ライフサイエンスコーパス: FEV1

1 FEV1 decline in individuals with asthma-COPD overlap wit

2 FEV1 decline was greater in smokers (P < 0.001), but the

3 FEV1 percentage predicted was significantly different be

4 FEV1:fvc (p=0.0075) and FeNO (p<0.0001), but not broncho

5 ouncil dyspnea score (r = 0.34; P < 0.0001), FEV1% predicted (r = -0.33; P < 0.0001), and the radiolo

6 spite ongoing use of asthma medications, (2) FEV1 of less than 70% of predicted value, (3) daily or a

7 pb or greater (OR, 1.72; 95% CI, 1.14-2.59), FEV1/FVC ratio decrements (OR, -0.22 SDU; 95% CI, -0.36

8 or FRC-HI, vs 21% and 41% in patients with a FEV1 > 80%).

9 evalence of HI was higher in patients with a FEV1 <60% predicted (93% for RV-HI and 71% for FRC-HI, v

10 11; P = .002) and experienced an accelerated FEV1 decline by 13.2 mL/y in the LHS (P = .007) and by 1

11 y events were not associated with additional FEV1 decline.

12 Besides accelerating adult FEV1 decline, cigarette smoking also modifies how early-

13 63) CNTO3157 provided no protection against FEV1 decrease (least squares mean: CNTO3157 [n = 30] = -

14 55.4% of EBV and 6.5% of SoC subjects had an FEV1 improvement of 12% or more (P < 0.001).

15 irflow limitation phenotype (A Limit) had an FEV1/FVC z score of less than -1.64 but not A Trpg.

16 cerbation in the year before the study or an FEV1 <60% or >/=60% of predicted.

17 time, but the proportion of patients with an FEV1/FVC ratio <0.7 decreased at 6, 12, 18, and 24 month

18 8, 9.6]), mean FEV1 (-166 ml [-332, -1]) and FEV1 /FVC ratio (-4.6%, [-8.1, -1.1]) at 12 years.

19 r = 0.54), exacerbation rate (r = 0.41), and FEV1 (r = -0.46).

20 r = 0.35), exacerbation rate (r = 0.47), and FEV1 (r = -0.61).

21 ction (FEV1/forced vital capacity < 0.85 and FEV1 < 100% predicted) than in BECs from children with a

22 te highly with sweat chloride test, BMI, and FEV1% predicted values.

23 decrease in FVC (forced vital capacity) and FEV1 (forced expiratory volume in 1 s) of 0.03 L [95% co

24 odest correlations between NET complexes and FEV1, symptoms evaluated by using the COPD assessment te

25 nts, and between endothelial dysfunction and FEV1 or FEV1/FVC in HeartSCORE participants (all P > 0.0

26 ociation between endothelial dysfunction and FEV1, FEV1/FVC, low-attenuation area/visual emphysema, a

27 me overcrowding, and pollution exposure) and FEV1 and FVC trajectories between ages 43 and 60-64 year

28 x, BMI, smoking index, biomass exposure, and FEV1.

29 DLCO, FEV1, and FEV1/FVC were found to be valuable parameters in determi

30 g emphysematous changes were DLCO, FEV1, and FEV1/FVC, in that order.

31 gnificantly (P < 0.001) reduced CRR, FR, and FEV1 and increased FENO , EOS, PAI-1, FXIII, and CD in p

32 and lower limit of normal values for FVC and FEV1 than those in other Hispanic/Latino background grou

33 r lung function decline, assessed by FVC and FEV1, is accelerated in women who undergo menopause.

34 -resolution computed tomographic images, and FEV1/FVC ratios less than 0.8 or greater than 0.9 (<0.7

35 r whom we had symptomatology information and FEV1 measurements, respectively.

36 p between the Jacobian determinant, MAL, and FEV1 decline.

37 and less than the lower limit of normal, and FEV1 of less than 80% of the predicted normal value.

38 concentrations with respiratory outcomes and FEV1 in percent predicted (FEV1%) were estimated by surv

39 % CI: 1.27, 3.46, p=0.004, respectively] and FEV1 decreased (beta=-0.143; 95% CI: -0.248, -0.039, p=0

40 Associations between smoking and FEV1/FVC ratios were different between asthma phenotypes

41 y correlated with FENO, R5, R20, R5-R20 and %FEV1.

