ライフサイエンスコーパス: vital capacity

1 ed also with airway obstruction (FEV1/forced vital capacity).

2 iratory volume in 1 second (FEV1) and forced vital capacity.

3 ned improvement in skin thickness and forced vital capacity.

4 function based on predicted values of forced vital capacity.

5 -term associations of pollutants with forced vital capacity.

6 rters of these abnormalities were low forced vital capacity.

7 l rating scale and measurement of the forced vital capacity.

8 of strength and a slight increase in forced vital capacity.

9 A similar pattern emerged for forced vital capacity.

10 Similar results were obtained for forced vital capacity.

11 rced expiratory flow at 25% to 75% of forced vital capacity.

12 lung injury score and inversely with forced vital capacity.

13 ound some evidence of less decline in forced vital capacity.

14 or influencing IPF prognosis was the percent vital capacity.

15 ive muscle weakness accompanied by decreased vital capacities.

16 that resulted in significant improvements in vital capacity (10%).

17 ; P = 1.1 x 10(-5), respectively) and forced vital capacity (-100 +/- 21 mL; P = 2.7 x 10(-6) and -10

18 confidence interval: -5.2, -0.1) and forced vital capacity (-2.4%, 95% confidence interval: -4.7, -0

19 w magnesium intake showed deficits in forced vital capacity (-2.8%, 95% confidence interval: -5.4, -0

20 y volume in 1 second (FEV1) (388 mL), forced vital capacity (298 mL), and the FEV1/forced vital capac

21 ignificantly lower percent predicted: forced vital capacity (61.5+/-16 versus 80.5+/-14; P<0.0001), m

22 4.6 vs. 88.4 +/- 5.6%; P = 0.03) and forced vital capacity (83.2 +/- 4.7 vs. 109.2 +/- 6.0%; P = 0.0

23 e associated with a 2.4% decrement in forced vital capacity (95% confidence interval (CI): -4.0, -0.7

24 vital capacity, and 6-month change in forced vital capacity, a decrease in forced vital capacity rema

25 types used to assess asthma severity: forced vital capacity, a sensitive measure of airway obstructio

26 volume in the first second (FEV1) and forced vital capacity after adjustment for sex, age, height, we

27 5% of forced vital capacity, and FEV1/forced vital capacity (all P < .0001).

28 he rate of decline of leg and grip strength, vital capacity, ALS Functional Rating Scale-Revised, and

29 ed 13% to 20% of the association with forced vital capacity and 29% to 42% of the association with em

30 hildren were able to produce a second forced vital capacity and a second forced expired volume in 0.7

31 tively and positively correlated with forced vital capacity and age, respectively.

32 extent, and the percentage predicted forced vital capacity and carbon monoxide diffusing capacity.

33 y fibrosis as determined by change in forced vital capacity and death.

34 Forced vital capacity and diffusing capacity for carbon monoxid

35 ne was evaluated on the basis of inspiratory vital capacity and FEV(1).

36 n C, were associated with deficits in forced vital capacity and FEV1 in boys.

37 s associated with lower mean residual forced vital capacity and forced expiratory volume in 1 s in me

38 on, pulmonary function tests revealed stable vital capacity and forced expiratory volume in 1 second

39 We observed a modest reduction in forced vital capacity and forced expiratory volume in one secon

40 Forced vital capacity and mid-expiratory flow did not significa

41 The rate of progression of the forced vital capacity and of the ALS Functional Rating Scale-Re

42 th increased airflow limitation (FEV1/forced vital capacity and residual volume/total lung capacity r

43 ally in upper lung parts, and correlation to vital capacity and to markers for hyperinflation and air

44 as associated with a decrease in FVC (forced vital capacity) and FEV1 (forced expiratory volume in 1

45 is, gender, smoking history, baseline forced vital capacity, and 6-month change in forced vital capac

46 with a decreased total lung capacity, forced vital capacity, and diffusing capacity for carbon monoxi

