ライフサイエンスコーパス: forced expiratory volume

1 ere assigned based on percentage of expected forced expiratory volume.

2 FEV1/forced vital capacity (FVC) ratio, and forced expiratory volume after exhaling 75% of vital cap

3 scores and lung parameters such as decreased forced expiratory volume and increased residual volume c

4 logical measurements of lung function (i.e., forced expiratory volumes and diffusing capacities).

5 values were significantly increased, whereas forced expiratory volume at 0.5 seconds (FEV(0.5)) signi

6 in baseline airflow were not significant for forced expiratory volume at 0.5 seconds (mean z score fo

7 nflammatory profile in children with reduced forced expiratory volume at 0.5 seconds (P = .02).

8 The neonatal forced expiratory volume at 0.5 seconds was inversely as

9 is was linearly associated with the ratio of forced expiratory volume at 1 s to forced vital capacity

10 on, there is a fall in total lung volume and forced expiratory volume at 100 ms.

11 All patients completed pre-operative forced expiratory volume capacity (FEV1), diffusing capa

12 All patients completed tests of preoperative forced expiratory volume capacity in 1 s (FEV1) and diff

13 Forced expiratory volume decreased and sputum volume inc

14 In those with low predicted postoperative forced expiratory volume during first second (FEV(1)) or

15 ciation with the pulmonary function measure--forced expiratory volume (FEV(1)) % of predicted value.

16 tcomes included percent-predicted one-second forced expiratory volume (FEV1%), forced vital capacity

17 ort uses symptoms, exacerbation history, and forced expiratory volume (FEV1)% to categorise patients

18 V-infected participants but similar 1-second forced expiratory volume (FEV1), especially in those wit

19 stage 2 airflow limitation (ratio of FEV1 to forced expiratory volume [FEV1/FVC] less than 70% plus F

20 ene, has been previously associated with the forced expiratory volume/forced vital capacity ratio.

21 high-density lipoprotein (HDL) cholesterol, forced expiratory volume, grip strength, HbA1c, longevit

22 lung function measures as z scores at birth (forced expiratory volume in 0.5 seconds [FEV0.5], forced

23 between groups except for the mean change in forced expiratory volume in 0.5 seconds, which was 38 mL

24 Girls had higher prebronchodilator forced expiratory volume in 0.5 seconds/forced vital cap

25 pronounced, with boys demonstrating reduced forced expiratory volume in 0.5 seconds/forced vital cap

26 November 2011, including all patients with a forced expiratory volume in 1 s <50% baseline.

27 h Arg117His-CFTR and percentage of predicted forced expiratory volume in 1 s (% predicted FEV1) of at

28 , height, body-mass index, percent predicted forced expiratory volume in 1 s (%FEV1), risk of Pseudom

29 - 37.4 vs. 396.2 +/- 32.1 L/min; P = 0.007), forced expiratory volume in 1 s (75.2 +/- 4.6 vs. 88.4 +

30 e change from baseline in pre-bronchodilator forced expiratory volume in 1 s (FEV(1) ); eosinophilic

31 forced vital capacity (FVC) (P </= 0.01) and forced expiratory volume in 1 s (FEV(1)) (P </= 0.05) (m

32 anges correlated with the late-phase fall in forced expiratory volume in 1 s (FEV(1)) after whole-lun

33 y endpoints were change in prebronchodilator forced expiratory volume in 1 s (FEV(1)) and the rate of

34 We tested genome-wide association with forced expiratory volume in 1 s (FEV(1)) and the ratio o

35 th trials (BDP/FF/G vs BDP/FF) were pre-dose forced expiratory volume in 1 s (FEV(1)) at week 26 and

36 ial demonstrated significant improvements in forced expiratory volume in 1 s (FEV(1)) from baseline,

37 dy, significantly improves prebronchodilator forced expiratory volume in 1 s (FEV(1)) in a subset of

38 al effects of 474 smoking-associated CpGs on forced expiratory volume in 1 s (FEV(1)) in UK Biobank (

39 ge caused an early change (0-2 h) in minimum forced expiratory volume in 1 s (FEV(1)) of -1.091 l (95

40 e relation between dietary food patterns and forced expiratory volume in 1 s (FEV(1)) or respiratory

41 history of 10 or more pack-years, a ratio of forced expiratory volume in 1 s (FEV(1)) to forced vital

42 d in 107 patients with stable COPD [x +/- SD forced expiratory volume in 1 s (FEV(1)): 34.5 +/- 16.5]

43 had substantial deficits in 8-year growth of forced expiratory volume in 1 s (FEV(1), -81 mL, p=0.01

44 M(10)) and lung function: postbronchodilator forced expiratory volume in 1 s (FEV(1), primary outcome

45 etween DHEA-sulfate and percentage predicted forced expiratory volume in 1 s (FEV(1)PP).

