ライフサイエンスコーパス: airflow limitation

1 y variable respiratory symptoms and variable airflow limitation.

2 evelopment of severe asthma and/or worsening airflow limitation.

3 d activity loss was significantly related to airflow limitation.

4 s, and correlate these sites with expiratory airflow limitation.

5 oil and examined the mechanism of expiratory airflow limitation.

6 putative effect on causing fixed expiratory airflow limitation.

7 asthma that was independent of the degree of airflow limitation.

8 had a reduced ventilatory ceiling because of airflow limitation.

9 on was stratified by country and severity of airflow limitation.

10 ults in largely irreversible and progressive airflow limitation.

11 ditional common characteristic is reversible airflow limitation.

12 ith COPD and explore their relationship with airflow limitation.

13 ed with the AA genotype demonstrated greater airflow limitation.

14 ere airflow limitation, and 0.1% very severe airflow limitation.

15 rrelated with the type 2 immune response and airflow limitation.

16 y disease (COPD) is characterized by chronic airflow limitation.

17 post-bronchodilator measures for those with airflow limitation.

18 deration in the diagnosis of asthma based on airflow limitation.

19 lly characterized by incompletely reversible airflow limitation.

20 decline is a rare feature of biomass-induced airflow limitation.

21 be associated with severe exacerbations and airflow limitation.

22 diseases, both of which are characterized by airflow limitation.

23 d to ensure proper evaluation of severity of airflow limitation.

24 isk increased significantly with severity of airflow limitation.

25 status and smoking history, and severity of airflow limitation.

26 roke and the risk increases with severity of airflow limitation.

27 concentrations were further associated with airflow limitation.

28 (H)2-mediated eosinophilic inflammation, and airflow limitation.

29 s significantly correlate with the degree of airflow limitation.

30 with ischemic heart disease: 11.3% had mild airflow limitation, 15.8% moderate airflow limitation, 3

31 ator spirometry, to identify the presence of airflow limitation, 18,475 subjects (99%) were assigned

32 had mild airflow limitation, 15.8% moderate airflow limitation, 3.3% severe airflow limitation, and

33 assessment of (1) symptoms, (2) severity of airflow limitation, (3) history of exacerbations, and (4

34 patients with fixed as compared to variable airflow limitation (69.76 vs 43.84 pg/ml, P < 0.05) and

35 Most patients with airflow limitation (70.6%) had no previous spirometry te

36 osure (PE) to dust and fumes (P = 0.006) and airflow limitation (AFL) (P = 0.033).

37 measures as z-score, and a classification of airflow limitation (AL) based on this parameter has rece

38 y smokers, and those with severe obstructive airflow limitation, although unpredictable transient des

39 Enrollment criteria included irreversible airflow limitation and AECOPD requiring corticosteroids,

40 We sought to prospectively assess airflow limitation and airway inflammation in children 4

41 P < 0.001), which increased with severity of airflow limitation and are suggestive of hypertensive or

42 We evaluated the effects of airflow limitation and arousal on digital vascular tone

43 ion does not mediate the association between airflow limitation and atherosclerosis.

44 Instead, airflow limitation and endothelial dysfunction seem to b

45 ith asthma had more respiratory symptoms and airflow limitation and higher levels of inflammatory and

46 To test the hypothesis that airflow limitation and hyperinflation are associated wit

47 n of asthma is associated with the degree of airflow limitation and hyperinflation.

48 ty in the asthmatic airway are correlated to airflow limitation and hyperreactivity.

49 nificantly down-regulated in smokers without airflow limitation and in patients with COPD compared wi

50 tein level, was decreased in smokers without airflow limitation and in patients with COPD, and correl

51 lable, and inexpensive global measurement of airflow limitation and lung function.

52 ributable to variation in the definitions of airflow limitation and the treatment of people with asth

53 .8% moderate airflow limitation, 3.3% severe airflow limitation, and 0.1% very severe airflow limitat

54 mpassing 8 never-smokers, 10 smokers without airflow limitation, and 12 smokers with COPD.

55 We contrasted clinical features, airflow limitation, and albuterol responsiveness in adul

56 by enhanced airway inflammation, reversible airflow limitation, and asthma-related symptoms.

57 ntioxidants is related to the development of airflow limitation, and hence dietary supplementation ma

58 d in lungs of never-smokers, smokers without airflow limitation, and patients with COPD; and in C57BL

59 and CMH, how symptoms during life related to airflow limitation at 60-64 years, and how CMH duration

60 Airflow limitation at day 0 was reversible after broncho

61 prospectively investigated the mechanism of airflow limitation before and after targeted emphysemato

62 but without current or previous evidence of airflow limitation, bronchial reversibility, or airway h

63 s with COPD older than 40 years, with severe airflow limitation, bronchitic symptoms, and a history o

64 ermediate-onset wheezers showed irreversible airflow limitation by 18 years.

65 y disease (COPD) is characterized by chronic airflow limitation caused by a combination of airways di

66 We find a major determinant of airflow limitation common to these diseases is the ratio

67 wn, but they may contribute to the resultant airflow limitation commonly seen in asthma.

