ライフサイエンスコーパス: bronchial hyperresponsiveness

1 der characterized by airway inflammation and bronchial hyperresponsiveness.

2 was >37.8ppb, 25 of 38 subjects (65.7%) had bronchial hyperresponsiveness.

3 was >37.8ppb, 29 of 43 subjects (67.4%) had bronchial hyperresponsiveness.

4 liferation and MMP-1 protein associated with bronchial hyperresponsiveness.

5 eral blood eosinophilia, high level of FENO, bronchial hyperresponsiveness.

6 mediated inflammation, tissue remodeling and bronchial hyperresponsiveness.

7 77 gene with asthma and with the severity of bronchial hyperresponsiveness.

8 se-dust-mite-induced airway inflammation and bronchial hyperresponsiveness.

9 There was some evidence of associations with bronchial hyperresponsiveness.

10 d inflammation and, if appropriate, negative bronchial hyperresponsiveness.

11 es, whereas others are shared with atopy and bronchial hyperresponsiveness.

12 osinophils, mucin levels in the airways, and bronchial hyperresponsiveness.

13 showed better lung mechanics, but unaltered bronchial hyperresponsiveness.

14 h could explain its genetic association with bronchial hyperresponsiveness.

15 ase and phosphodiesterase also contribute to bronchial hyperresponsiveness.

16 novel therapeutic targets for the control of bronchial hyperresponsiveness.

17 erity of airway narrowing or the severity of bronchial hyperresponsiveness.

18 is of asthma, elevated serum IgE levels, and bronchial hyperresponsiveness.

19 e of beta2 agonists has been known to induce bronchial hyperresponsiveness.

20 region for linkage to asthma, serum IgE, and bronchial hyperresponsiveness.

21 associated with clinical signs of atopy and bronchial hyperresponsiveness.

22 ascular lung inflammation, and inhibition of bronchial hyperresponsiveness 6 wk after administration

23 (IL9) as a determining factor in controlling bronchial hyperresponsiveness, a hallmark of the disease

24 e to allergen, and prevented the increase in bronchial hyperresponsiveness after allergen challenge.

25 symptoms, reversible airflow obstruction, or bronchial hyperresponsiveness after having all asthma me

26 olled symptoms, and normal lung function and bronchial hyperresponsiveness, along with a high express

27 Subjects had bronchial hyperresponsiveness, an FEV1 < or = 70% of pre

28 tant in the inflammatory response leading to bronchial hyperresponsiveness and asthma.

29 implicated in determining susceptibility to bronchial hyperresponsiveness and asthma.

30 n for genes that determine susceptibility to bronchial hyperresponsiveness and atopy in animal models

31 y of the Genetics and Environment of Asthma, bronchial hyperresponsiveness and atopy) (170 with and 1

32 Viral respiratory infections can cause bronchial hyperresponsiveness and exacerbate asthma.

33 assumed coughing occurs as a consequence of bronchial hyperresponsiveness and inflammation, but the

34 gnosed asthma and atopy at 7(1/2) years, and bronchial hyperresponsiveness and lung function at 8(1/2

35 atory disease characterized by inflammation, bronchial hyperresponsiveness and narrowing of the airwa

36 In patients with moderate to severe bronchial hyperresponsiveness and nasal polyposis, the c

37 regression analysis, only moderate to severe bronchial hyperresponsiveness and nasal polyps were inde

38 s strongly associated with susceptibility to bronchial hyperresponsiveness and protection from allerg

39 ated with severe peribronchial eosinophilia, bronchial hyperresponsiveness, and augmented IL-13 and I

40 arly childhood is associated with asthma and bronchial hyperresponsiveness, and faster weight growth

41 cle growth, MMP-1 levels are associated with bronchial hyperresponsiveness, and MMP-1 activation are

42 CHI3L1 is a susceptibility gene for asthma, bronchial hyperresponsiveness, and reduced lung function

43 Transient bronchial hyperresponsiveness appears to be the predomin

44 Allergen-induced increases in serum IgE and bronchial hyperresponsiveness are exaggerated in periost

45 role for IL-9 in the complex pathogenesis of bronchial hyperresponsiveness as a risk factor for asthm

46 participants underwent lung function tests, bronchial hyperresponsiveness assessment and sputum indu

47 terized by reversible airway obstruction and bronchial hyperresponsiveness associated with T(H)2 cell

48 inkage to qualitative measures of asthma and bronchial hyperresponsiveness (BHR) (p > 0.10) or to qua

49 on with the key asthma-related phenotypes of bronchial hyperresponsiveness (BHR) and atopy.

50 Bronchial hyperresponsiveness (BHR) and nitric oxide pro

51 Bronchial hyperresponsiveness (BHR) can be present in su

52 Bronchial hyperresponsiveness (BHR) describes the exagge

53 been shown to induce airway inflammation and bronchial hyperresponsiveness (BHR) in mice.

