ライフサイエンスコーパス: asbestosis

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1 portant in idiopathic pulmonary fibrosis and asbestosis.

2 s of lung cancer among men with radiographic asbestosis.

3 thout radiographic or functional evidence of asbestosis.

4 ng biopsy shortly before his death confirmed asbestosis.

5 ther this was conditional on the presence of asbestosis.

6 tively predict subsequent risk of death from asbestosis.

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

8 [95% confidence interval (CI), 1.7-7.6]), by asbestosis among nonsmokers (rate ratio = 7.40 [95% CI,

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

10 Asbestosis and silicosis are incurable and may be progre

11 Asbestosis and silicosis occurrence is predictable among

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

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

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

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

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

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

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

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

20 Asbestosis further increases the lung cancer risk and, c

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

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

23 Although asbestosis is generally considered to be a slowly progre

24 Asbestosis is observed in approximately 200,000 patients

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

26 Bronchoalveolar macrophages from asbestosis patients showed increased expression of sever

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

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

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

30 e pulmonary fibrotic disorders silicosis and asbestosis, respectively.

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

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

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

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

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

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

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

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