46 Adult subjects (percentage of predicted forced expiratory volume in 1 s (FEV1 ) 60-85%) were ran

47 t was change from baseline in evening trough forced expiratory volume in 1 s (FEV1 ) at Week 24.

48 point was change from baseline at week 12 in forced expiratory volume in 1 s (FEV1 in L) in patients

49 n as assessed by the percentage of predicted forced expiratory volume in 1 s (FEV1%).

50 The change in forced expiratory volume in 1 s (FEV1) after administrat

51 utcomes were on-treatment rate of decline in forced expiratory volume in 1 s (FEV1) and a composite o

52 ) Normative Aging Study whose lung function [forced expiratory volume in 1 s (FEV1) and forced vital

53 irometrically; that is, as the ratio between forced expiratory volume in 1 s (FEV1) and forced vital

54 Study 1 measured change in forced expiratory volume in 1 s (FEV1) and provocative c

55 Improvement in trough forced expiratory volume in 1 s (FEV1) and the increased

56 sociation study (GWAS) so far (n=48,201) for forced expiratory volume in 1 s (FEV1) and the ratio of

57 secondary endpoints were pre-bronchodilator forced expiratory volume in 1 s (FEV1) and total asthma

58 y secondary endpoints were prebronchodilator forced expiratory volume in 1 s (FEV1) and total asthma

59 ol was non-inferior to tiotropium for trough forced expiratory volume in 1 s (FEV1) at week 12 (prima

60 ere, upper lobe-predominant emphysema with a forced expiratory volume in 1 s (FEV1) between 20% and 4

61 ed 40-80 years and had a post-bronchodilator forced expiratory volume in 1 s (FEV1) between 50% and 7

62 Biobank, from the middle and extremes of the forced expiratory volume in 1 s (FEV1) distribution amon

63 Although documents have traditionally used forced expiratory volume in 1 s (FEV1) for staging, clin

64 been associated with accelerated decline in forced expiratory volume in 1 s (FEV1) in patients with

65 randomly assigned (1:1) adults with COPD, a forced expiratory volume in 1 s (FEV1) less than 50% pre

66 ystic fibrosis, age at least 18 years, and a forced expiratory volume in 1 s (FEV1) of 40% or more th

67 Patients (aged >/=12 years) with a forced expiratory volume in 1 s (FEV1) of 50-90% predict

68 symptomatic asthma and a pre-bronchodilator forced expiratory volume in 1 s (FEV1) of 60-90% predict

69 gnosis of cystic fibrosis, percent predicted forced expiratory volume in 1 s (FEV1) of 70 or more, an

70 d with a postbronchodilator reversibility in forced expiratory volume in 1 s (FEV1) of at least 12% a

71 onic obstructive pulmonary disease who had a forced expiratory volume in 1 s (FEV1) of less than 50%

72 gible patients had COPD, post-bronchodilator forced expiratory volume in 1 s (FEV1) of less than 50%,

73 e patients with COPD had post-bronchodilator forced expiratory volume in 1 s (FEV1) of lower than 50%

74 efficacy endpoint of both studies was trough forced expiratory volume in 1 s (FEV1) on day 169, which

75 r study 1 was maximum percentage decrease in forced expiratory volume in 1 s (FEV1) over 4-10 h after

76 lternative to and more sensitive method than forced expiratory volume in 1 s (FEV1) to assess treatme

77 -reported asthma and a postbronchodilatatory forced expiratory volume in 1 s (FEV1) to forced vital c

78 lowed up by questionnaires until age 5, when forced expiratory volume in 1 s (FEV1) was measured by s

79 Among obese patients, the forced expiratory volume in 1 s (FEV1) was significantly

80 hen adjusted for sex, body-mass index (BMI), forced expiratory volume in 1 s (FEV1), and PA:A greater

81 condary endpoints included prebronchodilator forced expiratory volume in 1 s (FEV1), Asthma Control Q

82 duals, we studied genome-wide association of forced expiratory volume in 1 s (FEV1), forced vital cap

83 hese functional volumes were correlated with forced expiratory volume in 1 s (FEV1), forced vital cap

84 Indices were forced expiratory volume in 1 s (FEV1), forced vital cap

85 and pulmonary function levels, including the forced expiratory volume in 1 s (FEV1), in general popul

86 metimes associated with an acute decrease in forced expiratory volume in 1 s (FEV1).