42 The geographical, anthropometrics, FEV1, dyspnea, comorbidities, and health status scores w

43 COPD was defined as FEV1/forced vital capacity (FVC) of less than 70% and le

44 litis obliterans syndrome grade and baseline FEV1% predicted (P = 0.04).

45 eded to treat was not influenced by baseline FEV1 but was influenced by the history of exacerbations.

46 ve of a history of exacerbations or baseline FEV1.

47 ity was greatest for subjects whose baseline FEV1/FVC value was closest to the diagnostic threshold,

48 At baseline, FEV1 bronchodilator responsiveness was the most importan

49 associated with a lower post-bronchodilator FEV1 compared with those not sensitised to fungi ((73.0

50 dicted value, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.70 or less, a s

51 ng prebronchodilator and post-bronchodilator FEV1, FVC, FEV1/FVC, and maximum mid-expiratory flow (MM

52 ry (1-4) on the basis of post-bronchodilator FEV1.

53 COPD was defined as post-bronchodilator FEV1/FVC <0.7.

54 imitation was defined as post-bronchodilator FEV1/FVC less than 0.70.

55 ometrically defined as a post-bronchodilator FEV1/FVC less than the lower limit of normal.

56 ges 43 and 60-64 years related to concurrent FEV1 decline.

57 were persons with no COPD or with mild COPD (FEV1 >/=60% predicted, no exacerbation in the past year)

58 iotropium in patients with symptomatic COPD, FEV1 of less than 50%, and a history of exacerbations.

59 Subjects recorded daily FEV1 and FVC for up to 490 days.

60 DLCO, FEV1, and FEV1/FVC were found to be valuable parameters

61 determining emphysematous changes were DLCO, FEV1, and FEV1/FVC, in that order.

62 % CI 0.052-0.109; p<0.001) and 2-h post-dose FEV1 by 0.117 L (0.086-0.147; p<0.001) compared with BDP

63 endpoints were pre-dose FEV1, 2-h post-dose FEV1, and Transition Dyspnea Index (TDI) focal score, al

64 ndpoint was change from baseline in pre-dose FEV1 at week 52.

65 At week 26, BDP/FF/GB improved pre-dose FEV1 by 0.081 L (95% CI 0.052-0.109; p<0.001) and 2-h po

66 The three co-primary endpoints were pre-dose FEV1, 2-h post-dose FEV1, and Transition Dyspnea Index (

67 For week 52 pre-dose FEV1, fixed triple was superior to tiotropium (mean diff

68 ed with other asthma outcomes scores, except FEV1, but shared relatively low common variance with the

69 D, exacerbations were associated with excess FEV1 decline, with the greatest effect in Global Initiat

70 presenting with an isolated decline in FEV1 (FEV1 First) had significantly higher PRM(fSAD) than cont

71 forced expiratory volume in 1 second [FEV1 ; FEV1 <65% vs >/=65% predicted], inhaled beclomethasone d

72 on between endothelial dysfunction and FEV1, FEV1/FVC, low-attenuation area/visual emphysema, and dif

73 a younger gestational age had a lower FEV1, FEV1/forced vital capacity (FVC) ratio, and forced expir

74 levels were negatively associated with FEV1, FEV1/FVC, and MMEF.

75 We used linear mixed models to fit FEV1 decline based on reported exacerbations or acute re

76 , and total lung capacity) and lesser flows (FEV1 and forced expiratory flow, midexpiratory phase), a

77 arly-life home overcrowding (P = 0.009), for FEV1 at 43 years.

78 for 5-year survival was slightly higher for FEV1 expressed as percentage of predicted than as z-scor

79 None of the SNPs identified for FEV1/forced vital capacity replicated in the independent

80 ife was also associated with odds ratios for FEV1 and FVC less than the lower limit of normal (LLN) (

81 ns were observed with reduced lung function (FEV1 % of predicted value < 90%).

82 ranulocytic asthma had better lung function (FEV1 % pred) [median (IQR): 71.5 (59.0-88.75) vs 69.0 (5

83 Measures of lung function (FEV1, forced vital capacity [FVC], and forced expiratory

84 hodilator and post-bronchodilator FEV1, FVC, FEV1/FVC, and maximum mid-expiratory flow (MMEF).

85 proximately 0.5 SD for most variables (e.g., FEV1; mean z-score, -1.00 vs. -1.53; mean difference, 0.

