ライフサイエンスコーパス: asbestosis

1 plaques, and 1,353 (32.0%) had radiographic asbestosis.

2 ure to cigarettes, asbestos, and presence of asbestosis.

3 s of lung cancer among men with radiographic asbestosis.

4 thout radiographic or functional evidence of asbestosis.

5 ng biopsy shortly before his death confirmed asbestosis.

6 ther this was conditional on the presence of asbestosis.

7 portant in idiopathic pulmonary fibrosis and asbestosis.

8 tively predict subsequent risk of death from asbestosis.

9 aths during the subsequent 10 yr were due to asbestosis, according to the best clinical and radiologi

10 [95% confidence interval (CI), 1.7-7.6]), by asbestosis among nonsmokers (rate ratio = 7.40 [95% CI,

11 ntial mechanisms and therapeutic targets for asbestosis and other diseases (asthma, smoking-related i

12 Asbestosis and silicosis are incurable and may be progre

13 Asbestosis and silicosis occurrence is predictable among

14 development of lung fibrosis in the forms of asbestosis and silicosis, respectively.

15 r eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques.

16 umerous diseases, including gout, silicosis, asbestosis, and atherosclerosis.

17 acco smoking, asbestos exposure, presence of asbestosis, and pleural plaques.

18 s known to cause cellular damage, leading to asbestosis, bronchogenic carcinoma, and mesothelioma in

19 is) raised the risk of subsequent death from asbestosis by 2- to 6-fold.

20 Residual confounding by subclinical asbestosis, exposure to unmeasured lung carcinogens, or

21 olar macrophages isolated from patients with asbestosis express higher amounts of MARCO and have grea

22 continue to be diagnosed with mesothelioma, asbestosis, fibrosis and lung carcinoma because of the l

23 Asbestosis further increases the lung cancer risk and, c

24 Recorded mortality from asbestosis has increased markedly in the United States i

25 Here, we show that patients with asbestosis have higher levels of mitochondrial Ca(2+) co

26 athogenesis of fibrosis induced by asbestos (asbestosis), in part by generating reactive oxygen speci

27 Although asbestosis is generally considered to be a slowly progre

28 Asbestosis is observed in approximately 200,000 patients

29 risk also increased with worsening pulmonary asbestosis (p = 0.03 for trend).

30 Bronchoalveolar macrophages from asbestosis patients showed increased expression of sever

31 We found that alveolar macrophages from asbestosis patients spontaneously produce high levels of

32 he mitochondria of alveolar macrophages from asbestosis patients, and mitochondrial import requires t

33 d exposure parameters among individuals with asbestosis quantitatively predict subsequent risk of dea

34 e pulmonary fibrotic disorders silicosis and asbestosis, respectively.

35 index, Charlson comorbidity index, smoking, asbestosis, rheumatoid arthritis with interstitial lung

36 of death (expressed as a percentage) due to asbestosis rose sharply with increasing interstitial fib

37 onchiectasis, pulmonary fibrosis, silicosis, asbestosis, sarcoidosis, and tuberculosis.

38 e, we confirm that macrophages isolated from asbestosis subjects are resistant to apoptosis and show

39 e ratio = 14.4 [95% CI, 10.7-19.4]) and with asbestosis, supra-additive (rate ratio = 36.8 [95% CI, 3

40 opathies, such as gout, atherosclerosis, and asbestosis, trigger inflammation and tissue remodeling b

41 hat may explain the different pathologies of asbestosis versus silicosis.

42 t of cigarette smoking on risk of death from asbestosis was small and disappeared after adjustment fo

43 characterizing a murine inhalation model of asbestosis, we provide the first evidence showing activa

44 sothelioma and the occurrence of deaths from asbestosis were indicative of high levels of asbestos ex

45 ite- and chrysotile-induced inflammation and asbestosis were used to study the localization of p65, a

46 in lung macrophages from human subjects with asbestosis, while it was absent in mice harboring a cond