87 ve comparator groups, as was the decrease in forced expiratory volume in 1 s (net difference -0.038 L

88 onary function testing demonstrated improved forced expiratory volume in 1 s (p=0.003) in the hMSC-tr

89 ble disease, and with a percentage predicted forced expiratory volume in 1 s (ppFEV(1)) of 40-90%, in

90 IL-25(+) cells correlated inversely with the forced expiratory volume in 1 s (r = -0.639; P = 0.01).

91 es of lung function (percentage of predicted forced expiratory volume in 1 s [FEV(1)] and frequency o

92 ntial difference; sweat chloride >40 mmol/L; forced expiratory volume in 1 s [FEV1] >/= 40% and </= 9

93 ung function measures sequentially (ratio of forced expiratory volume in 1 s [FEV1] to forced vital c

94 ithin 1 year (defined as post-bronchodilator forced expiratory volume in 1 s [FEV1] to forced vital c

95 te asthma were enrolled in pairs matched for forced expiratory volume in 1 s and ethnic origin, accor

96 Acute iloprost inhalation reduced forced expiratory volume in 1 s and mid-volume forced ex

97 Other outcomes included lung function (forced expiratory volume in 1 s and morning peak expirat

98 xidant diet had a lower percentage predicted forced expiratory volume in 1 s and percentage predicted

99 ower mean residual forced vital capacity and forced expiratory volume in 1 s in men after adjustment

100 and to decrease future risk (as predicted by forced expiratory volume in 1 s level and exacerbations

101 iciency (serum concentration <11 muM) with a forced expiratory volume in 1 s of 35-70% (predicted).

102 y, were applied to test the association with forced expiratory volume in 1 s percent predicted values

103 Posttransplantation peak forced expiratory volume in 1 s was worse in patients wi

104 ase in FVC (forced vital capacity) and FEV1 (forced expiratory volume in 1 s) of 0.03 L [95% confiden

105 XCL11 was predictive of a greater decline in forced expiratory volume in 1 s, 6 months later.

106 Secondary endpoints, including forced expiratory volume in 1 s, peak expiratory flow, u

107 terms of exacerbations, asthma control, and forced expiratory volume in 1 s.

108 Forced expiratory volume in 1 s/forced vital capacity (F

109 cipants, methacholine PC20 (20% reduction in forced expiratory volume in 1 s; a prespecified secondar

110 ed as at least a 12% and 200 mL reduction in forced expiratory volume in 1 sec (FEV(1)) or forced vit

111 At 1 h post-morning dose on Day 6, forced expiratory volume in 1 sec (FEV1 ) was measured u

112 ) on specific airway resistance (sR(aw)) and forced expiratory volume in 1 sec (FEV1) before and afte

113 ng mass was the only measure associated with forced expiratory volume in 1 sec (FEV1) decline, with e

114 We measured forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and blood DNA

115 in D (25-OHD) levels and pulmonary function (forced expiratory volume in 1 sec [FEV(1)] %predicted) w

116 , we separated patients with an obstructive (forced expiratory volume in 1 sec [FEV(1)]: vital capaci

117 ive decline in pulmonary allograft function (forced expiratory volume in 1 sec [FEV1]) in absence of

118 er lung function [average reduction in FEV1 (forced expiratory volume in 1 sec) for a 10% increase in

119 at both moderate and elevated temperatures (forced expiratory volume in 1 sec, -12.4% vs. -7.5%, p >

120 but did not exhibit decreased posttransplant forced expiratory volume in 1 sec.

121 luded wheezing, coughing, and 12% decline in forced expiratory volume in 1 sec.

122 d with forced vital capacity % predicted and forced expiratory volume in 1 second % predicted (P < 0.

