on h

147 s observed after adjustment for occupational asbestos exposure.

148 ant mesothelioma is strongly associated with asbestos exposure.

149 hic evidence of lung changes consistent with asbestos exposure.

150 n an urban setting, and with a potential for asbestos exposure.

151 ar of birth, sex, and potential occupational asbestos exposure.

152 lved and that mesothelioma predominates upon asbestos exposure.

153 ss mesothelioma - the cancer often linked to asbestos exposure.

154 f the pleura and is strongly associated with asbestos exposure.

155 an aggressive cancer largely associated with asbestos exposure.

156 ancer that is commonly associated with prior asbestos exposure.

157 M) is an aggressive neoplasm associated with asbestos exposure.

158 on homeostasis, with a more marked effect in asbestos exposure.

159 For example, environmental asbestos exposures associated with a former mine in Libb

160 bestos, many issues related to environmental asbestos exposures remain unresolved.

161 ronchiolar epithelial cells after chrysotile asbestos exposures.

162 that at least one effect of iron-containing asbestos fiber exposure was mediated by ROS production.

163 consistent across two cohorts with differing asbestos fiber exposures and intensity.

164 Wittenoom Township residents and 2) a mixed-asbestos-fiber, mixed-occupation group.

165 on molecular signature of long-CNT- and long-asbestos-fiber-induced pathology.

166 luorescent tagging and imaging of chrysotile asbestos fibers and prepared samples with a distribution

167 The so-called amphibole asbestos fibers are enriched with mineral iron ions, abl

168 Much available evidence suggests that asbestos fibers damage cells through the production of R

169 observations of the diffusion of individual asbestos fibers in water.

170 hat instillation of either long CNTs or long asbestos fibers into the pleural cavity of mice induces

171 termates, BAP1(+/-) mice exposed to low-dose asbestos fibers showed significant alterations of the pe

172 Among asbestos fibers, crocidolite is considered the most and

173 Combined with biopersistence of asbestos fibers, we hypothesize that this creates an env

174 uence the biological activities of these two asbestos fibers.

175 h aspect ratio, such as carbon nanotubes and asbestos fibres, have been shown to cause length-depende

176 Community exposure to asbestos from contaminated vermiculite ore from Libby, M

177 distinguish healthy persons with exposure to asbestos from patients with mesothelioma.

178 mice to carbon nanotubes mimics exposure to asbestos, from initial and chronic inflammation, through

179 icles and pathogens; however, a receptor for asbestos has not been identified.

180 including exposure to radon, cooking fumes, asbestos, heavy metals, and environmental tobacco smoke,

181 In both mice and hamsters injected with asbestos, HMGB1 was specifically detected in the nuclei,

182 was addressed by instillation of crocidolite asbestos in a series of wild-type or SPARC-null mice.

183 anscriptional changes induced by crocidolite asbestos in A549 human lung epithelial cells.

184 al ban, the current and future prevalence of asbestos in brakes is uncertain, suggesting the need for

185 ces for aggregate formation and transport of asbestos in confined spaces.

186 Intratracheal injection of crocidolite asbestos in mice leads to pulmonary inflammation and inj

187 g workers who were occupationally exposed to asbestos in South Carolina.

188 tured carbon nanotubes (CNTs) are similar to asbestos in terms of their fibrous shape and biopersiste

189 fferences between crocidolite and chrysotile asbestos in terms of their transcriptional effects and t

190 rus has emerged as a potential cofactor with asbestos in the development of diffuse malignant mesothe

191 sregulation is a critical mode of action for asbestos in the induction of pleural mesothelioma.

192 ung carcinogens, such as cigarette smoke and asbestos, in pulmonary epithelial cells.

193 Asbestos increased expression of several CREB target gen

194 Asbestos increases lung cancer mortality among nonsmoker

195 wn to cause lung cancer, cigarette smoke and asbestos, induce pulmonary inflammation, and pulmonary i

196 Asbestos induced a dose-dependent increase in nuclear DN

197 esothelial cells showed rapid and protracted asbestos-induced cAMP response element binding protein (

198 Malignant mesothelioma (MM) is an asbestos-induced cancer arising on the mesothelial surfa

199 to secrete TNF-alpha, which protects HM from asbestos-induced cell death and triggers a chronic infla

200 sease, and provide mechanistic links between asbestos-induced cell death, chronic inflammation, and c

201 othelial cell lines enhanced spontaneous and asbestos-induced double-strand breaks, indicated by gamm

202 mmation and lung remodeling are hallmarks of asbestos-induced fibrosis, but the molecular mechanisms

203 type, and is required for the development of asbestos-induced fibrosis.

