ライフサイエンスコーパス: asbestos exposure

1 ancer that is commonly associated with prior asbestos exposure.

2 ar duct regions by 24 hours after the single asbestos exposure.

3 9 patients had a history of asbestos exposure.

4 ere made to identify cancers attributable to asbestos exposure.

5 ermline genetic mutations, in the absence of asbestos exposure.

6 2% in British seamen were related to onboard asbestos exposure.

7 ly fatal tumour that is causally linked with asbestos exposure.

8 ce of cancer in naval personnel from onboard asbestos exposure.

9 hogenic germline mutations, independently of asbestos exposure.

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

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

12 s observed after adjustment for occupational asbestos exposure.

13 ant mesothelioma is strongly associated with asbestos exposure.

14 hic evidence of lung changes consistent with asbestos exposure.

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

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

17 lved and that mesothelioma predominates upon asbestos exposure.

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

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

20 d neoplasm that is typically associated with asbestos exposure.

21 ted to TP53 mutation status and occupational asbestos exposure.

22 , and are often associated with occupational asbestos exposure.

23 lls after mechanical wounding or crocidolite asbestos exposure.

24 information including cigarette smoking and asbestos exposure.

25 vitamin A carotenoids, tobacco exposure, and asbestos exposure.

26 an aggressive cancer largely associated with asbestos exposure.

27 to develop fibroproliferative lesions after asbestos exposure.

28 likely to have been confounded by smoking or asbestos exposure.

29 osis and work-related histories of long term asbestos exposure.

30 ronchiolar epithelial cells after chrysotile asbestos exposures.

31 e induction of fibrosis in workers with high asbestos exposures.

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

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

34 ent in individuals at high risk of MM due to asbestos exposure, although those with the 1125A polymor

35 om mesothelial cells and are associated with asbestos exposure and approximately 50% contain simian v

36 Mesothelioma arises in a context of asbestos exposure and chronic inflammation, which would

37 er adjustment for the confounding effects of asbestos exposure and cigarette smoking.

38 The relation between asbestos exposure and colorectal cancer remains controve

39 Malignant mesothelioma has been linked to asbestos exposure and generally has a poor prognosis bec

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

41 lignant mesothelioma (MM) is associated with asbestos exposure and the presence of SV40 viral sequenc

42 Occupational asbestos exposure and TP53 mutation were significantly a

43 The relationship between asbestos exposure and upper-lobe location of tumor was a

44 al membranes which are often associated with asbestos exposure and with Simian virus 40 (SV40) infect

45 ome, exposure to tobacco smoke, occupational asbestos exposure, and additional molecular alterations

46 in the United States are not associated with asbestos exposure, and only a minority of people exposed

47 r, not all mesotheliomas are associated with asbestos exposure, and only a small minority of people e

48 onmental history revealed no other source of asbestos exposure, and the initial clinical diagnosis wa

49 nterval, 1.5-15.4) compared to those without asbestos exposure, and this association remained after a

50 of lung cancer; smoking history; history of asbestos exposure; and intakes of yellow-orange vegetabl

51 nflammation occurred after 10 and 20 days of asbestos exposure as evidenced by increases in total pro

52 omas, clinicians should continue to consider asbestos exposure as the most likely and most thoroughly

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

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

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

56 Asbestos exposure causes activation of extracellular sig

57 e tumors, 14.6% had a history of significant asbestos exposure compared with 5.4% of those with lower

58 involved in lung injury and remodeling after asbestos exposure could aid in defining mechanisms of ai

59 r among those with a history of occupational asbestos exposure (crude odds ratio, 4.8; 95% confidence

60 The case-control study confirmed that asbestos exposure did not account for the observed assoc

61 f adenocarcinomas (p < 0.02), but history of asbestos exposure did not predict tumor histology.

62 e favors adenocarcinomas, but the history of asbestos exposure does not appear to influence the tumor

63 er-lobe location while those associated with asbestos exposure favor a lower-lobe location.

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

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

66 Asbestos exposure has been proposed as a risk factor for

67 with lung cancer, both cigarette smoking and asbestos exposure histories favor an upper-lobe location

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

69 100 fiber-years per milliliter of cumulative asbestos exposure in a cohort study of textile workers i

70 alized to the mitochondrial matrix following asbestos exposure in lung macrophages via direct interac

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

72 Asbestos exposure increased mitochondrial Ca(2+) influx

73 These data suggest that asbestos exposure increases the likelihood of mutation a

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

75 y all lung cancer, and it is well known that asbestos exposure interacts synergistically with tobacco

76 Asbestos exposure is an important environmental mediator

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

78 Asbestos exposure is one important environmental cause o

79 Asbestos exposure is strongly associated with the develo

80 Asbestos exposure is the major known risk factor for mes

81 mouse studies have focused on the effect of asbestos exposure, leaving the effects of genetic mutati

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

83 examine the effects of cigarette smoking and asbestos exposure on location and histology of lung canc

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

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

86 4 [CI, 4.32 to 38.28]) and extraoccupational asbestos exposure (OR, 8.42 [CI, 2.77 to 30.58]).

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

88 istory of lung cancer (p = 0.03), history of asbestos exposure (p = 0.02), less intake of yellow-oran

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

90 [95% CI, 4.0-13.7]), and by smoking without asbestos exposure (rate ratio = 10.3 [95% CI, 8.8-12.2])

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

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

93 PDGF-AA isoform expression immediately after asbestos-exposure, suggest a scenario in which a potent

94 c studies have established tobacco smoke and asbestos exposures synergistically interact to enhance l

95 th k-ras mutations had significantly greater asbestos exposures than those without mutations (P < 0.0

96 he case also had many risk factors including asbestos exposure that had not yet been linked with Beni

97 nant mesothelioma is a rare tumour caused by asbestos exposure that originates mainly from the pleura

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

99 ms increases the percent of HM that survives asbestos exposure, thus increasing the pool of asbestos-

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

101 a comprehensive characterization of possible asbestos exposure to investigate asbestos as the potenti

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

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

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

105 In contrast to some prior reports, asbestos exposure was also associated with an upper-lobe

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

107 We aimed to test whether occupational asbestos exposure was associated with k-ras codon 12 mut

108 case of a 65-year-old accountant whose only asbestos exposure was during a summer job 50 years earli

109 No history of asbestos exposure was elicited by careful questioning or

110 A dose-response trend based on years of asbestos exposure was less evident.

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

112 Asbestos exposure was most specifically associated with

113 e association of k-ras mutation and reported asbestos exposure was not dependent on the presence of r

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

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

116 ls selected from 1,150 men with occupational asbestos exposure who had undergone pulmonary function t

117 sible associations of tobacco carcinogen and asbestos exposure with DAP-kinase promoter methylation,

118 e was an association of smoking duration and asbestos exposure with FHIT exon loss, indicating that c

119 aggressive, incurable cancer associated with asbestos exposure, with a long latency and poor overall

120 asbestosis were indicative of high levels of asbestos exposure, with an expectation of cases of asbes