ライフサイエンスコーパス: airway mucus

1 ycoproteins, the principal macromolecules in airway mucus.

2 ight serve as therapeutic targets to control airway mucus.

3 rway mucus and identify agents that decrease airway mucus.

4 pe A receptors (GABA(A)Rs) are implicated in airway mucus.

5 ological sections confirmed that Dex reduced airway mucus.

6 mM nitrite (NO2) at pH 6.5, which mimics CF airway mucus.

7 uction of MUC5AC mucin, a major component of airway mucus.

8 lveolar enlargement and excess production of airway mucus.

9 expression were not significantly reduced by airway mucus.

10 Levels of airway mucus, airway eosinophils, and peribronchial CD4+

11 uation of viral load, protein concentration, airway mucus, airway reactivity, or ILC2 numbers.

12 al disease (signified by formation of excess airway mucus and accumulation of M2-differentiating lung

13 by which cigarette smoke/nicotine regulates airway mucus and identify agents that decrease airway mu

14 reduced lung IL-13 protein levels, decreased airway mucus and reactivity, attenuated weight loss, and

15 MUC5AC mucin is a major component of airway mucus, and its expression is modulated by a TNF-a

16 ane fusion processes, including secretion of airway mucus, antibody, insulin, gastric acids, and ions

17 respiring anaerobically within the thickened airway mucus, at a pH of approximately 6.5.

18 (concentrated) mucus in the CF lung impairs airway mucus clearance, which initiates bacterial infect

19 ies of in vitro binding to immobilized human airway mucus confirmed the inhibitory effect of encapsul

20 and epithelium, and the barrier function of airway mucus contribute significantly to this problem.

21 Abundant airway mucus contributes to airway obstruction in RSV di

22 ion, IgE levels, eosinophil recruitment, and airway mucus, demonstrating induction of allergic sensit

23 Airway glands, which produce most airway mucus, do so in response to both acetylcholine (A

24 cystic fibrosis (CF) mucus ex vivo and mouse airway mucus ex situ.

25 ns, the primary macromolecular components of airway mucus, facilitate airway clearance by mucociliary

26 llergen- or nicotine/cigarette smoke-induced airway mucus formation in NHBE cells, murine airways, or

27 Nicotine-induced airway mucus formation is independent of IL-13, and alph

28 the allergen-induced mucous cell metaplasia, airway mucus formation, and the expression of mucus-rela

29 ological ligand for alpha7-nAChRs to trigger airway mucus formation.

30 Airway mucus forms the structural basis of the local inn

31 C5B, provide the organizing framework of the airways mucus gel and are major contributors to its rheo

32 The airways mucus gel performs a critical function in defend

33 of serum-specific IgE, cellular infiltrates, airway mucus goblet cells, and airway responsiveness wer

34 tine and allergens are strong stimulators of airway mucus; however, the mechanism of mucus modulation

35 nstrated that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and

36 dies demonstrated that M. pneumoniae induces airway mucus hypersecretion by modulating the STAT/EGFR-

37 However, its function in modulating airway mucus hypersecretion in asthma remains undefined.

38 f anti-hypersecretory drugs for treatment of airway mucus hypersecretion in asthma.

39 Airway mucus hypersecretion is a feature of many patient

40 Airway mucus hypersecretion is a key pathophysiologic fe

41 Airway mucus hypersecretion is a key pathophysiological

42 clinical implications for the management of airway mucus hypersecretion.

43 on the physical and transport properties of airway mucus in spontaneously breathing dogs.

44 Airway mucus is a hallmark of respiratory syncytial viru

45 Excessive airway mucus is an important cause of morbidity and mort

46 cent data indicate that cystic fibrosis (CF) airway mucus is anaerobic.

47 mphocyte recruitment were decreased, as were airway mucus, levels of specific proinflammatory mediato

48 mice had higher lung leukocyte counts, more airway mucus metaplasia, greater lung levels of some Th2

49 disease, the effects of these antagonists on airway mucus morphology were assessed in isolated perfus

50 s may be required for effective treatment of airway mucus obstruction in CF.

51 ide a novel therapeutic target to ameliorate airway mucus obstruction in lung diseases.

52 nductance regulator, a Cl ion channel, cause airway mucus obstruction leading to fatal lung disease.

53 ological studies and cell counts revealed no airway mucus obstruction or inflammation in the lungs of

54 d that hypoxic epithelial necrosis caused by airway mucus obstruction precedes neutrophilic inflammat

55 ns, treated Slc26a9-deficient mice exhibited airway mucus obstruction, which did not occur in wild-ty

56 radicable by antibiotics and responsible for airway mucus overproduction that contributes to airway o

57 In the thick CF airway mucus, P. aeruginosa forms antibiotic- and phagoc

58 Airway mucus plays a critical role in clearing inhaled t

59 ed that may serve to identify occult central airway mucus plugging in the ventilated asthmatic patien

60 l airspace enlargement, but had no effect on airway mucus plugging, bacterial infection, or pulmonary

61 In in vivo models of airway mucus plugs, neutrophil migration was inhibited b

62 Laboratory RSV strains differentially induce airway mucus production in mice.

63 ers, increased eosinophil apoptosis, reduced airway mucus production, and attenuated airway hyperresp

64 -induced airway inflammation, with increased airway mucus production, oxidative stress, inflammatory

65 Blocking the chemokines also decreased airway mucus production.

66 bronchioalveolar lavage fluid, and enhanced airway mucus production.

67 a mice results from significant decreases in airway mucus production.

68 peribronchiolar inflammation, and increased airway mucus production.

69 CTL inhibited eosinophil infiltration in the airway, mucus production, and cytokine accumulation in t

70 development of eosinophilic inflammation of airways, mucus production, and bronchial hyperreactivity

71 poxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils ind

72 nflux of eosinophils into the lungs, but not airway mucus release.

73 ns, but no approved or effective therapy for airway mucus retention in patients with chronic bronchit

74 inflammatory, and infectious insults induce airway mucus secretion and goblet cell metaplasia to pre

75 The dominant neural control of human airway mucus secretion is cholinergic.

76 , rhinorrhea, coughing, bronchoconstriction, airway mucus secretion, dysphagia, altered gastrointesti

77 SL) hyperabsorption generates a concentrated airway mucus that interacts with P. aeruginosa to promot

78 the airways, cilia function in concert with airway mucus to mediate the critical function of mucocil

79 ance regulator (CFTR) leads to impairment of airway mucus transport and to chronic lung diseases resu

80 sity would contribute to the accumulation of airway mucus which is characteristic of this disease.