204 ew insights into the molecular mechanisms of asbestos-induced genotoxicity.

205 We show that asbestos-induced HM cell death is a regulated form of ne

206 The incidence of asbestos-induced human cancers is increasing worldwide,

207 In vitro studies showed that asbestos-induced inflammasome/inflammation activation in

208 ylation of p16/Ink4a and p19/Arf in CNT- and asbestos-induced inflammatory lesions precedes mesotheli

209 germline BAP1 mutations might influence the asbestos-induced inflammatory response that is linked to

210 es in chemotherapy worldwide, the history of asbestos-induced lung disease casts a long shadow over f

211 C-delta as a potential therapeutic option in asbestos-induced lung diseases.

212 cient for Arf are susceptible to accelerated asbestos-induced malignant mesothelioma (MM).

213 t knockout mice also revealed the process of asbestos-induced mesothelial to fibroblastic transition

214 xhibited a significantly higher incidence of asbestos-induced mesothelioma than wild-type (WT) litter

215 alterations that we previously identified in asbestos-induced MMs arising in Nf2 (+/-) mice.

216 SOD protects the lung in both bleomycin- and asbestos-induced models of pulmonary fibrosis.

217 e mitochondria-associated ROS, which mediate asbestos-induced nuclear mutagenic events and inflammato

218 ignaling, a pathway previously implicated in asbestos-induced oncogenesis of human mesothelial cells.

219 hat has now been independently implicated in asbestos-induced oncogenesis.

220 At 3 days, asbestos-induced peribronchiolar cell proliferation in w

221 ER stress in macrophages was associated with asbestos-induced pulmonary fibrosis.

222 ein, Rac1, in macrophages are protected from asbestos-induced pulmonary fibrosis.

223 ed in the bronchoalveolar lavage fluid after asbestos-induced pulmonary injury, and this response is

224 lable iron (Fe) is proposed to contribute to asbestos-induced toxicity through the production of reac

225 Asbestos-induced translocation of Cu,Zn-SOD to the IMS w

226 Using a series of experiments, we found that asbestos induces a fibroblastic transition of mesothelia

227 ther, our data are the first to suggest that asbestos induces mesothelial to fibroblastic transition

228 Our studies are the first to show that asbestos induces PKD phosphorylation in lung epithelial

229 estos exposure, the exact mechanism by which asbestos induces this neoplasm and other asbestos-relate

230 tion (LCM) of distal bronchioles in a murine asbestos inhalation model, we show that osteopontin (OPN

231 mation and fibrogenesis in a murine model of asbestos inhalation, we used transgenic (Tg) mice expres

232 p-PKD in lung homogenates and in situ after asbestos inhalation.

233 Asbestos is a known human carcinogen, and recent regulat

234 Although asbestos is a well-known lung carcinogen, the pleural pl

235 PKCdelta-dependent PKD phosphorylation by asbestos is causally linked to a cellular pathway that i

236 The mineral asbestos is considered the main causative agent of this

237 Asbestos is cytotoxic to human mesothelial cells (HM), w

238 d for current and future generations because asbestos is difficult to be disposed off.

239 Inhalation of crystalline silica and asbestos is known to cause the progressive pulmonary fib

240 Although exposure to asbestos is now regulated, patients continue to be diagn

241 lies and not others, and whether exposure to asbestos is required for development of mesothelioma in

242 (CNTs) raises concern that they may pose an asbestos-like inhalation hazard, leading to the developm

243 iopersistent properties and thus may pose an asbestos-like inhalation hazard.

244 e site of mesothelioma development, produced asbestos-like length-dependent responses.