123 competence (OR, 3.58; 95% CI, 1.75 to 7.31); forced expiratory volume in 1 second < 80% (OR, 2.59; 95

124 talized 58 times and had significantly worse forced expiratory volume in 1 second ( FEV1 forced expir

125 2) and 4.0 percentage points lower predicted forced expiratory volume in 1 second (95% CI, -6.6 to -1

126 flation, r = -0.8; 95% CI: -0.94, 0.42), and forced expiratory volume in 1 second (airway obstruction

127 bations, improved prebronchodilator (pre-BD) forced expiratory volume in 1 second (FEV(1) ) and quali

128 ose with severe persistent disease, can have forced expiratory volume in 1 second (FEV(1) ) values >=

129 ed and HP (3)He MRI VDP were correlated with forced expiratory volume in 1 second (FEV(1)) (model: r

130 e of total fiber intake had a 60.2-ml higher forced expiratory volume in 1 second (FEV(1)) (p for tre

131 with findings at quantitative CT (r = 0.75), forced expiratory volume in 1 second (FEV(1)) (r = -0.68

132 measurements were positively correlated with forced expiratory volume in 1 second (FEV(1)) (r = 0.65,

133 n whose mothers had received vitamin A had a forced expiratory volume in 1 second (FEV(1)) and a forc

134 relationship between longitudinal changes in forced expiratory volume in 1 second (FEV(1)) and CT-qua

135 African ancestry was inversely related to forced expiratory volume in 1 second (FEV(1)) and forced

136 the authors developed prediction models for forced expiratory volume in 1 second (FEV(1)) and the pr

137 nge from baseline in percentage of predicted forced expiratory volume in 1 second (FEV(1)) at week 4.

138 nt predicted forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV(1)) compared w

139 was the relative change in prebronchodilator forced expiratory volume in 1 second (FEV(1)) from basel

140 tients were at least 40 years of age, with a forced expiratory volume in 1 second (FEV(1)) of 70% or

141 were symptomatic, had a post-bronchodilator forced expiratory volume in 1 second (FEV(1)) of 80% or

142 Using linear mixed models, we analyzed the forced expiratory volume in 1 second (FEV(1)) of both ac

143 f longitudinal changes in postbronchodilator forced expiratory volume in 1 second (FEV(1)) reversibil

144 When compared with smokers with the largest forced expiratory volume in 1 second (FEV(1)) to forced

145 Forced expiratory volume in 1 second (FEV(1)) was <80% p

146 the patients was 65.0+/-7.8 years; the mean forced expiratory volume in 1 second (FEV(1)) was 41.1+/

147 Maximum forced expiratory volume in 1 second (FEV(1)) was measur

148 inical prognostic scores (Liou and CF-ABLE), forced expiratory volume in 1 second (FEV(1)), and risk

149 iations of prematurity and birth weight with forced expiratory volume in 1 second (FEV(1)), forced vi

150 y function impairment, as evidenced by lower forced expiratory volume in 1 second (FEV(1)), was assoc

151 ow obstruction with lower values of ratio of forced expiratory volume in 1 second (FEV(1))-to-functio

152 the groups in the rate of change (slope) in forced expiratory volume in 1 second (FEV(1)).

153 through week 24 in the percent of predicted forced expiratory volume in 1 second (FEV(1)).

154 ric measures forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV(1)).

155 In mixed models, the rate of decline in forced expiratory volume in 1 second (FEV(1))/forced vit

156 re decline in lung function measurements for forced expiratory volume in 1 second (FEV1) (388 mL), fo

157 siblings (P = 0.010) and is associated with forced expiratory volume in 1 second (FEV1) (P = 0.030).

158 , P = .02) were significant variables, while forced expiratory volume in 1 second (FEV1) and airway d

159 ions between exposures and annual changes in forced expiratory volume in 1 second (FEV1) and FEV1 as

160 5 years of age, measured as the increases in forced expiratory volume in 1 second (FEV1) and forced v

161 ermined by their history and their values of forced expiratory volume in 1 second (FEV1) and forced v

162 e, 6574 had COPD, defined as a ratio between forced expiratory volume in 1 second (FEV1) and forced v

163 Forced expiratory volume in 1 second (FEV1) and forced v

164 The pulmonary function measures of forced expiratory volume in 1 second (FEV1) and its rati

165 Other outcomes included the forced expiratory volume in 1 second (FEV1) and scores o

166 icacy end points were percent changes in the forced expiratory volume in 1 second (FEV1) and the 6-mi

167 by measuring forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) at baseline,

168 from baseline in the percentage of predicted forced expiratory volume in 1 second (FEV1) at week 24.