86 nal age at birth had a lower FEV1 but higher FEV1/FVC ratio (P < .05).

87 nfant weight gain was associated with higher FEV1 but lower FEV1/FVC ratio and FEF75 in childhood (P

88 ody, reduced exacerbation rates and improved FEV1 in patients with uncontrolled asthma, particularly

89 ximately 0.5 z-scores ( approximately 5%) in FEV1 and FVC compared with African American peers from t

90 apy (n = 899), mean changes from baseline in FEV1 were 142 ml (95% confidence interval [CI], 126 to 1

91 eosinophilic inflammation and the change in FEV1 .

92 2% (P < 0.001), with a mean +/- SD change in FEV1 at 6 months of 20.7 +/- 29.6% and -8.6 +/- 13.0%, r

93 between study arms in 52-week mean change in FEV1 slope (mean slope difference, 0.00 L, 95% confidenc

94 between-group difference in median change in FEV1 was 7.0% (97.5% CI, 3.4% to infinity; 1-sided P < .

95 he primary outcome was the 52-week change in FEV1.

96 Changes in FEV1, residual volume, 6-minute-walk distance, St. Georg

97 Secondary outcomes included changes in FEV1, St. George's Respiratory Questionnaire (SGRQ), 6-m

98 levels were associated with more decline in FEV1 (467 vs. 320 mL) (P = 0.02).

99 ients presenting with an isolated decline in FEV1 (FEV1 First) had significantly higher PRM(fSAD) tha

100 s associated with 1.00 ml/yr less decline in FEV1 (P < 0.001) and 1.55 ml/yr less decline in FVC (P <

101 ssociated with 2.54 ml/yr greater decline in FEV1 (P < 0.001) and 3.27 ml/yr greater decline in FVC (

102 ation of histamine inducing a 20% decline in FEV1 (PC20 ) </=16 mg/mL showed a sensitivity of 87% and

103 whereas patients with concurrent decline in FEV1 and FVC had significantly higher PRM(PD) than contr

104 The multivariable-adjusted decline in FEV1 in asthma-COPD overlap with early-onset asthma was

105 The mean (SD) rate of decline in FEV1 was 39.0 (58.6) ml/yr.

106 MAL2 (threshold, 36.9%), the mean decline in FEV1 was 56.4 (68.0) ml/yr versus 43.2 (59.9) ml/yr for

107 of COPD exacerbations, mortality, decline in FEV1, and response to both inhaled and systemic corticos

108 : 1.03, 1.10) for asthma, a 9 ml decrease in FEV1 (95% CI: 2.0-15 mL decrease) and a 16 ml decrease i

109 ration of allergen causing a 15% decrease in FEV1 (allergen PC15) that was maximal and approximately

110 and the AA/AG genotypes had a 5% decrease in FEV1 /FVC (P<.001).

111 he primary end point was maximal decrease in FEV1 during 10 days after inoculation.

112 For every 200-ml decrease in FEV1, all-cause mortality increased by 11.0% in those wi

113 2 level was associated with a 5% decrease in FEV1/forced vital capacity ratio (beta = -0.05; 95% CI,

114 as significantly associated with decrease in FEV1: beta=-0.0012 (95% CI: -0.0019, -0.0006) and FVC: b

115 We noted no differences in FEV1 slopes between the immediate and deferred ART group

116 of mannitol required to reach a 15% drop in FEV1 , or mannitol reactivity, expressed as the response

117 the response dose ratio (RDR: max % fall in FEV1 /cumulative dose), when comparing ICS/IND/TIO to IC

118 ty increased and was associated with fall in FEV1 and worsening asthma symptoms.

119 ter and an increment of 200 ml or greater in FEV1 after bronchodilator administration.

120 ferences between the randomisation groups in FEV1 or fraction of exhaled nitric oxide.

121 The mean relative improvement in FEV1 between the treatment group versus the control grou

122 greater than or equal to 10% improvement in FEV1 with parenteral corticosteroid.

123 There were small improvements in FEV1 and Pc20 for both mild/ moderate and severe asthmat

124 /mL or less, which led to a 20% reduction in FEV1 (PC20).