47 Spirometric outcomes (FEV(1), forced vital capacity, and FEV(1)/forced vital capacity ratio)

48 rced expiratory flow at 25% to 75% of forced vital capacity, and FEV1/forced vital capacity (all P <

49 cted FEV1 [ppFEV1], percent predicted forced vital capacity, and FEV1/forced vital capacity ratio) we

50 dequate and functional rating scales, forced vital capacity, and patient survival have been the measu

51 forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) we

52 iratory volume in 1 second (FEV1) and forced vital capacity, and the 10-year incidence of coronary he

53 orced expiratory flow between 25% and 75% of vital capacity, and the ratio between residual volume an

54 expiratory volume in 1 second (FEV1), forced vital capacity, and total lung capacity were categorized

55 s associated with greater lung volumes (FVC, vital capacity, and total lung capacity) and lesser flow

56 The primary endpoint, change in forced vital capacity as a percentage of the predicted normal v

57 orced expiratory flow between 25% and 75% of vital capacity as the dependent variable.

58 ced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted value

59 ced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted value

60 For example, the decrease in forced vital capacity associated with a 70-ppb/month greater cu

61 ced expiratory volume in 1 second and forced vital capacity associated with a decrease of 1 standard

62 d 3 years (27 patients; p<0.0001) and forced vital capacity at 1 year (58 patients; p=0.009), 2 years

63 up had a decline in percent predicted forced vital capacity at 48 weeks (p=0.0373).

64 of forced expiratory volume at 1 s to forced vital capacity at age 22 years.

65 iratory volume in 1 second (FEV1) and forced vital capacity below 0.7.

66 sured the mean mixed expired NO content of a vital-capacity breath using chemiluminescence in patient

67 xpected, there was an abrupt decrease in her vital capacity, but unexpectedly, it increased during th

68 h initial mRSS >14) or an increase in forced vital capacity by more than 10%.

69 myopathies by analysing longitudinal forced vital capacity data in a large international cohort.

70 istically significant increase in ALS-forced vital capacity decline in SOD1(A4V) compared with SOD1(n

71 re similar in all 3 groups, while the forced vital capacity decreased significantly in the relaxin gr

72 crease in mRSS or decrease of >10% in forced vital capacity) despite treatment with cyclophosphamide

73 tonometry, retinal photography, audiometry, vital capacity determinations, a health questionnaire on

74 gnancy was negatively associated with forced vital capacity (difference in standard deviation score -

75 e activity, pulmonary function tests (forced vital capacity, diffusing capacity for carbon monoxide),

76 ng involvement in SSc, as well as the forced vital capacity, diffusing capacity for carbon monoxide,

77 mined together with 6-month change in forced vital capacity, diffusing capacity for carbon monoxide,

78 survival was independent of age, sex, forced vital capacity, diffusing capacity of carbon monoxide, M

79 f disease severity, including a lower forced vital capacity, diffusion capacity for carbon monoxide,

80 hange in longitudinal measurements of forced vital capacity during a 60-week treatment period.

81 atory flow between 25% and 75% of the forced vital capacity (FEF(25-75)) (-16.2%, 95% confidence inte

82 xpiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), -5.5%, 95% CI: -10.5, -0.3)

83 xpiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), 48%; total airway resistanc

84 forced expiratory flow at 75% of the forced vital capacity (FEF(75)) (-8.3%, 95% confidence interval

85 xpiratory flow between 25% and 75% of forced vital capacity (FEF25-75) was associated with the persis

86 forced expiratory flow at 50% of functional vital capacity [FEF50], and provocative dose of methacho

87 rced expiratory volume after exhaling 75% of vital capacity (FEF75), whereas those born with a smalle

88 forced expiratory flow at 75% of the expired vital capacity (FEF75).

89 ed expiratory volume in 1 second over forced vital capacity (FEV(1)/FVC) was measured in 4,267 nonast

90 irst second (FEV(1)) and its ratio to forced vital capacity (FEV(1)/FVC), an indicator of airflow obs

91 d (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC).