169 ys, with a difference of 0.079 (P=0.01); the forced expiratory volume in 1 second (FEV1) before bronc

170 solute change in the percentage of predicted forced expiratory volume in 1 second (FEV1) from the bas

171 ents with lymphangioleiomyomatosis, the mean forced expiratory volume in 1 second (FEV1) increased by

172 Reduced low forced expiratory volume in 1 second (FEV1) is reportedl

173 eal-life study was to compare the changes in forced expiratory volume in 1 second (FEV1) of omalizuma

174 ght to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time.

175 The forced expiratory volume in 1 second (FEV1) showed a sim

176 te change in the percentage of the predicted forced expiratory volume in 1 second (FEV1) through week

177 pulmonary disease (COPD) requires a ratio of forced expiratory volume in 1 second (FEV1) to forced vi

178 and moderately correlated with the ratio of forced expiratory volume in 1 second (FEV1) to forced vi

179 bstruction by spirometry, using the ratio of forced expiratory volume in 1 second (FEV1) to forced vo

180 Forced expiratory volume in 1 second (FEV1) values obtai

181 .77; P < .0001) with percentage predicted of forced expiratory volume in 1 second (FEV1) was observed

182 h intermittent culture positivity and higher forced expiratory volume in 1 second (FEV1) were most li

183 ardised format (CRQ-SAS), pre-bronchodilator forced expiratory volume in 1 second (FEV1), and safety.

184 effect of either benralizumab regimen on the forced expiratory volume in 1 second (FEV1), as compared

185 es were changes from baseline to 6 months in forced expiratory volume in 1 second (FEV1), forced vita

186 Forced expiratory volume in 1 second (FEV1), forced vita

187 Spirometry measures: forced expiratory volume in 1 second (FEV1), forced vita

188 pid decline in lung function, as measured by forced expiratory volume in 1 second (FEV1), forced vita

189 h and decline on the basis of graphs showing forced expiratory volume in 1 second (FEV1), representin

190 es), low-frequency reactance area (ALX), and forced expiratory volume in 1 second (FEV1).

191 change in the area under the curve (AUC) for forced expiratory volume in 1 second (FEV1).

192 acity (VC), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV1).

193 ucing the maximum percentage decrease in the forced expiratory volume in 1 second (FEV1).

194 s ratio (OR) = 3.10, 95% CI: 1.65, 5.78) and forced expiratory volume in 1 second (OR = 2.35, 95% CI:

195 alized subjects had significantly worse FEV1 forced expiratory volume in 1 second (P = .02) and (3)He

196 ficant correlation (P < .01) with changes in forced expiratory volume in 1 second (r = 0.70), forced

197 forced expiratory volume in 1 second ( FEV1 forced expiratory volume in 1 second ) (P < .0001), CT R

198 measure of lung function (prebronchodilator forced expiratory volume in 1 second [FEV(1)]) in more t

199 adiographic and PFT (percentage of predicted forced expiratory volume in 1 second [FEV(1)], percentag

200 year, asthma hospitalization in prior year, forced expiratory volume in 1 second [FEV1 ; FEV1 <65% v

201 0 to 80 years of age, had COPD (defined by a forced expiratory volume in 1 second [FEV1] of less than

202 y history of lung cancer, and lung function (forced expiratory volume in 1 second [FEV1]).

203 viation of Pao2 correlated with PFT metrics (forced expiratory volume in 1 second [FEV1]/forced vital

204 oxide (Dlco%) than with airflow obstruction (forced expiratory volume in 1 second [FEV1]/vital capaci

205 s syndrome, anti-TNFalpha treatment improved forced expiratory volume in 1 second and 6-min walk dist

206 Mean forced expiratory volume in 1 second and diffusing capac

207 A priori determined covariates were forced expiratory volume in 1 second and diffusion capac

208 Forced expiratory volume in 1 second and forced vital ca

209 We tested genome-wide association with forced expiratory volume in 1 second and the ratio of fo

210 d greater improvement relative to placebo in forced expiratory volume in 1 second at Day 28 (102 mL [

211 The prebronchodilator forced expiratory volume in 1 second at week 52 was high

212 ion of methacholine required to decrease the forced expiratory volume in 1 second by 20% (PC20).