125 In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated w

126 treatment step, the greatest variability in FEV1 over time, and the greatest sensitivity to methacho

127 The full model, including FEV1, also had modestly superior discriminatory power th

128 Age, body mass index, FEV1, PC20, fraction of exhaled nitric oxide, blood eosi

129 I, chronic Pseudomonas aeruginosa infection, FEV1/FVC (forced vital capacity), PA:A greater than 1, a

130 h the late phenotype had the highest initial FEV1 but experienced the greatest loss of lung function.

131 After omalizumab initiation, FEV1 improved at 6 months in responder patients and then

132 ssociated with increased airflow limitation (FEV1/forced vital capacity and residual volume/total lun

133 cterized by differences in mean longitudinal FEV1 trajectories.

134 Lower FEV1 is associated with increased prevalence of atherosc

135 Lower FEV1 was independently associated with increased atheros

136 The severe group had a lower FEV1 and more eosinophilic inflammation compared to mild

137 eline, both groups of asthmatics had a lower FEV1 and Pc20 and increased eosinophilic inflammation co

138 ize for gestational age at birth had a lower FEV1 but higher FEV1/FVC ratio (P < .05).

139 ican American subjects (n = 264) had a lower FEV1 percent predicted (80% vs 85%, P < .01), greater to

140 n with a younger gestational age had a lower FEV1, FEV1/forced vital capacity (FVC) ratio, and forced

141 significantly worse asthma control and lower FEV1.

142 in was associated with higher FEV1 but lower FEV1/FVC ratio and FEF75 in childhood (P < .05).

143 Adult SA continued to manifest lower FEV1 and worse asthma control as compared with NONSA aft

144 eater limitation of activity, slightly lower FEV1, FVC, and inspiratory capacity, and greater airway-

145 enotypes (AA/AG), were associated with lower FEV1 /FVC in subjects with asthma (beta=-1.25, CI: -2.14

146 was also significantly associated with lower FEV1/FVC (P = 0.04), its contribution relative to PRM(FS

147 ut unchanged FEV1 (P = 0.94), yielding lower FEV1/FVC ratios (P < 0.001).

148 to early, middle, and late timing of maximal FEV1 loss, in the overall cohort (n = 18,387).

149 Mean FEV1 % pred of 75.1%, median values of 300/mm(3) of bloo

150 educed sensitization (3.37[1.18, 9.6]), mean FEV1 (-166 ml [-332, -1]) and FEV1 /FVC ratio (-4.6%, [-

151 53 years, 59-69% were female, and had a mean FEV1 percentage of predicted normal of 63-84%.

152 The adjusted mean FEV1 decline increased by -3.8 ml/yr (95% CI, -6.3 to -2

153 roups exhibited a small but significant mean FEV1% predicted improvement after TA (SA group mean diff

154 The mean FEV1 at baseline was 60.0% of the predicted value.

155 The mean FEV1 percent predicted for cases was 42.5% (14.2%); for

156 The mean age was 71 years, mean FEV1 was 1.3 L, and 59% had evidence of mild/moderate co

157 inophil group had significantly lower median FEV1 percentage predicted than the low sputum eosinophil

158 early-life exposures impact on both midlife FEV1 and FVC.

159 Malnourished African children had a normal FEV1/FVC ratio but significant reductions of approximate

160 spiratory impairment, as shown by the normal FEV1/FVC ratio.

161 ter the last dose, all IOS outcomes, but not FEV1 or FEF(25-75), were significantly better with formo

162 children with asthma and airway obstruction (FEV1/forced vital capacity < 0.85 and FEV1 < 100% predic

163 The analysis of FEV1 change from baseline to week 4 showed a statistical

164 ociated with an additional loss (-6.1 mL) of FEV1 (p = 0.001) between 1981 and 2011.

165 (-21.8 ml; -43.9 to 0.2) and higher odds of FEV1 less than 80% predicted (1.41; 1.03-1.93).

166 based on z-score or percentage predicted of FEV1 in patients with chronic obstructive pulmonary dise

167 The lowest quartile of FEV1 at 7 years was associated with ACOS (odds ratio, 2.

168 The lowest quartile of FEV1/FVC ratio at 7 years was associated with ACOS (odds

169 Mean (SD) rate of FEV1 decline in ml/yr for GOLD (Global Initiative for Ch

170 fifth decade and not an accelerated rate of FEV1 decline.

