ライフサイエンスコーパス: airflow limitation

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

2 concentrations were further associated with airflow limitation.

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

4 s significantly correlate with the degree of airflow limitation.

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

6 d activity loss was significantly related to airflow limitation.

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

8 oil and examined the mechanism of expiratory airflow limitation.

9 putative effect on causing fixed expiratory airflow limitation.

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

11 had a reduced ventilatory ceiling because of airflow limitation.

12 of mucous plugging and its association with airflow limitation.

13 ation inhomogeneity and spirometry to assess airflow limitation.

14 ne) were not associated with air trapping or airflow limitation.

15 y variable respiratory symptoms and variable airflow limitation.

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

17 ults in largely irreversible and progressive airflow limitation.

18 ditional common characteristic is reversible airflow limitation.

19 ith COPD and explore their relationship with airflow limitation.

20 ed with the AA genotype demonstrated greater airflow limitation.

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

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

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

24 post-bronchodilator measures for those with airflow limitation.

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

26 lly characterized by incompletely reversible airflow limitation.

27 erized by incompletely reversible expiratory airflow limitation.

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

29 be associated with severe exacerbations and airflow limitation.

30 not associated with emphysema or severity of airflow limitation.

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

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

33 isk increased significantly with severity of airflow limitation.

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

35 caused by HMW agents showed a higher risk of airflow limitation (1.76 [1.07-2.91]), whereas OA due to

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

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

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

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

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

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

42 med at identifying circulating biomarkers of airflow limitation across different stages of life.

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

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

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

46 but smaller airways, which causes expiratory airflow limitation and abnormal respiratory mechanics bu

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

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

49 linical history of COPD, along with moderate airflow limitation and an increased risk of exacerbation

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

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

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

53 The risk of airflow limitation and chronic obstructive pulmonary dis

54 Instead, airflow limitation and endothelial dysfunction seem to b

55 signature of serum proteins associated with airflow limitation and evaluate their relation to lung f

56 bronchial airway hyperreactivity and chronic airflow limitation and has been described as leading to

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

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

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

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

61 f mucus plugs and emphysema in mechanisms of airflow limitation and hypoxemia in smokers with chronic

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

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

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

65 ulmonary disease, moderate-severe expiratory airflow limitation and radiologically determined bronchi

66 to numerous diverse stimuli, contributing to airflow limitation and symptoms including breathlessness

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

68 Background Fixed airflow limitation and ventilation heterogeneity are com

69 .8% moderate airflow limitation, 3.3% severe airflow limitation, and 0.1% very severe airflow limitat

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

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

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

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

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

75 ulmonary disease, moderate-severe expiratory airflow limitation, and radiologically determined bronch

76 functional abnormalities, in the absence of airflow limitation, and who may develop persistent airfl

77 [95% CI, 1.66-4.24]; P < .001) but not with airflow limitation (aOR, 1.07 [95% CI, .71-1.62]; P = .7

78 and cardiac markers and support the role of airflow limitation as independent predictor of mortality

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

80 Airflow limitation at day 0 was reversible after broncho

81 Understanding of airflow limitation based on the structural changes of as

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

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

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

85 A measure of airflow limitation but not vital capacity was associated

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

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

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

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

90 Airflow limitation compatible with chronic obstructive p

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

92 ng sites, aged at least 40 years, with known airflow limitation (defined as a post-bronchodilator FEV

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

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

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

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

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

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

99 te (Estimate = -1.757, p = 0.048) and severe airflow limitation (Estimate = -3.200, p = 0.022) than B

100 was associated with increased risk of severe airflow limitation (Estimate =2.073, p = 0.048), while o

101 uretic peptide, high-sensitivity troponin I, airflow limitation (FEV(1)), lung hyperinflation (residu

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

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

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

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

106 the entire sample, even after adjusting for airflow limitation, gas trapping, and diffusing capacity

107 07 arbitrary units; p < 0.001), whereas mild airflow limitation (> 200 ml/second) had no effect (1.00

108 ged 40-85 years, had moderate to very severe airflow limitation, had elevated blood eosinophil counts

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

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

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

112 besity-associated insulin resistance (IR) in airflow limitation in asthma is uncertain.

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

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

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

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

117 nchioles (pre-TBs/TBs), underlie progressive airflow limitation in chronic obstructive pulmonary dise

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

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

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

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

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

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

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

125 1)%pred) classifications for the severity of airflow limitation in terms of exertional breathlessness

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

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

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

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

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

131 airways and reduced airway resistance, while airflow limitation in the LFEV(1) is due to increased ai

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

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

134 Airflow limitation is a hallmark of chronic obstructive

135 Although airflow limitation is associated with additional morbidi

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

137 rimarily of young, obese females with severe airflow limitation, little eosinophilic inflammation, an

138 urrently available classifications combining airflow limitation measurements with clinical parameters

139 Treatments for airflow limitation might improve survival and both respi

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

141 und Longitudinal progression to irreversible airflow limitation occurs in approximately 10% of patien

142 ns were associated with air trapping but not airflow limitation (odds ratio 1.19, 95% confidence inte

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

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

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

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

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

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

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

150 a propria in asthma patients with concurrent airflow limitation or severe disease.

151 w limitation, and who may develop persistent airflow limitation over time.

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

153 Induction of airflow limitation produced significant phase difference

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

155 s: FEV(1)/FVC and FEV(1)%pred as measures of airflow limitation severity show similar predictions of

156 NT5a mRNA was associated with severe asthma, airflow limitation, sputum eosinophilia and Th2, and Th1

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

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

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

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

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

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

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

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

165 ire and were classed as having or not having airflow limitation through pulmonary function tests befo

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

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

168 The prevalence of asthma with airflow limitation was 1.1% (0.9-1.4), representing 13.1

169 A signature of 5 circulating biomarkers of airflow limitation was associated with both impaired lun

170 Airflow limitation was associated with greater respirato

171 Airflow limitation was defined as post-bronchodilator FE

172 Airflow limitation was defined as post-bronchodilator sp

173 Airflow limitation was observed in 30.5% of patients wit

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

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

176 y symptoms, history of smoking exposure, and airflow limitation with FEV(1)/FVC < 0.70.

177 haracterized by progressive and irreversible airflow limitation, with individual body composition inf