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

3 ing excessive neutrophil infiltration in the cystic fibrosis lung.

4 pathogen that can aggressively colonize the cystic fibrosis lung.

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

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

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

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

9 tection of bacteria in explanted whole human Cystic Fibrosis lungs.

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

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

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

13 aureus are the most common colonizers of the cystic fibrosis lung, and frequently overlap to cause ch

14 Using the cystic fibrosis lung as an example, we cultured an avera

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

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

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

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

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

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

21 The severity of cystic fibrosis lung disease has considerable heritabili

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

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

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

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

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

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

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

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

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

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

32 dase ameliorates the two pivotal features of cystic fibrosis lung disease, inflammation and infection

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

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

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

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

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

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

39 hannel (beta-ENaC), a model with features of Cystic Fibrosis lung disease.

40 ium abscessus pulmonary infection and severe cystic fibrosis lung disease.

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

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

43 (desert soil biocrust wetting) and clinical (cystic fibrosis lung) examples, our ability to recover m

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

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

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

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

48 rom biofilm-associated infections, including cystic fibrosis lung infection(4), as well as medical de

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

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

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

52 LasR(-) lineages frequently arise in cystic fibrosis lung infections and their detection corr

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

54 rincipal pathogens associated with wound and cystic fibrosis lung infections.

55 and are commonly found in chronic wound and cystic fibrosis lung infections.

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

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

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

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

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

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

62 Culture-independent studies of cystic fibrosis lung microbiota have provided few mechan

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

64 udomonas aeruginosa strains to an artificial cystic fibrosis lung sputum media.

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

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