ライフサイエンスコーパス: FEV1

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

2 FEV1 percentage predicted was significantly different be

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

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

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

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

7 y events were not associated with additional FEV1 decline.

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

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

10 An FEV1 of 1.50 L or less had a sensitivity of 87% and spec

11 55.4% of EBV and 6.5% of SoC subjects had an FEV1 improvement of 12% or more (P < 0.001).

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

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

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

15 8, 9.6]), mean FEV1 (-166 ml [-332, -1]) and FEV1 /FVC ratio (-4.6%, [-8.1, -1.1]) at 12 years.

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

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

18 er smokers with PRISm (FEV(1)/FVC >= 0.7 and FEV1 < 80%) in COPDGene was used to stratify subjects in

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

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

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

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

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

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

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

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

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

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

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

30 nnual rates of change in BMI, FEV1, FVC, and FEV1:FVC ratio were 0.22 kg/m2/year, -25.50 mL/year, -21

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

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

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

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

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

36 % CI: 1.27, 3.46, p=0.004, respectively] and FEV1 decreased (beta=-0.143; 95% CI: -0.248, -0.039, p=0

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

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

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

40 Airway obstruction was defined as FEV1/FVC ratio <0.7.

41 Defining airflow obstruction as FEV1:FVC less than 0.70 provided discrimination of COPD-

42 obstruction, which was defined by a baseline FEV1:FVC less than a range of fixed thresholds (0.75 to

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

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

45 ve of a history of exacerbations or baseline FEV1.

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

47 At baseline, FEV1 bronchodilator responsiveness was the most importan

48 ry defect and among groups based on the best FEV1 and FVC measurements (>80%, 60%-80%, and <60% predi

49 ry defect and among groups based on the best FEV1 and FVC measurements (>80%, 60-80% and <60%predicte

50 used to plot the linear relationship between FEV1 versus time before and after ECP.

51 cal significance of the relationship between FEV1 versus time before ECP initiation.

52 ears, average annual rates of change in BMI, FEV1, FVC, and FEV1:FVC ratio were 0.22 kg/m2/year, -25.

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

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

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

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

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

58 ung function after pulmonary exacerbation by FEV1% or in serial concentrations of plasma cathelicidin

59 olume in the first second to vital capacity (FEV1:FVC) less than 0.70 with respiratory symptoms.

60 e first second to the forced vital capacity (FEV1:FVC) of less than 0.70, yet this fixed threshold is

61 operative forced expiratory volume capacity (FEV1), diffusing capacity of the lung for carbon monoxid

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

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

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

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

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

67 % 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

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

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

70 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

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

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

73 use these key genes to successfully estimate FEV1/FVC ratios across patients, via support-vector-mach

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

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

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

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

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

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

80 The optimal fixed FEV1:FVC threshold was defined by the best discriminatio

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

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

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

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

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

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

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

88 ereas only 12.4% of those with LTL >=6.5 had FEV1% <80% (RR = 2.53, 95%CI = [1.70-3.76]).

89 ample, 29.9% of those with LTL <6.5 kbps had FEV1% <80% whereas only 12.4% of those with LTL >=6.5 ha

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

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

92 eosinophilic inflammation and the change in FEV1 .

93 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

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

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

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

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

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

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

103 Patients whose decline in FEV1 before ECP was statistically significant (P < 0.05)

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 r LTL and greater yearly rates of decline in FEV1% (0.46%/year, 95%CI = [0.05-0.87]) and in the FEV1/

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

109 steeper BMI increases had faster declines in FEV1 (r = -0.16) and FVC (r = -0.26) and slower declines

110 ) and FVC (r = -0.26) and slower declines in FEV1:FVC ratio (r = 0.11) (all P values < 0.0001).

111 : 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

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

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

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

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

116 2 level was associated with a 5% decrease in FEV1/forced vital capacity ratio (beta = -0.05; 95% CI,

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

118 ; P < .001) but no significant difference in FEV1 decline (-31 vs -33 mL/y; difference, 2 mL/y; 95% C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 cterized by differences in mean longitudinal FEV1 trajectories.

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

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

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

138 significantly worse asthma control and lower FEV1.