213 Kaplan-Meier curves showed patients with forced expiratory volume in 1 second decline >=5% and >=

214 Oxygen requirement >2 L/min at diagnosis and forced expiratory volume in 1 second decline >=5% postin

215 The decline in forced expiratory volume in 1 second during the referenc

216 ion tests revealed stable vital capacity and forced expiratory volume in 1 second in all cases after

217 Overall, the mean (+/-SE) increase in forced expiratory volume in 1 second in the treated subj

218 Forced expiratory volume in 1 second is an important pre

219 Forced expiratory volume in 1 second just before ECP was

220 e model that predicted PRM gas trapping, the forced expiratory volume in 1 second normalized to the f

221 Prebronchodilator ratio of forced expiratory volume in 1 second over forced vital c

222 icantly associated with a greater decline in forced expiratory volume in 1 second per 10 years (basel

223 HSV or T2-weighted VIP were associated with forced expiratory volume in 1 second percentage predicte

224 OPD (r, -0.80; P < .001) and correlated with forced expiratory volume in 1 second percentage predicte

225 piratory volume in 1 second and the ratio of forced expiratory volume in 1 second to forced vital cap

226 e (renal), serum albumin (hepatic), ratio of forced expiratory volume in 1 second to forced vital cap

227 % CI: -0.93, -0.64; P<.001) and the ratio of forced expiratory volume in 1 second to forced vital cap

228 difference in the z scores for the ratio of forced expiratory volume in 1 second to forced vital cap

229 ut airway obstruction, defined by a ratio of forced expiratory volume in 1 second to the forced vital

230 fidence interval (CI): -198, -7) mL, and for forced expiratory volume in 1 second was -90 (95% CI: -1

231 d mean reduction from baseline in the trough forced expiratory volume in 1 second was 38 ml greater i

232 ge from baseline in the percent of predicted forced expiratory volume in 1 second was 8.7% (range, 2.

233 Lower forced expiratory volume in 1 second was also associated

234 change in SUV(max) and percentage predicted forced expiratory volume in 1 second was negatively corr

235 Patients with an irreversible decline in forced expiratory volume in 1 second were identified and

236 Greater effects on forced expiratory volume in 1 second were observed in th

237 y in poor pulmonary function patients [FEV1 (forced expiratory volume in 1 second) or DLCO (diffusion

238 (exacerbations, asthma-control days, and the forced expiratory volume in 1 second) to determine wheth

239 were 92% for forced vital capacity, 93% for forced expiratory volume in 1 second, 116% for total lun

240 dence interval [CI], 67-345 mL; P = .004 and forced expiratory volume in 1 second, 143 mL higher; 95%

241 ate, renal dysfunction, atrial fibrillation, forced expiratory volume in 1 second, and C-reactive pro

242 ity of the lungs for carbon monoxide (DLCO), forced expiratory volume in 1 second, and forced vital c

243 Safety, pharmacokinetics, forced expiratory volume in 1 second, asthma control que

244 measures of respiratory function, including forced expiratory volume in 1 second, forced vital capac

245 of effect modification by race/ethnicity for forced expiratory volume in 1 second, forced vital capac

246 , IQR(N) correlated with obstruction markers forced expiratory volume in 1 second-to-forced vital cap

247 he severity of asthma and inversely with the forced expiratory volume in 1 second.

248 tly correlated with the percentage predicted forced expiratory volume in 1 second.

249 n defect percentage were correlated with the forced expiratory volume in 1 second.

250 A similar trend was observed for forced expiratory volume in 1 second.

251 x, estimated glomerular filtration rate, and forced expiratory volume in 1 second.

252 alth care use and lung function, measured by forced expiratory volume in 1 second.

253 e in 1 second, forced vital capacity, or the forced expiratory volume in 1 second/forced vital capaci

254 atment failure, asthma control days, and the forced expiratory volume in 1 second; a two-sided P valu

255 also decreased in patients with HLA-Ab (mean forced expiratory volume in 1 second=49%) when compared

256 ) when compared with the control group (mean forced expiratory volume in 1 second=66%, P<0.05).