54 The severity of bronchial hyperresponsiveness (BHR) is a fundamental fea

55 Bronchial hyperresponsiveness (BHR) is a phenotypic hall

56 Bronchial hyperresponsiveness (BHR) is an important, but

57 The bronchial hyperresponsiveness (BHR) test is useful to di

58 physiology of lung allergic inflammation and bronchial hyperresponsiveness (BHR) that characterize as

59 topathologic alterations of the airways, and bronchial hyperresponsiveness (BHR) were assessed.

60 asthma is increased airway irritability, or bronchial hyperresponsiveness (BHR) which is still poorl

61 25 yr later, 38 subjects (21%) did not show bronchial hyperresponsiveness (BHR)(PC20 > 16 mg/ml), 45

62 inophil counts in relation to lung function, bronchial hyperresponsiveness (BHR), and asthma control

63 e airway eosinophilia, mucus overproduction, bronchial hyperresponsiveness (BHR), and immunogloubulin

64 fraction of exhaled nitric oxide (Feno), low bronchial hyperresponsiveness (BHR), and low bronchodila

65 he associations of parental asthma severity, bronchial hyperresponsiveness (BHR), and total and speci

66 the lack of bronchoprotection is related to bronchial hyperresponsiveness (BHR), and whether the bro

67 inflammation; associated phenotypes include bronchial hyperresponsiveness (BHR), elevated total seru

68 of airway Mycoplasma pneumoniae infection on bronchial hyperresponsiveness (BHR), lung inflammation,

69 Bronchial hyperresponsiveness (BHR), often undetected in

70 characteristic features of asthma, including bronchial hyperresponsiveness, bronchoconstriction, airw

71 corticosteroid-unresponsive inflammation and bronchial hyperresponsiveness driven by IL-13.

72 he presence of nocturnal asthma, more severe bronchial hyperresponsiveness, exercise-induced asthma,

73 n, the importance of T cell costimulation in bronchial hyperresponsiveness had not been characterized

74 uch as high total serum immunoglobulin E and bronchial hyperresponsiveness, have been linked by numer

75 ronin 60.1 inhibits leucocyte diapedesis and bronchial hyperresponsiveness in a murine model of aller

76 mplementary roles of FENO and FOT to predict bronchial hyperresponsiveness in adult stable asthmatic

77 R5 or R20 and FENO can predict the level of bronchial hyperresponsiveness in adult stable asthmatics

78 rphisms showing association with severity of bronchial hyperresponsiveness in asthma patients.

79 Adenosine has been suggested to induce bronchial hyperresponsiveness in asthmatics, which is be

80 Bronchial hyperresponsiveness in at-risk neonates preced

81 67 restored the sGC signaling and attenuated bronchial hyperresponsiveness in CS-exposed mice.

82 ease) is strongly associated with asthma and bronchial hyperresponsiveness in different populations.

83 Bronchial hyperresponsiveness in mild to moderate asthma

84 Bronchial hyperresponsiveness is a characteristic featur

85 ay smooth muscle function to the extent that bronchial hyperresponsiveness is ablated, consistent wit

86 10) of the likelihood ratio (LOD), 2.94) and bronchial hyperresponsiveness (LOD, 3.93).

87 mice, compared with WT mice, had diminished bronchial hyperresponsiveness (lung airway resistance);

88 s suggest that a gene controlling asthma and bronchial hyperresponsiveness maybe located in this regi

89 asthma through the assessment of nonspecific bronchial hyperresponsiveness (NSBH) is a key step in th

90 ; 95% CI, 1.37-3.85; P = 0.002), but not for bronchial hyperresponsiveness or atopy.

91 ither by the immunopathogenesis of asthma or bronchial hyperresponsiveness, or uncovered by the whole

92 as significantly associated with more severe bronchial hyperresponsiveness (P < .0001) and with curre

93 ide evidence for linkage between DXYS154 and bronchial hyperresponsiveness (P = 0.000057) or asthma (

94 levels (P=1.1 x 10(-13)), asthma (P=0.047), bronchial hyperresponsiveness (P=0.002), and measures of

95 Bronchial hyperresponsiveness-related symptoms were asso

96 nto health care ("reported asthma") and (2) "bronchial hyperresponsiveness-related symptoms," defined

97 es in support of HLA-G as a novel asthma and bronchial hyperresponsiveness susceptibility gene in the

98 we evaluated these patients before and after bronchial hyperresponsiveness to acetylcholine (ACh) or

99 ese correlations in patients with normalized bronchial hyperresponsiveness to ACh or Hist.

100 adult patients with asthma having normalized bronchial hyperresponsiveness to ACh or Hist.

101 his study was to assess the relation between bronchial hyperresponsiveness to dry, cold air at age 6

102 ypes [total and allergen-specific serum IgE, bronchial hyperresponsiveness to methacholine, forced ex

103 sGCalpha1(-/-) mice exposed to CS exhibited bronchial hyperresponsiveness to serotonin.

104 Because improvement in bronchial hyperresponsiveness was associated with a redu

105 e were ventilated with a flexiVent setup and bronchial hyperresponsiveness was determined using acety

106 The presence of bronchial hyperresponsiveness was measured with a methac