245 Exposure to erionite, an asbestos-like mineral, causes unprecedented rates of mal

246 Moreover, the very high costs of asbestos litigation have a significant impact on the who

247 In studies of the health effects of asbestos, lung cancer death is subject to misclassificat

248 health effects of occupational exposures to asbestos, many issues related to environmental asbestos

249 Asbestos may initiate mitochondria-associated ROS, which

250 lings collected from the abandoned Woodsreef Asbestos Mine in New South Wales, Australia as a strateg

251 were collected, and occupational exposure to asbestos, mineral wool (MW), and silica were assessed by

252 all percentage of vehicle brake linings with asbestos observed, it appears that the prior federal ban

253 ontext, standard estimates for the effect of asbestos on lung cancer death were similar to estimates

254 st to OPN wild-type mice (OPN(+/+)) inhaling asbestos, OPN null mice (OPN(-/-)) exposed to asbestos s

255 Pulmonary fibrosis after asbestos or bleomycin exposure was evaluated in 129SJ/wi

256 exposed to an intratracheal instillation of asbestos or bleomycin.

257 gene expression associated with crocidolite asbestos or cristobalite silica exposures in primary hum

258 present findings are specific to chrysotile asbestos or would be observed after inhalation of other

259 Asbestos- or bleomycin-induced lung fibrosis, AEC mtDNA

260 CO acts as an initial signaling receptor for asbestos, polarizes macrophages to a profibrotic M2 phen

261 othelioma development and shows that CNT and asbestos pose a similar health hazard.

262 ouble reading of CT scans focusing on benign asbestos-related abnormalities.

263 approximately 200,000 patients annually and asbestos-related deaths are estimated at 4,000 annually.

264 the 5,402 male subjects participating in an asbestos-related disease screening program conducted fro

265 critical initial step in the pathogenesis of asbestos-related disease, and provide mechanistic links

266 ve resulted in high rates of nonoccupational asbestos-related disease.

267 Asbestos-related diseases continue to result in approxim

268 ich asbestos induces this neoplasm and other asbestos-related diseases is still not well understood.

269 sting of both novel and previously described asbestos-related genes/gene products.

270 Better protection of individuals from asbestos-related health effects will require stimulation

271 f action of nonmutagenic carcinogens such as asbestos remain poorly characterized.

272 Therefore, asbestos research is of great interest to a large audien

273 The workshop also featured asbestos research supported by the National Institute of

274 s regarding genes that are important for the asbestos response.

275 negatively associated, and a higher cover of asbestos roofs and exposed soil was positively associate

276 sbestos, OPN null mice (OPN(-/-)) exposed to asbestos showed less eosinophilia in bronchoalveolar lav

277 her ionizing or ultraviolet radiation, or to asbestos, survive genotoxic stress, resulting in a highe

278 y of mortality in a cohort of South Carolina asbestos textile workers (1940-2001).

279 s: studies of lung cancer mortality among 1) asbestos textile workers and 2) uranium miners.

280 ly higher conditional probability of banning asbestos than did those ratifying one or no Convention (

281 avoiding known carcinogens (e.g., tobacco or asbestos) to intervening with anticarcinogenic strategie

282 avoiding known carcinogens (e.g., tobacco or asbestos) to intervening with anticarcinogenic strategie

283 or surface area of fibers) when interpreting asbestos toxicity; d) asbestos exposure to susceptible p

284 parental and rho(0) SAE cells in response to asbestos treatment.

285 In order to gauge the current prevalence of asbestos use in automotive brake applications, the Calif

286 ion with a threat of litigation, has reduced asbestos use in brake linings.

287 Chrysotile accounts for more than 90% of the asbestos used worldwide, but its capacity to induce mali

288 ondria are a potential cytoplasmic target of asbestos using a mitochondrial DNA-depleted (rho(0)) hum

289 The tons of asbestos utilized in the past remain a health hazard for

290 We recently reported that crocidolite asbestos was able to interact with the cell membranes of

291 in the in vivo lung response to crocidolite asbestos was addressed by instillation of crocidolite as

292 Similarly, asbestos was capable of activating caspase-1 in a Nalp3-

293 The response to long CNTs and long asbestos was characterized by acute inflammation, leadin

294 No asbestos was found in low mileage vehicles presumed to h

295 Additionally, no asbestos was found in the heavy-duty vehicle brake shoe

296 In contrast, the effects of asbestos were minimal in rho(0) SAE cells.

297 percent of person-years involved exposure to asbestos, with a median exposure of 3.30 fiber-years/mL

298 ssive malignancy associated with exposure to asbestos, with poor prognosis and no effective therapies

299 cer among high-risk individuals (smokers and asbestos workers) who were given high doses of beta-caro

300 lic health officials, politicians, unions of asbestos workers, lawyers and the public at large.