68 Airflow limitation compatible with chronic obstructive p

69 With regard to the causes of airflow limitation, CT can be used to quantify the two m

70 tinguishable, but many patients with chronic airflow limitation demonstrate features of both conditio

71 flammation-predominant asthma and persistent airflow limitation despite high-intensity anti-inflammat

72 enge stopped and FENO rose temporally as the airflow limitation developed.

73 The degree of airflow limitation did not predict levels of free testos

74 ) is a major pathophysiologic consequence of airflow limitation during exercise in patients with chro

75 ntilation (V E), lung volume, and expiratory airflow limitation (EAFL) were measured during each 1-mi

76 oading in elderly subjects with mild chronic airflow limitation (FEV(1)/FVC: 61 +/- 4%), we studied 1

77 xpression was also associated with increased airflow limitation (FEV1/forced vital capacity and resid

78 ations with decline in FEV1 and incidence of airflow limitation for adults who were free from COPD at

79 We determined the relative contribution of airflow limitation, gas exchange abnormalities, and pulm

80 07 arbitrary units; p < 0.001), whereas mild airflow limitation (> 200 ml/second) had no effect (1.00

81 reported that patients with mild to moderate airflow limitation have a lower exercise capacity than a

82 ed oxidative stress in patients with chronic airflow limitation; however, the population-based eviden

83 nspiratory airflow (V(I)max) and inspiratory airflow limitation (IFL) were assessed.

84 els in sputum are associated with persistent airflow limitation in asthma patients with airway eosino

85 ts on the lung parenchyma that contribute to airflow limitation in asthmatics, and we hypothesize tha

86 The aim of the ALICE (Airflow Limitation in Cardiac Diseases in Europe) study

87 lationship of airway TGF-beta1 expression to airflow limitation in children with asthma was also asse

88 Emphysema is a key contributor to airflow limitation in chronic obstructive pulmonary dise

89 C because of CS exposure might contribute to airflow limitation in COPD.

90 that oxidative stress may be associated with airflow limitation in men, and that gender differences m

91 Maximal expiratory airflow limitation in only four elderly asthmatics and o

92 ) study was to investigate the prevalence of airflow limitation in patients with ischemic heart disea

93 tly associated with respiratory symptoms and airflow limitation in severely alpha(1)AT-deficient indi

94 etic factors and is strongly associated with airflow limitation in smaller airways.

95 Airway remodeling burden is not limited to airflow limitation in the assessment of COPD severity an

96 re less likely to have undergone testing for airflow limitation in the community at the time of initi

97 ne in adulthood, and development of moderate airflow limitation in the general adult population.

98 iation between atopy and post-bronchodilator airflow limitation in the general population aged 40 yea

99 iation between atopy and post-bronchodilator airflow limitation in the general population appears to

100 ls from 4,724 subjects with mild-to-moderate airflow limitation in the Lung Health Study.

101 Nonsurvivors were older and had more severe airflow limitation, increased dyspnea, higher BODE score

102 Although airflow limitation is associated with additional morbidi

103 Although airflow limitation is common, no previous studies have e

104 urrently available classifications combining airflow limitation measurements with clinical parameters

105 Treatments for airflow limitation might improve survival and both respi

106 COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress fr

107 associated with a higher risk of subsequent airflow limitation (odds ratio [95% confidence interval]

108 h emphysema were matched for the severity of airflow limitation of those with bronchiolitis.

109 disease (COPD) is defined by the presence of airflow limitation on spirometry, yet subjects with COPD

110 g people with known pulmonary disease and/or airflow limitation on spirometry.

111 The no airflow limitation or air-trapping criteria (None) pheno

112 nt asthma (defined as wheeze and presence of airflow limitation or airway hyper-reactivity, or both).

113 ficant for spirometric phenotypes related to airflow limitation or COPD.

114 The airflow limitation phenotype (A Limit) had an FEV1/FVC z

115 Induction of airflow limitation produced significant phase difference

116 ated with increased risk of incident stage 2 airflow limitation (ratio of FEV1 to forced expiratory v

117 ntiating asthma from other causes of chronic airflow limitation, such as chronic obstructive pulmonar

118 evidence that CRTH2 receptors contribute to airflow limitation, symptoms and eosinophilic airway inf

119 ic obstructive pulmonary disease with severe airflow limitation, symptoms of chronic bronchitis, and

120 commended for patients with COPD with severe airflow limitation, symptoms of chronic bronchitis, and

121 ording to simple clinical measures (level of airflow limitation, symptoms, and frequency of previous

122 e pulmonary component is characterized by an airflow limitation that is not fully reversible.

123 Pulmonary function testing revealed severe airflow limitation (the FEV1 ranging from 22% to 56% of

124 a with low cumulated smoking exposure and no airflow limitation, those with COPD, those with asthma-C

125 y, 6-AMCH, DHC and 4-OPA would not result in airflow limitation to the airways.

126 onship between chronic respiratory symptoms, airflow limitation, treatment requirements, and semiquan

127 Airflow limitation was associated with greater respirato

128 Airflow limitation was defined as post-bronchodilator FE

129 Airflow limitation was defined as post-bronchodilator sp

130 Airflow limitation was observed in 30.5% of patients wit

131 ean +/- SD) who had fixed, severe expiratory airflow limitation with a mean FEV1 = 0.73 +/- 0.1 L (me

132 eceiving pressure support in whom we induced airflow limitation with a Starling resistor.