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 or influencing IPF prognosis was the percent vital capacity.

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

4 ned improvement in skin thickness and forced vital capacity.

5 function based on predicted values of forced vital capacity.

6 -term associations of pollutants with forced vital capacity.

7 rters of these abnormalities were low forced vital capacity.

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

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

10 A similar pattern emerged for forced vital capacity.

11 sease course, but there was no change in his vital capacity.

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

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

14 ive muscle weakness accompanied by decreased vital capacities.

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

16 s up to 48 weeks post-ART initiation (forced vital capacity, 206 mL higher; 95% confidence interval [

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

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

19 women; mean age 66.1 years [SD 9.3]; forced vital capacity 83.7% [SD 14.2]; diffusing capacity for c

20 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

21 of predicted values and were 92% for forced vital capacity, 93% for forced expiratory volume in 1 se

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

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

24 5% of forced vital capacity, and FEV1/forced vital capacity (all P < .0001).

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

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

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

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

29 Forced vital capacity and diffusing capacity for carbon monoxid

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

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

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

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

34 ratory-related events, lung function (forced vital capacity and gas transfer), and patient-reported o

35 first symptoms; loss of ambulation; fall in vital capacity and left ventricular ejection fraction; i

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

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

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

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

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

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

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

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

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

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

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

47 ed amyotrophic functional rating scale, slow vital capacity, and upper motor neuron score) and betwee

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

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

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

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

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

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

54 5.2%, and C/C 9.5%; p = 0.003), lower forced vital capacity at diagnosis (median percentage A/A 92.0,

55 Forced vital capacity at F-FDG PET/CT inversely correlated with

56 signal associated with FEV(1), FEV(1)/forced vital capacity, atopy, and age of asthma onset.

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

58 with reduced prebronchodilator FEV(1)/forced vital capacity (beta coefficient, -0.10; 95% CI, -0.19 t

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

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

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

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

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

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

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

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

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

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

69 mposite measure of ALS function and a stable vital capacity during a 12-month period.

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

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

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

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

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

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

76 Forced expiratory volume in 1 s/forced vital capacity (FEV(1)/FVC) but not FVC was related to m

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

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

79 x 10(-8)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC: r(g) = 0.137, p = 2.0 x 10(-

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

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

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

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

84 forced expired volume in the first second to vital capacity (FEV1:FVC) less than 0.70 with respirator

85 ory volume in the first second to the forced vital capacity (FEV1:FVC) of less than 0.70, yet this fi

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

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

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

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

90 ond forced expiratory volume (FEV1%), forced vital capacity (FVC%), and the FEV1/FVC ratio.

91 estrictive spirometric pattern [60 <= forced vital capacity (FVC) < 80% predicted] vs. 21.2% with a m

92 0 pack-years or more, and had an FEV1/forced vital capacity (FVC) <0.7.

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

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

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

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

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

98 ratory Volume in one second (FEV(1)), Forced Vital Capacity (FVC) and FEV(1)/FVC).

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

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

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

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

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

104 ed decline in percentage of predicted forced vital capacity (FVC) and stabilised 6-min walking distan

105 orming forced respiratory cycles, the Forced Vital Capacity (FVC) and the Forced Expiratory Volume in

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

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

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

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

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

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

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

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

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

115 This resulted from a lower forced vital capacity (FVC) in HIV-infected participants but si

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

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

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

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

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

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

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

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

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

125 classifiable ILD, a percent predicted forced vital capacity (FVC) of 45% or higher and percent predic

126 fibrosis and percentage of predicted forced vital capacity (FVC) of 55% or greater were enrolled and

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

128 fibrosis within the past 3 years and forced vital capacity (FVC) of 80% predicted or higher were eli

129 can Thoracic Association guidelines), forced vital capacity (FVC) of at least 45%, 6MWD of 150-450 m,

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

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

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

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

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

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

136 ion of alpha-T levels with FEV(1) and forced vital capacity (FVC) percent predicted.

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

138 ry volume in 1 second (FEV(1))-to-functional vital capacity (FVC) ratio (-1.7 vs -0.7) and greater pr

139 1 second (FEV(1)) (r = -0.68), FEV(1)/forced vital capacity (FVC) ratio (r = -0.74) (P < .001).

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

141 The degree of FEV(1)/forced vital capacity (FVC) ratio impairment was the largest pr

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

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

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

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

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

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

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

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

150 Forced vital capacity (FVC) was associated with moderate-to-vig

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

152 iratory volume in 1 second (FEV1) and forced vital capacity (FVC) were lower in the HIV+ compared to

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

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

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

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

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

158 piratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and forced expiratory flow at 25-7

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

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

161 expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and physical activity were assesse

162 ume in 1 s (FEV(1), primary outcome), forced vital capacity (FVC), and respiratory or allergic sympto

163 expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and their ratio (FEV1:FVC).