92 rced expiratory volume in 1 second to forced vital capacity (FEV(1):FVC ratio; pulmonary), hemoglobin

93 EV1) and FEV1 as a percentage of inspiratory vital capacity (FEV1%VC) were assessed with linear mixed

94 n 1 s (FEV1) and the ratio of FEV1 to forced vital capacity (FEV1/FVC) in the general population.

95 based on the forced expiratory volume/forced vital capacity (FEV1/FVC) ratio and then using the perce

96 was negatively correlated with FEV1, forced vital capacity, FEV1/forced vital capacity ratio, transf

97 operating volumes (10%, 30%, 60% and 90% of vital capacity) followed by three peals of voluntary and

98 tile) was associated with deficits in forced vital capacity for both boys and girls and with deficits

99 Asian values for forced vital capacity, forced expiratory volume in 1 s (FEV(1))

100 onary parameters of response included forced vital capacity, forced expiratory volume in 1 second, an

101 baseline to 12 months in measures of forced vital capacity, functional residual capacity, serum vasc

102 0 pack-years or more, and had an FEV1/forced vital capacity (FVC) <0.7.

103 orrelated with the absolute change in forced vital capacity (FVC) (% predicted values) and the placeb

104 monoxide, and the ratio of FEV(1) to forced vital capacity (FVC) (P <.01) but not with FVC and total

105 trations were associated with maximum forced vital capacity (FVC) (P </= 0.01) and forced expiratory

106 (p for trend < 0.001), 55.2-ml higher forced vital capacity (FVC) (p = 0.001), 0.4% higher FEV(1)/FVC

107 equired 12% or greater improvement in forced vital capacity (FVC) and 1 point or greater decrease in

108 1) Serial measurement of forced vital capacity (FVC) and carbon monoxide diffusing capac

109 ures were change in percent predicted forced vital capacity (FVC) and change in single-breath diffusi

110 tween 3 and 7 years of age and higher forced vital capacity (FVC) and FEV1 values at age 15 years (0.

111 rced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genomes Proj

112 e assessed lung function by measuring forced vital capacity (FVC) and forced expiratory volume in 1 s

113 acterized by the spirometric measures forced vital capacity (FVC) and forced expiratory volume in 1 s

114 significantly lower percent predicted forced vital capacity (FVC) and forced expiratory volume in 1 s

115 Forced vital capacity (FVC) and total lung capacity (TLC) were

116 e in 1 second (FEV1) and its ratio to forced vital capacity (FVC) are used in the diagnosis and monit

117 imary outcome was estimated change in forced vital capacity (FVC) at 30 weeks (mean follow-up) in pat

118 nt was change in percentage predicted forced vital capacity (FVC) at week 72.

119 Similar associations were seen for forced vital capacity (FVC) but not for the FEV(1):FVC ratio.

120 as defined as a decrease in predicted forced vital capacity (FVC) by 10% or more, a decrease in 6 min

121 sociation (discovery P = 0.0007) with Forced Vital Capacity (FVC) downstream of BANP on chromosome 16

122 iratory volume in 1 second (FEV1) and forced vital capacity (FVC) during that period (referred to as

123 d expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) have been reported.

124 s negatively associated with FEV1 and forced vital capacity (FVC) in adolescents with and without ast

125 associated with FEV1 and its ratio to forced vital capacity (FVC) in never-smokers.

126 y is associated with lower FEV(1) and forced vital capacity (FVC) in Puerto Rican children independen

127 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC) in the SpiroMeta consortium (n = 20

128 cores were associated with changes in forced vital capacity (FVC) in two cohorts.

129 creased by 118+/-330 ml (P=0.06), the forced vital capacity (FVC) increased by 390+/-570 ml (P<0.001)

130 Change in forced vital capacity (FVC) is widely accepted as a surrogate f

131 We recruited 20 SSc patients with a forced vital capacity (FVC) of <85% predicted, dyspnea on exert

132 ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.70 or less, a smoking history

133 tion, lung transplant, or decrease in forced vital capacity (FVC) of 10% or greater or decrease in di

134 nchodilation and a ratio of FEV(1) to forced vital capacity (FVC) of 70% or less.