257 Airway obstruction was defined as forced expiratory volume in 1-second (FEV1)/forced vital

258 ilution) in eight patients with severe COPD (forced expiratory volume in 1s (FEV(1) ) +/- SEM = 0.9 +

259 onchial hyperresponsiveness to methacholine, forced expiratory volume in 1s (FEV1 ) and atopy and ast

260 ction (specific airways resistance [sR(aw)], forced expiratory volume in 1s [FEV1]) and airway reacti

261 rd some measure of expiration, such as FEV1 (Forced Expiratory Volume in 1s), because airway constric

262 preceding day was associated with a reduced forced expiratory volume in 8-yr-olds; -32.4 ml; 95% CI:

263 ent contributors to ACQ-6 score were R20 and forced expiratory volume in one second (% pred.), and th

264 sease and whether the first treatment year's forced expiratory volume in one second (FEV(1) ) predict

265 les, the Forced Vital Capacity (FVC) and the Forced Expiratory Volume in one second (FEV(1)) can be i

266 hat were found to be associated with similar forced expiratory volume in one second (FEV(1)) measurem

267 levels of these six genes and lung function (Forced Expiratory Volume in one second (FEV(1)), Forced

268 ancer is genetically correlated with reduced forced expiratory volume in one second (FEV(1): r(g) = 0

269 /= 0.35 kUA /L) (n = 418) and lung function [forced expiratory volume in one second (FEV1 ) and force

270 hypertonic saline with placebo improved the forced expiratory volume in one second (FEV1) between th

271 ation; secondary measures included change in forced expiratory volume in one second (FEV1), weight, a

272 Forced expiratory volume in one second accounted for les

273 odest reduction in forced vital capacity and forced expiratory volume in one second following broncho

274 ry of cancer, family history of lung cancer, forced expiratory volume in one second percent predicted

275 In 12 COPD patients (forced expiratory volume in one second: 58 +/- 17%pred.)

276 ization, serum total immunoglobulin E (IgE), forced expiratory volume in one-second (FEV1) and forced

277 the results from a standard spirometry test, forced expiratory volume in one-second percent (FEV1 %),

278 ence in change for the secondary outcomes of forced expiratory volume in the first second (0.0 L; 95%

279 clinically important lung-function measures: forced expiratory volume in the first second (FEV(1)) an

280 ratio values correlated positively with the forced expiratory volume in the first second (FEV(1), %)

281 The primary outcome measure was change in forced expiratory volume in the first second (FEV1) at 2

282 We performed GWAS of the rate of change in forced expiratory volume in the first second (FEV1) in 1

283 ounds, and a prolonged expiratory phase; his forced expiratory volume in the first second (FEV1) is 1

284 ratory Questionnaire (MCID, 4) and change in forced expiratory volume in the first second (FEV1; MCID

285 de Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and

286 Forced expiratory volume in the first second increased f

287 very 6 months for 5 years and measured child forced expiratory volume in the first second of expirati

288 f 5 patients, 4 (80%) had improvement of the forced expiratory volume in the first second of expirati

289 In a mixed-model analysis, change in forced expiratory volume in the first second of expirati

290 difference for change in postbronchodilator forced expiratory volume in the first second of expirati

291 ty criteria included age of 6 to 18 years, a forced expiratory volume in the first second of expirati

292 -3.05; P < .001; I(2) = 0%), lowest baseline forced expiratory volume in the first second of expirati

293 mean BMI of 21.6 [IQR, 18.2-26.1], mean [SD] forced expiratory volume in the first second of expirati

294 onary disease (COPD) requires a ratio of the forced expiratory volume in the first second to the forc

295 (95% CI, 0.03 L to infinity) (P = .002) for forced expiratory volume in the first second, +21 m (95%

296 ustment for age, sex, race, body mass index, forced expiratory volume in the first second, pack-years

297 Lung function (forced expiratory volume in the first three-quarters of

298 tcome; secondary outcomes included change in forced expiratory volume, Mini Asthma Quality of Life Qu

299 Lower forced expiratory volume, PA:A>1, and hyperinflation cor

300 s of peak VO2 were peak heart rate (r=0.33), forced expiratory volume (r=0.33), pulmonary hypertensio