171 and nondietary risk factors, slower rates of FEV1 and FVC decline by 23.6 (95% CI: 16.6, 30.7) and 37

172 inear mixed effects modeling of the ratio of FEV1 to FVC was used to identify distinct lung function

173 nct phenotypes by evaluating trajectories of FEV1 decline.

174 The effect of oral corticosteroids on FEV1 , Pc20, airway inflammation and serum cytokines was

175 0 showed a significant interaction effect on FEV1 with dust mite allergen level in PRGOAL (interactio

176 3A) were shown to have an additive effect on FEV1/FVC levels in the genetic risk score analysis; were

177 was no effect of any early-life exposure on FEV1 decline.

178 asthma status and the PAI-1 polymorphism on FEV1 /FVC (P=.03).

179 ifies the estimated effect of rs117902240 on FEV1 in children with asthma.

180 s because of the known effects of smoking on FEV1 decline.

181 between endothelial dysfunction and FEV1 or FEV1/FVC in HeartSCORE participants (all P > 0.05).

182 t least one exacerbation in the past year or FEV1 less than 60% of predicted without exacerbation in

183 he muscle metaboreflex, in 18 COPD patients (FEV1 /FVC ratio < 70%), 9 also classified as chronically

184 Improvement in peak FEV1 within 3 hours after dosing at 24 weeks (primary en

185 therapy improved the primary end point, peak FEV1 within 3 hours after dosing (5 mug, 139 mL [95% CI,

186 wer prebronchodilator and postbronchodilator FEV1 and prebronchodilator forced expiratory flow at 25%

187 ent at 6 months, pre- and postbronchodilator FEV1 remained stable at 12, 18, and 24 months.

188 ted prebronchodilator and postbronchodilator FEV1 were 72.7% (SD, 21.4%) and 78.2% (SD, 20.7%), respe

189 capacity (FVC), pre- and postbronchodilator FEV1, residual volume (RV), and total lung capacity (TLC

190 e associated with reduced postbronchodilator FEV1 and FVC percent predicted.

191 nd asthma subgrouped with postbronchodilator FEV1 percent predicted value of less than 80%, it was ai

192 t was change from baseline prebronchodilator FEV1 at week 12.

193 quares mean difference) in prebronchodilator FEV1 after 12 weeks than did placebo (placebo group: 224

194 Mean prebronchodilator FEV1 showed improvement in responders at 6 months, while

195 t screening, had a morning prebronchodilator FEV1 of more than 50% to 90% predicted at screening, and

196 In children, after TA only prebronchodilator FEV1 distinguished SA from NONSA.

197 this penumbra of lung at risk would predict FEV1 decline.

198 s in both cohorts (per 25% lower % predicted FEV1: odds ratio [OR], 1.76; 95% confidence interval [CI

199 COR participants) (per 25% lower % predicted FEV1: OR, 1.35; 95% CI, 1.02-1.77; P = 0.03 for coronary

200 es (1.4% decrease in percentage of predicted FEV1 per 1 SD increase in log Gal-3; 95% confidence inte

201 solute change in the percentage of predicted FEV1 was 6.8 percentage points for tezacaftor-ivacaftor

202 annual rate of decline in percent predicted FEV1 (ppFEV1) in treated patients was compared with that

203 No significant changes in percent predicted FEV1 were observed (change from baseline at Week 24, +2.

204 Baseline ACT score, percent predicted FEV1, degree of bronchodilator response, and ICS adheren

205 ciation of NO2 levels with percent predicted FEV1, fraction of exhaled nitric oxide, or asthma sympto

206 ical covariates (age, sex, percent predicted FEV1, self-reported gastroesophageal reflux, St. George'

207 to 10-point improvement in percent predicted FEV1.

208 in IL-6 low patients (mean percent predicted FEV1=70.8% [SD 19.5] vs 78.3% [19.7]; p=0.002), and the

209 icantly correlated with percentage predicted FEV1 (r = -0.74; P = .0028) and FV (r = 0.74; P = .0002)

210 related positively with percentage predicted FEV1.

211 e changes in the percentage of the predicted FEV1 in favor of tezacaftor-ivacaftor over placebo were

212 ve change in the percentage of the predicted FEV1 through week 24 (calculated as a percentage) was a

213 tory outcomes and FEV1 in percent predicted (FEV1%) were estimated by survival and linear regression

214 6: P<0.05), but not with FEV1 (% predicted), FEV1 /FVC or bronchodilator reversibility.