135 piratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.70 as assessed by sp

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

137 or FF scores and greater declines in forced vital capacity (FVC) or DL(CO) at 6 months.

138 ession, as measured by the decline in forced vital capacity (FVC) or vital capacity, in patients with

139 The primary outcome was the change in forced vital capacity (FVC) over a 60-week period.

140 PEA showed a lower decrease in their forced vital capacity (FVC) over time as compared with untreate

141 ollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio,

142 1 second (FEV(1)) (r = -0.68), FEV(1)/forced vital capacity (FVC) ratio (r = -0.74) (P < .001).

143 ough the correlation between the FEV1/forced vital capacity (FVC) ratio and 129Xe VDP (r=-0.95, P<.00

144 The FEV1/forced vital capacity (FVC) ratio is used as a criterion for ai

145 xpiratory volume in 1 second (FEV(1))/forced vital capacity (FVC) ratio with increasing age was faste

146 estational age had a lower FEV1, FEV1/forced vital capacity (FVC) ratio, and forced expiratory volume

147 ratory volume in 1 second (FEV(1)) to forced vital capacity (FVC) ratio, those with chronic obstructi

148 d decrease in FEV(1) and its ratio to forced vital capacity (FVC) stratified a priori by asthma statu

149 5) and obese (BMI > or = 30) men, but forced vital capacity (FVC) tended to decrease with increasing

150 ory volume in 1 second (FEV(1)) and a forced vital capacity (FVC) that were significantly higher than

151 d expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) under the lower limit of normal (LL

152 Forced vital capacity (FVC) was highly correlated with body len

153 ; p < 0.001) and the average adjusted forced vital capacity (FVC) was reduced by 287.8 ml (95% CI: 13

154 n phenotype (A Trpg) was defined as a forced vital capacity (FVC) z score of less than -1.64 or an in

155 Forced vital capacity (FVC), a spirometric measure of pulmonary

156 rced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), airway responsiveness as indicated

157 volume between 50% and 75% of expired forced vital capacity (FVC), and (2) the fraction of the FVC ex

158 expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and 6-minute walk distance.

159 ide association study (GWAS) of FEV1, forced vital capacity (FVC), and FEV1/FVC in 1144 Hutterites ag

160 morphisms in 15 genes with TEW, FEV1, forced vital capacity (FVC), and FEV1/FVC ratio was studied in

161 rced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and forced expiratory flow between

162 correlated with vital capacity (VC), forced vital capacity (FVC), and forced expiratory volume in 1

163 piratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and ratio of FEV(1) to FVC.

164 y mass index, percentage of predicted forced vital capacity (FVC), and the ratio of forced expiratory

165 ratory efficacy measurements included forced vital capacity (FVC), carbon monoxide diffusing capacity

166 volume in the first second (FEV1) and forced vital capacity (FVC), even after adjustment for age, hei

167 l associations with percent predicted forced vital capacity (FVC), FEV(1)/FVC ratio, and PC(20) were

168 rced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC, and diffusing capacity f

169 We measured forced vital capacity (FVC), forced expiratory volume in 1 sec

170 Secondary outcome measures were forced vital capacity (FVC), manual muscle testing (MMT), quali

171 iratory volume in 1 second (FEV1) and forced vital capacity (FVC), obtained by spirometry, were used

172 xpiratory volume in 1 sec (FEV(1)) or forced vital capacity (FVC), or both, after administration of a

173 Lung function parameters (forced vital capacity (FVC), pre- and postbronchodilator FEV1,

174 ible patients, stratified by baseline forced vital capacity (FVC), serum LOXL2 (sLOXL2) concentration

175 Forced vital capacity (FVC), the forced expiratory flow between

176 atory volume in one-second (FEV1) and forced vital capacity (FVC).

177 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC).