164 int was the annual rate of decline in forced vital capacity (FVC), assessed over a 52-week period.

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

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

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

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

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

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

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

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

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

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

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

176 r age, being HIV+, and having reduced forced vital capacity (FVC).

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

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

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

180 e in the first second (FEV(1), %) and forced vital capacity (FVC, %) values.

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

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

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

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

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

186 fined as a post-bronchodilator FEV(1)/forced vital capacity [FVC] ratio <=0.70) and a specialist-veri

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

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

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

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

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

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

193 on expiratory flow variables (FEV(1), forced vital capacity [FVC], FEV(1)/FVC ratio, and forced expir

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

195 expiratory volume in 1 second to the forced vital capacity greater than or equal to 70% (HR, 1.67, P

196 ator forced expiratory flow at 25% to 75% of vital capacity growth were as follows: 182 mL/y (95% CI,

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

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

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

200 ed with mortality after adjusting for forced vital capacity (HR 2.47, 95% CI 1.48-4.15; p=0.0063), an

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

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

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

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

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

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

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

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

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

210 core >1), and impaired lung function (forced vital capacity <=75% predicted) conducted in 39 UK speci

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

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

213 -0.70, P < .001), ratio of FEV(1) to forced vital capacity (model: r = -0.73, P < .001; MRI: r = -0.

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

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

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

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

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

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

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

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

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

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

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

225 ator forced expiratory flow at 25% to 75% of vital capacity over 1 year among sensitized/exposed asth

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

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

228 tients' HRCT scan scores (P < .0001), forced vital capacity (P = .0017), FEV(1) (P = .037), and total

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

230 P = .001) whereas mean ADC (P = .17), forced vital capacity (P = .12), and diffusing capacity of the

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

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

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

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

235 % to -1.2%/month percentage predicted forced vital capacity, P < .04 and from -1.2 to 0.6 ALS Functio

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

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

238 sures of pulmonary dysfunction (PaO2, forced vital capacity percentage predicted, total lung capacity

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

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

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

242 ian values correlated with changes in forced vital capacity (R = -0.38; 95% CI: -0.25, -0.49; P < .00

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

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

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

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

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

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

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

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

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

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

253 EV(1) (r = -0.35; P = .04) and FEV(1)/forced vital capacity ratio (r = -0.41; P = .01).

254 rced expiratory volume in 1 second-to-forced vital capacity ratio (r = -0.70; 95% confidence interval

255 ) (r = 0.65, P < .001), the FEV(1)-to-forced vital capacity ratio (r = 0.81, P < .001), and diffusing

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

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

258 Subjects with preserved FEV(1)-to-forced vital capacity ratio and reduced FEV(1) percentage predi

259 1) percent predicted and an FEV(1)-to-forced vital capacity ratio at age 50 years (-3.36% [95% CI = -

260 ned COPD as postbronchodilator FEV(1)/forced vital capacity ratio below the lower limit of normal, as

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

262 he mean (SD) prebronchodilator FEV(1)/forced vital capacity ratio was 80.2% (9.0%).

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

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

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

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

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

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

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

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

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

272 on monoxide, total lung capacity, and forced vital capacity (rho = -0.76, -0.70, and -0.62, respectiv

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

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

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

276 , but assisted ventilation rating and forced vital capacity showed moderate correlations with tidal v

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

278 up enrolled adults with ALS and sitting slow vital capacity (SVC) 60%-90 % of predicted from 11 sites

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

280 neurofilament H subunit levels, and the slow vital capacity; the time to death, tracheostomy, or perm

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

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

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

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

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

286 5 Hz (R5) was significantly correlated with vital capacity (VC), forced vital capacity (FVC), and fo

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

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

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

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

291 rving weekly, the mean difference for forced vital capacity was -102 (95% confidence interval (CI): -

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

293 A measure of airflow limitation but not vital capacity was associated with overall mortality in

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

295 0 mL and >/=12% increase in FEV(1) or forced vital capacity) was present in 20 (9.0%) participants.

296 Clinical function and vital capacity were measured.

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

298 on monoxide, total lung capacity, and forced vital capacity were rho = -0.65, -0.70, and -0.57, respe

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

300 of the lungs for carbon monoxide and forced vital capacity, were performed at each examination.