215 ontrol Test score, FEV1 (percent predicted), FEV1/forced vital capacity ratio (percent predicted), an

216 rced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and

217 s associated with reduced FEV1 to FVC ratio (FEV1/FVC), hyperinflation, and alveolar enlargement, but

218 heezy bronchitis was associated with reduced FEV1 that was evident by the fifth decade and not an acc

219 RATIONALE: Aging is associated with reduced FEV1 to FVC ratio (FEV1/FVC), hyperinflation, and alveol

220 L1RAP, and IL4R were associated with reduced FEV1/forced vital capacity ratio (beta = -0.11, -0.08, a

221 5 or 50% increase), (2) spirometric results (FEV1 >/=80% of predicted value or >/=15% increase), (3)

222 week 12 in forced expiratory volume in 1 s (FEV1 in L) in patients with baseline blood eosinophil co

223 decline in forced expiratory volume in 1 s (FEV1) and a composite of cardiovascular events.

224 nchodilator forced expiratory volume in 1 s (FEV1) and total asthma symptom score.

225 nchodilator forced expiratory volume in 1 s (FEV1) between 50% and 70% of the predicted value, a rati

226 t predicted forced expiratory volume in 1 s (FEV1) of 70 or more, and lung clearance index2.5 (LCI2.5

227 sibility in forced expiratory volume in 1 s (FEV1) of at least 12% at screening, from 52 clinical res

228 nchodilator forced expiratory volume in 1 s (FEV1) of less than 50%, at least one moderate-to-severe

229 age 5, when forced expiratory volume in 1 s (FEV1) was measured by spirometry.

230 tients, the forced expiratory volume in 1 s (FEV1) was significantly lower in IL-6 high than in IL-6

231 ndex (BMI), forced expiratory volume in 1 s (FEV1), and PA:A greater than 1, and in the validation co

232 y (ratio of forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] <70%, bronchodilato

233 nchodilator forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] ratio <0.7 in patie

234 gatively with the Asthma Control Test score, FEV1 (percent predicted), FEV1/forced vital capacity rat

235 tal of 152 participants (72% male; mean [SD] FEV1 percent predicted, 50.5% [21.2]; median [first quar

236 ubjects (age, 63.7 +/- 6.1 yr [mean +/- SD]; FEV1, % predicted, 29.3 +/- 6.5; residual volume, % pred

237 ated with forced expiratory volume in 1 sec (FEV1) decline, with each 10-g increase in lung mass asso

238 ts for forced expiratory volume in 1 second (FEV1) (388 mL), forced vital capacity (298 mL), and the

239 d with forced expiratory volume in 1 second (FEV1) (P = 0.030).

240 dicted forced expiratory volume in 1 second (FEV1) from the baseline value to the average of the week

241 ges in forced expiratory volume in 1 second (FEV1) of omalizumab responders and nonresponders at 6 mo

242 dicted forced expiratory volume in 1 second (FEV1) through week 24 (calculated in percentage points);

243 ted of forced expiratory volume in 1 second (FEV1) was observed; correspondingly median FV (r = 0.86;

244 on the forced expiratory volume in 1 second (FEV1), as compared with placebo.

245 howing forced expiratory volume in 1 second (FEV1), representing spirometric measurements performed f

246 ion [forced expiratory volume in one second (FEV1 ) and forced vital capacity (FVC)] (n = 414).

247 gE), forced expiratory volume in one-second (FEV1) and forced vital capacity (FVC).

248 year, forced expiratory volume in 1 second [FEV1 ; FEV1 <65% vs >/=65% predicted], inhaled beclometh

249 ction (forced expiratory volume in 1 second [FEV1]).

250 orced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in

251 minimization to balance groups for age, sex, FEV1 percent predicted, and baseline exercise capacity a

252 attern of emphysema in relation to age, sex, FEV1, smoking index, biomass exposure, and BMI.

253 growth, leading to a proportionately smaller FEV1 and FVC without respiratory impairment, as shown by

254 defined as post-bronchodilator spirometric (FEV1 /FVC) ratio <lower limit of normal.