178 ry volume (FEV) after 1 second (FEV1)/forced vital capacity (FVC).

179 easured using percentage of predicted forced vital capacity (FVC).

180 int was the annual rate of decline in forced vital capacity (FVC).

181 tory volume in one second (FEV1 ) and forced vital capacity (FVC)] (n = 414).

182 d expiratory volume in 1 s (FEV1) and forced vital capacity (FVC)] was measured at 2 and up to 5 visi

183 ar, and the primary end point was the forced vital capacity (FVC, expressed as a percentage of the pr

184 ed expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] <70%, bronchodilator reversibility

185 s [FEV(1)] 46.8% of predicted, FEV(1)/forced vital capacity [FVC] 54.6%, and postsalbutamol reversibi

186 Spirometry (forced vital capacity [FVC] and forced expiratory volume in 1 s

187 physiologic parameters of breathing (forced vital capacity [FVC] and single-breath diffusing capacit

188 ed expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] ratio <0.7 in patients with symptom

189 adult lung function (FEV1/forced expiratory vital capacity [FVC] ratio and FEV1) as the number of ri

190 he greatest decline in lung function (forced vital capacity [FVC]% predicted) in the early years afte

191 volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave veloc

192 ond [FEV(1)], percentage of predicted forced vital capacity [FVC]) results were compared by using ana

193 Measures of lung function (FEV1, forced vital capacity [FVC], and forced expiratory flow between

194 expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and peak expiratory flow rate [PEF

195 expiratory volume in 1 second [FEV1]/forced vital capacity [FVC], Pearson r = -0.69, P < .001; perce

196 We conclude that a 6-month change in forced vital capacity gives additional prognostic information t

197 g a spirometer to trigger scanning at 90% of vital capacity (group 2, spirometric gating study).

198 rosis (defined as death or decline in forced vital capacity >10% at 12 months after study enrolment)

199 d forced expiratory flow after 25% to 75% of vital capacity had been expelled (FEF25-75).

200 LS Functional Rating Scale-Revised or forced vital capacity, having at least 25% improvement at 6 mon

201 may help counteract postoperative decreased vital capacity; however, the evidence for the role of in

202 including rash, alopecia, and reduced forced vital capacity, improved markedly in patients with these

203 rced expiratory volume in 1 second to forced vital capacity in 48,201 individuals of European ancestr

204 reas the relationship between age and forced vital capacity in patients with Bethlem myopathy was not

205 atory volume in 1 second (FEV(1)) and forced vital capacity in the CARDIA cohort.

206 he decline in forced vital capacity (FVC) or vital capacity, in patients with idiopathic pulmonary fi

207 Vital capacity increased 11% (mean) within 9 months in 3

208 f postnatal lung growth and differentiation: vital capacity, inspiratory capacity, compliance, non-pa

209 A reduced forced vital capacity is prevalent in patients with adult conge

210 h asthma and airway obstruction (FEV1/forced vital capacity < 0.85 and FEV1 < 100% predicted) than in

211 rate/severe airflow obstruction (FEV1/forced vital capacity <0.70 and FEV1 < 80% of predicted value)

212 ty: age > or =65 years at enrollment, forced vital capacity <50% predicted, clinically significant ar

213 xpiratory volume in 1 second (FEV(1))/forced vital capacity <70% and FEV(1 )<80% predicted.

214 ve therapy, as assessed by either the forced vital capacity (mean change IFNalpha -8.2 versus placebo

215 and forced expiratory flow at 50% of forced vital capacity (mean z score for cases vs control subjec

216 A total of 486 forced vital capacity measurements obtained in 145 patients wer

217 in other outcome measures, including forced vital capacity, measures of oral aperture and hand exten

218 did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functio

219 Secondary outcomes were forced vital capacity, number of pulmonary exacerbations, weigh

220 below 85% of those predicted for both forced vital capacity (odds ratio (OR) = 3.10, 95% CI: 1.65, 5.

