ライフサイエンスコーパス: asbestos

1 ptional alterations induced by both types of asbestos.

2 smoking and occupational exposures including asbestos.

3 tochondria are a major cytoplasmic target of asbestos.

4 e caution afforded known carcinogens such as asbestos.

5 y vehicle brake linings contained chrysotile asbestos.

6 ronchiolar epithelial cells of mice inhaling asbestos.

7 g roles in the apoptotic response induced by asbestos.

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

9 inflammation after inhalation of chrysotile asbestos.

10 as well as cell proliferation in response to asbestos.

11 l and resistance to the cytotoxic effects of asbestos.

12 taphases in HM exposed to both TNF-alpha and asbestos.

13 appaB signaling in mediating HM responses to 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 ressive tumors usually caused by exposure to asbestos.

19 ity to mesothelioma upon chronic exposure to asbestos.

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

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

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

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

24 y rare, aberrant metaphases in HM exposed to asbestos and an increased mitotic rate with fewer irregu

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

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

27 Asbestos and H2O2 diminished AEC SIRT3 protein expressio

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

29 This makes asbestos and mesothelioma research a public health issue

30 % CI, 4.2-23.2) for subjects exposed to both asbestos and MW and for subjects exposed to both asbesto

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

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

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

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

35 Inhalation of asbestos and oxidant-generating pollutants causes injury

36 Both asbestos and particulates alter lung iron homeostasis, w

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

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

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

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

41 We tested the hypothesis that asbestos and Simian virus (SV40) are cocarcinogens.

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

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

44 Asbestos and SV40 in combination had a costimulatory eff

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

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

47 In vivo, macrophages phagocytize asbestos and, in response, release TNF-alpha and other c

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

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

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

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

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

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

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

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

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

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

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

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

60 Asbestos bodies in lymphoma-associated PDMM were lower t

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

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

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

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

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

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

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

68 Asbestos carcinogenesis has been linked to the release o

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

70 finding raised an apparent paradox: How can asbestos cause MM if HM exposed to asbestos die?

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

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

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

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

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

76 1.21-4.85) after adjustment for smoking and asbestos cumulative exposure index.

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

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

79 of mesothelial and inflammatory cells around asbestos deposits.

80 Only a fraction of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting

81 : How can asbestos cause MM if HM exposed to asbestos die?

82 In vitro, asbestos does not induce transformation of primary human

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

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

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

86 ons of people have been exposed worldwide to asbestos, especially during the second half of the twent

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Asbestos-exposed mice harboring a conditional deletion o

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

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

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

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

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

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

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

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

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

110 Asbestos-exposed PKCdelta knockout (PKCdelta-/-) mice ex

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

112 levels of the profibrotic cytokine, IL-4, in asbestos-exposed wild-type mice but not PKCdelta-/- mice

113 ession of lung MMP12 and MMP13 compared with asbestos-exposed wild-type mice.

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

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

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

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

118 4 [CI, 4.32 to 38.28]) and extraoccupational asbestos exposure (OR, 8.42 [CI, 2.77 to 30.58]).

119 [95% CI, 4.0-13.7]), and by smoking without asbestos exposure (rate ratio = 10.3 [95% CI, 8.8-12.2])

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

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

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

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

124 Asbestos exposure has been proposed as a risk factor for

125 100 fiber-years per milliliter of cumulative asbestos exposure in a cohort study of textile workers i

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

127 Asbestos exposure increased mitochondrial Ca(2+) influx

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

129 Asbestos exposure is one important environmental cause o

130 Asbestos exposure is strongly associated with the develo

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

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

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

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

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

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

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

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

139 Asbestos exposure was most specifically associated with

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

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

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

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

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

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

146 s observed after adjustment for occupational asbestos exposure.

147 ant mesothelioma is strongly associated with asbestos exposure.

148 hic evidence of lung changes consistent with asbestos exposure.

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

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

151 lved and that mesothelioma predominates upon asbestos exposure.

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

153 an aggressive cancer largely associated with asbestos exposure.

154 ancer that is commonly associated with prior asbestos exposure.

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

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

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

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

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

160 ronchiolar epithelial cells after chrysotile asbestos exposures.

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

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

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

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

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

166 Among asbestos fibers, crocidolite is considered the most and

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

168 uence the biological activities of these two asbestos fibers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Asbestos increased expression of several CREB target gen

188 Asbestos increases lung cancer mortality among nonsmoker

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

190 Asbestos induced a dose-dependent increase in nuclear DN

191 We found that asbestos induced the secretion of TNF-alpha and the expr

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

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

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

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

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

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

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

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

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

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

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

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

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

205 ibrotic agent, but the mechanisms leading to asbestos-induced lung diseases are unclear.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Asbestos is a known human carcinogen, and recent regulat

229 Asbestos is a known inflammatory, carcinogenic, and fibr

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

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

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

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

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

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

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

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

238 imary human mesothelial cells (HM); instead, asbestos is very cytotoxic to HM, causing extensive cell

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

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

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

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

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

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

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

246 arcinogens and suggest that lower amounts of asbestos may be sufficient to cause MM in individuals in

247 Asbestos may initiate mitochondria-associated ROS, which

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

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

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

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

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

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

254 Mesothelial cells exposed to asbestos or bleomycin for 96 h acquired senescent-like m

255 exposed to an intratracheal instillation of asbestos or bleomycin.

256 gement also failed to senesce in response to asbestos or chemotherapeutic agents.

257 e mesothelial cells to DNA damage induced by asbestos or chemotherapeutic agents.

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

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

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

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

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

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

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

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

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

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

268 Asbestos-related diseases continue to result in approxim

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

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

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

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

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

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

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

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

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

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

283 and primary lung fibroblasts confirmed that asbestos transcriptionally up-regulates MMPs via an EGFR

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 he second half of the twentieth century when asbestos use increased significantly.

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

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

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

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

292 s from cotton, wood, metal, minerals, and/or asbestos was associated with nonchronic cough and/or phl

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

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

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

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

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

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

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.