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

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

141 Shorter LTL was associated with lower FEV1% and FVC% at baseline.

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

143 Biomass was associated with lower FEV1/FVC (raw values -7.0, p = 0.04; GLI pp -7.62, p = 0

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

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

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

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

148 est airway to lung ratio quartile had a mean FEV1 decline of -37 mL/y (15 mL/y), which did not differ

149 53 years, 59-69% were female, and had a mean FEV1 percentage of predicted normal of 63-84%.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 nct phenotypes by evaluating trajectories of FEV1 decline.

167 These results support the use of FEV1:FVC less than 0.70 to identify individuals at risk

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

169 0 showed a significant interaction effect on FEV1 with dust mite allergen level in PRGOAL (interactio

170 3A) were shown to have an additive effect on FEV1/FVC levels in the genetic risk score analysis; were

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

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

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

174 Predicted post-operative FEV1 and DLCO were derived from SC, PS and SPECT/CT.

175 lobectomy and measurement of post-operative FEV1 and DLCO.

176 , PS, SPECT/CT and the actual post-operative FEV1 and DLCO.

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

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

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

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

181 , the lung function in both groups was poor [FEV1 z-score median -2.05, IQR (-2.64, -1.41).

182 follow-up (defined as a postbronchodilation FEV1/FVC ratio of at least the lower limit of normal and

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

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

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

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

187 , PS, SPECT/CT, and the actual postoperative FEV1 and DLCO.

188 c lobectomy and measurement of postoperative FEV1 and DLCO.

189 Predicted postoperative FEV1 and DLCO were derived from SC, PS, and SPECT/CT.

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

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

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

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

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

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

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

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

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

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

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

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

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

203 to 10-point improvement in percent predicted FEV1.

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

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

206 related positively with percentage predicted FEV1.

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

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

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

210 6: P<0.05), but not with FEV1 (% predicted), FEV1 /FVC or bronchodilator reversibility.

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

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

213 orced vital capacity (FVC), and their ratio (FEV1:FVC).

214 possible association between LBW and reduced FEV1 (p = 5.69E-18, MR-PRESSO) and FVC (6.02E-22, MR-PRE

215 I) was significantly associated with reduced FEV1 and FVC (P < .05 for both).

216 tructive-restrictive impairment with reduced FEV1 and FVC in 75% of the patients.

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

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

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

220 5 or 50% increase), (2) spirometric results (FEV1 >/=80% of predicted value or >/=15% increase), (3)

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

222 f predicted forced expiratory volume in 1 s (FEV1%).

223 ve forced expiratory volume capacity in 1 s (FEV1) and diffusing capacity of the lungs for carbon mon

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

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

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

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

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

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

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

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

232 g ratio was 0.033 (0.004), and the mean (SD) FEV1 decline was -33 mL/y (31 mL/y).

233 D at a median of 3.1 years and the mean (SD) FEV1 decline was -36 mL/y (75 mL/y).

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

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

236 Forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) were lower in the

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

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

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

240 Forced expiratory volume in 1 second (FEV1) values obtained 6 months before (baseline) and 6 m

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

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

243 Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and physical activit

244 red by forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and their ratio (FEV

245 ned as forced expiratory volume in 1-second (FEV1)/forced vital capacity (FVC) ratio <0.7.

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

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

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

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

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

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

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

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

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

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

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

257 EV1%), forced vital capacity (FVC%), and the FEV1/FVC ratio.

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

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

260 ears; 95% CI, 38.0 to 66.8; P<.001), but the FEV1 decline did not differ significantly (-34 vs -36 mL

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

262 (0.46%/year, 95%CI = [0.05-0.87]) and in the FEV1/FVC ratio (0.19%/year, 95%CI = [0.03-0.36]).

263 Results of the FEV1 identification analysis were not replicated.

264 s occurred without a sustained effect on the FEV1.

265 changes in the lungs of PLWH when using the FEV1/FVC ratio as single diagnostic measure.

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

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

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

269 7]), and the key secondary end point, trough FEV1 (5 mug, 87 mL [95% CI, 19-154; P = .01]; 2.5 mug, 1

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

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

272 edicted one-second forced expiratory volume (FEV1%), forced vital capacity (FVC%), and the FEV1/FVC r

273 t similar 1-second forced expiratory volume (FEV1), especially in those with limited smoking experien

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

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

276 more timely implementation of ECP (ie, when FEV1 values >1.5 L) should be considered especially in p

277 Patients whose FEV1 decline exceeded 40 mL/month were 12 times more lik

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

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

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

281 ion by T cells significantly associated with FEV1 (R = 0.655, P = 0.006) and with time posttransplant

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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