221 ry fibrosis on chest radiograph and a forced vital capacity of <55% of predicted; 4) in the GI tract,

222 expiratory volume in 1 s (FEV(1)) to forced vital capacity of 0.70 or less after bronchodilators (an

223 patients had a cumulative decline in forced vital capacity of 2.3% per year (P < 0.0001) whereas the

224 demonstrated a cumulative decline in forced vital capacity of 2.6% per year (P < 0.0001).

225 iagnosed in the past 48 months, had a forced vital capacity of 55-90% of the predicted value, and a h

226 Patients with reduced force vital capacity of at least moderate severity had a 1.6-f

227 back extrapolation as a proportion of forced vital capacity of less than 5%, whereas all but 4 could

228 less than 80% and a ratio of FEV1 to forced vital capacity of less than 70%), and had a smoking hist

229 atients had amyotrophic lateral sclerosis, a vital capacity of more than 60% of that predicted for ag

230 fibrosis was independent of age, sex, forced vital capacity, or diffusing capacity of carbon monoxide

231 , P <.001) and the ratio of FEV(1) to forced vital capacity, or FVC, (r = -0.930, P <.001).

232 forced expiratory volume in 1 second, forced vital capacity, or the forced expiratory volume in 1 sec

233 and >/=10% decline, respectively, in forced vital capacity over the preceding 6-month period.

234 ine mRNA had a significant decline in forced vital capacity over time after the BAL, whereas patients

235 s characterized by considerably lower forced vital capacity (P < .001) and higher S(cond) (P = .001)

236 001) and C3 (P < .001), and decreased forced vital capacity (P = .013).

237 atio of maximal midexpiratory flow to forced vital capacity (p = 0.02), whereas exposure to ozone was

238 lower value for the percent predicted forced vital capacity (P<0.0001).

239 t improvements in mRSS (p<0.0001) and forced vital capacity (p<0.03) persisted.

240 phagia (OR=10.67; p=0.03) and reduced forced vital capacity (p=0.005).

241 e (P=0.007), a lower ratio of FEV1 to forced vital capacity (P=0.03), and a reduced carbon monoxide d

242 proportional to weight (P < .001) and forced vital-capacity (P = .001) and inversely proportional to

243 % to -1.2%/month percentage predicted forced vital capacity, P < .04 and from -1.2 to 0.6 ALS Functio

244 monas aeruginosa infection, FEV1/FVC (forced vital capacity), PA:A greater than 1, and previous exace

245 forced expiratory volume in 1 second, forced vital capacity, peak expiratory flow, diffusing capacity

246 cent predicted], 38.1 [13.9]%; FEV(1)/forced vital capacity [percent predicted], 40.9 [11.8]%; arteri

247 ith acute care visits, decreased FEV1/forced vital capacity percentage values, fraction of exhaled ni

248 Mean peak VO2 and forced vital capacity (% Pred) were significantly reduced (P<0.

249 ibutors to AQLQ(S) score were R20 and forced vital capacity (% pred.).

250 thickness positively correlated with forced vital capacity % predicted and forced expiratory volume

251 piratory volume in 1 second (FEV1) to forced vital capacity (r = 0.63, r = 0.67, and r = -0.60, respe

252 s of patients with CF correlated with forced vital capacity (r = 0.7; 95% confidence interval [CI]: 0

253 ratory volume in 1 second (r = 0.70), forced vital capacity (r = 0.84), and %VV (r = 0.56).

254 ased forced expiratory volume in 1 second to vital capacity ratio (<50%), lateral pleural puncture, a

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

256 C-C and C-UC groups, except for FEV1/forced vital capacity ratio (86% vs 82%, respectively; P < .01)

257 associated with a 5% decrease in FEV1/forced vital capacity ratio (beta = -0.05; 95% CI, -0.08 to -0.

258 L4R were associated with reduced FEV1/forced vital capacity ratio (beta = -0.11, -0.08, and -0.10; P

259 ; P = 0.021), as did a decreased FEV1/forced vital capacity ratio (FEV1 response increased 0.39% of b

260 asthma (P = .03) and decreased FEV(1)/forced vital capacity ratio (P = .03).