255 ), NO in exhaled breath (FENO ), spirometry (FEV1 ) and eosinophil count (EOS) in 36 patients with al

256 Among 630 children who completed spirometry, FEV1:FVC was less than 70% in ten (2%) children, of whom

257 The FEV1/FVC remained unchanged over time, but the proportio

258 mL), forced vital capacity (298 mL), and the FEV1/forced vital capacity ratio (3.7%) over the follow-

259 f decline in lung function, expressed as the FEV1 slope in mL/year; spirometry was done annually duri

260 We identified associations between the FEV1/FVC ratio and 5 common genetic variants in the iden

261 The decrease in the FEV1 /FVC ratio associated with the risk genotype was mo

262 Results of the FEV1 identification analysis were not replicated.

263 s occurred without a sustained effect on the FEV1.

264 reatment with currently available therapies (FEV1 <60% predicted and/or exacerbation risk).

265 mary end point analyzed was change in trough FEV1 (DeltaFEV1) from baseline to 8 to 12 weeks of treat

266 ndpoints were change from baseline in trough FEV1 and in St. George's Respiratory Questionnaire (SGRQ

267 7]), and the key secondary end point, trough FEV1 (5 mug, 87 mL [95% CI, 19-154; P = .01]; 2.5 mug, 1

268 with increased FVC (P = 0.004) but unchanged FEV1 (P = 0.94), yielding lower FEV1/FVC ratios (P < 0.0

269 Over 8.3 years of follow-up, FEV1 First patients with PRM(fSAD) greater than or equal

270 To define normal values, we used FEV1 values from participants in the National Health and

271 Key exclusion criteria were FEV1 less than 70% of predicted value or hospitalization

272 The primary outcomes were FEV1 decline, respiratory mortality, and biomarkers of s

273 Within smoker-stratified models, there were FEV1 deficits among ever-smokers associated with infant

274 ht to determine the relationship of AHR with FEV1 decline, respiratory mortality, and systemic inflam

275 e relationship of the PAI-1 risk allele with FEV1/FVC by multivariate linear regression, stratified b

276 I, 0.148 to 0.190; P < 0.001), and also with FEV1 change at follow-up (adjusted beta = -3.013; 95% CI

277 ND-E/I was independently associated with FEV1 (adjusted beta = -0.020; 95% confidence interval [C

278 tify common genetic variants associated with FEV1 and its ratio to forced vital capacity (FVC) in nev

279 g the first year of life was associated with FEV1 at age 16 years of -15.8 ml (95% confidence interva

280 e activity was independently associated with FEV1 decline (beta coefficient, -0.139; P = 0.001).

281 PRM(fSAD) and PRM(emph) were associated with FEV1 decline (P < 0.001 and P = 0.001, respectively).

282 (fSAD) but not PRM(emph) was associated with FEV1 decline (P < 0.001).

283 els (MAL2) was significantly associated with FEV1 decline.

284 ergen levels, but negatively associated with FEV1 in children exposed to high levels.

285 Rs117902240 was positively associated with FEV1 in children exposed to low dust mite allergen level

286 and tended to be negatively associated with FEV1% (beta=-0.59; 95% CI: -1.24, 0.05); bisphenol A ten

287 d NH3 levels were negatively associated with FEV1, FEV1/FVC, and MMEF.

288 ncentrations were negatively associated with FEV1/FVC ratio (P < .05).

289 s) remitting wheeze was only associated with FEV1/FVC ratio decrements (OR, -0.15 SDU; 95% CI, -0.25

290 Associations with FEV1 were also negative and proportionally similar.

291 ly) and a higher proportion of children with FEV1 of less than 80% predicted (odds ratio, 5.74; 95% C

292 within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted,

293 eutrophils, which positively correlated with FEV1 %predicted (r = 0.43; P = .008).

294 + T cells from small airways correlated with FEV1 (R = 0.834, P = 0.039).

295 of CDC42EP4 and DOCK5 transcript counts with FEV1/FVC ratio together support a role of CDC42 in the T

296 neutrophils (r=-0.46: P<0.05), but not with FEV1 (% predicted), FEV1 /FVC or bronchodilator reversib

297 ely correlated with FENO and positively with FEV1 (all P < 0.001).

298 I, PAI-1, FENO , and EOS and positively with FEV1 .

299 rocedure was the percentage of subjects with FEV1 improvement from baseline of 12% or greater.

300 led, 78 were randomized (age 67 +/- 8 years; FEV1 48 +/- 21% predicted), and 65 completed the trial (