ライフサイエンスコーパス: cystic fibrosis lung

1 Roc systems may sense the environment in the cystic fibrosis lung.

2 ile lifestyle to resilient biofilm as in the cystic fibrosis lung.

3 dominant mode of P. aeruginosa growth in the cystic fibrosis lung.

4 ing excessive neutrophil infiltration in the cystic fibrosis lung.

5 pathogen that can aggressively colonize the cystic fibrosis lung.

6 F508 CFTR and associated ERM proteins in the cystic fibrosis lung.

7 in a self-produced polymeric matrix--in the cystic fibrosis lung.

8 ces our understanding of pathogenesis in the cystic fibrosis lung.

9 upregulated AlgU during colonization of the cystic fibrosis lung and suggests opposing roles for thi

10 n-mediated anti-inflammatory activity in the cystic fibrosis lung and that lipoxins have therapeutic

11 nome analyses of B. cenocepacia infection in cystic fibrosis lungs and serves as a valuable resource

12 Focusing on a pathogen of the cystic fibrosis lung, Burkholderia cenocepacia, we seque

13 environment of low iron concentration in the cystic fibrosis lung can induce efflux-mediated resistan

14 Pseudomonas aeruginosa permanently colonizes cystic fibrosis lungs despite aggressive antibiotic trea

15 nstrate the in vivo contribution of IL-17 in cystic fibrosis lung disease and the therapeutic validit

16 The target cells for gene therapy of cystic fibrosis lung disease are the well differentiated

17 r development for treatment or prevention of cystic fibrosis lung disease has been limited by the ina

18 The severity of cystic fibrosis lung disease has considerable heritabili

19 esized that the presence of these markers of cystic fibrosis lung disease in the first 2 years of lif

20 and do not support a proposed mechanism for cystic fibrosis lung disease involving defective phagoso

21 The potential role of submucosal glands in cystic fibrosis lung disease is discussed.

22 progress independently of CFTR activity once cystic fibrosis lung disease is established.

23 s used to identify loci causing variation in cystic fibrosis lung disease severity.

24 s approach identified IFRD1 as a modifier of cystic fibrosis lung disease severity.

25 ate that IFRD1 modulates the pathogenesis of cystic fibrosis lung disease through the regulation of n

26 initiation of the first clinical trials for cystic fibrosis lung disease using recombinant adenoviru

27 e fluid from Scnn(+) mice, a murine model of cystic fibrosis lung disease which contains elevated con

28 transport processes and the pathogenesis of cystic fibrosis lung disease, however, are unclear.

29 al benefit of nebulized hypertonic saline in cystic fibrosis lung disease, with a proposed mechanism

30 y in pulmonary fibrosis is also prominent in cystic fibrosis lung disease.

31 gulator (CFTR) Cl(-) channel mutations cause cystic fibrosis lung disease.

32 ene transfer strategies for the treatment of cystic fibrosis lung disease.

33 fractures are common in adults with advanced cystic fibrosis lung disease.

34 g disease, especially patchy disease such as cystic fibrosis lung disease.

35 tant role in increasing the diversity of the cystic fibrosis lung environment and promoting patient s

36 hyperacidification of these compartments in cystic fibrosis lung epithelial cells.

37 xist in calprotectin-enriched airspaces of a cystic fibrosis lung explant.

38 coid and motile, isolates recovered from the cystic fibrosis lung frequently display a mucoid, nonmot

39 It has been reported that in cystic fibrosis lungs, in which P. aeruginosa adopts the

40 were to use the preclinical murine model of cystic fibrosis lung infection and inflammation to inves

41 he P. aeruginosa cell surface during chronic cystic fibrosis lung infection, where it is associated w

42 ox-active phenazine, pyocyanin (PCN), during cystic fibrosis lung infection.

43 robes and mammalian cells, especially during cystic fibrosis lung infection.

44 s kidney stones, bacterial endocarditis, and cystic fibrosis lung infections--and focus on the role o

45 adaptation of Pseudomonas aeruginosa to the cystic fibrosis lung is limited by genetic variation, wh

46 as products that promote inflammation in the cystic fibrosis lung is not known.

47 he medium; the secretion of these enzymes by cystic fibrosis lung isolate strain 38 was shown to be g

48 sigma factor MucA to promote mucoidy in some cystic fibrosis lung isolates.

49 Biofilm formation in the cystic fibrosis lung likely occurs under anaerobic condi

50 at misregulation of protease activity in the cystic fibrosis lung may alter fluid secretion and patho

51 gy of immotile natural isolates found in the cystic fibrosis lung mucus.

52 ocepacia is an opportunistic pathogen of the cystic fibrosis lung that elicits a strong inflammatory

53 Cystic fibrosis-lung transplant recipients (CF-LTRs) may