261 score, FEV1 (percent predicted), FEV1/forced vital capacity ratio (percent predicted), and forced exp

262 forced expiratory volume in 1 second/forced vital capacity ratio among white, African-American, and

263 A lower postbronchodilator FEV1/forced vital capacity ratio and a higher number of cigarette pa

264 ed expiratory volume in 1 s (FEV1) to forced vital capacity ratio of less than 0.7, without any restr

265 1), forced vital capacity, and FEV(1)/forced vital capacity ratio) are proposed as core outcomes for

266 icted forced vital capacity, and FEV1/forced vital capacity ratio) were performed in 4 white populati

267 aseline for every 1% decrease in FEV1/forced vital capacity ratio).

268 ith FEV1, forced vital capacity, FEV1/forced vital capacity ratio, transfer lung capacity of carbon m

269 ted with the forced expiratory volume/forced vital capacity ratio.

270 alence of asthma and decreased FEV(1)/forced vital capacity ratio.

271 forced vital capacity, a decrease in forced vital capacity remained an independent risk factor for m

272 ced expiratory volume in 1 second and forced vital capacity remained unchanged after BEP but increase

273 None of the SNPs identified for FEV1/forced vital capacity replicated in the independent cohorts.

274 r assessment of physical fitness were forced vital capacity, resting heart rate, hand grip strength,

275 rced expiratory volume in 1 second to forced vital capacity (rs=-0.72; 95% CI: -0.92, -0.52; P=.001)

276 ould be reviewed after 4 weeks, FEV1, forced vital capacity, S(acin), and S(cond) values showed marke

277 s neonates (forced expiratory flow at 50% of vital capacity second in neonates reduced by 0.34 z scor

278 volume in 1 second normalized to the forced vital capacity (standardized coefficients [betaS] = -0.6

279 ly, this group also had a decreased FVC/slow vital capacity (SVC).

280 olume in 1 s and percentage predicted forced vital capacity than did those consuming the high-antioxi

281 monary function tests (PFTs) included forced vital capacity, total lung capacity, forced expiratory v

282 b prevent about 50% of the decline in forced vital capacity typically seen in this disease; future tr

283 ced expiratory volume in 1 second and forced vital capacity using data collected from 1996 to 2000 in

284 cant improvement from baseline, while forced vital capacity values declined from baseline.

285 rced expiratory volume in 0.5 seconds/forced vital capacity values than did boys (mean difference, 0.

286 rced expiratory volume in 0.5 seconds/forced vital capacity values than did girls of equivalent age (

287 od asthma, is measured reproducibly in mixed vital capacity (VC) expirates.

288 5 Hz (R5) was significantly correlated with vital capacity (VC), forced vital capacity (FVC), and fo

289 We studied the predictive value of vital capacity (VC), static inspiratory and expiratory m

290 (forced expiratory volume in 1 sec [FEV(1)]: vital capacity [VC] <0.7) and a nonobstructive pattern (

291 (forced expiratory volume in 1 second [FEV1]/vital capacity [VC]).

292 , prothrombin time (P = 0.0005), and maximal vital capacity (VCmax) (P = 0.04); lower platelet count

293 rced expiratory volume in 1 second to forced vital capacity was -0.75 (95% confidence interval [CI],

294 tween the 25th and 75th percentile of forced vital capacity was also inversely associated with higher

295 hip between maximal motor ability and forced vital capacity was highly significant (P < 0.0001).

296 ual interstitial pneumonia, change in forced vital capacity was the best physiologic predictor of mor

297 0 mL and >/=12% increase in FEV(1) or forced vital capacity) was present in 20 (9.0%) participants.

298 ed expiratory volume in 1 second, and forced vital capacity were performed systematically before, dur

299 Age at diagnosis and most recent forced vital capacity were significant predictors of mortality

300 hazards models were used for FEV1 and forced vital capacity, with gender-specific lung function quart