ライフサイエンスコーパス: forced vital capacity

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

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

3 sustained improvement in skin thickness and forced vital capacity.

4 ung dysfunction based on predicted values of forced vital capacity.

5 fy long-term associations of pollutants with forced vital capacity.

6 ree-quarters of these abnormalities were low forced vital capacity.

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

8 ization 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 ator forced expiratory flow at 25% to 75% of forced vital capacity.

12 ed with lung injury score and inversely with forced vital capacity.

13 nd we found some evidence of less decline in forced vital capacity.

14 ml (95% confidence interval 0.2 to 49.6) in forced vital capacity.

15 - 19 mL; P = 1.1 x 10(-5), respectively) and forced vital capacity (-100 +/- 21 mL; P = 2.7 x 10(-6)

16 7%, 95% confidence interval: -5.2, -0.1) and forced vital capacity (-2.4%, 95% confidence interval: -

17 with low magnesium intake showed deficits in forced vital capacity (-2.8%, 95% confidence interval: -

18 piratory volume in 1 second (FEV1) (388 mL), forced vital capacity (298 mL), and the FEV1/forced vita

19 S had significantly lower percent predicted: forced vital capacity (61.5+/-16 versus 80.5+/-14; P<0.0

20 5.2 +/- 4.6 vs. 88.4 +/- 5.6%; P = 0.03) and forced vital capacity (83.2 +/- 4.7 vs. 109.2 +/- 6.0%;

21 ls) were associated with a 2.4% decrement in forced vital capacity (95% confidence interval (CI): -4.

22 forced vital capacity, and 6-month change in forced vital capacity, a decrease in forced vital capaci

23 o phenotypes used to assess asthma severity: forced vital capacity, a sensitive measure of airway obs

24 ratory volume in the first second (FEV1) and forced vital capacity after adjustment for sex, age, hei

25 5% to 75% of forced vital capacity, and FEV1/forced vital capacity (all P < .0001).

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

27 0% of children were able to produce a second forced vital capacity and a second forced expired volume

28 ts negatively and positively correlated with forced vital capacity and age, respectively.

29 disease extent, and the percentage predicted forced vital capacity and carbon monoxide diffusing capa

30 ulmonary fibrosis as determined by change in forced vital capacity and death.

31 Forced vital capacity and diffusing capacity for carbon

32 vitamin C, were associated with deficits in forced vital capacity and FEV1 in boys.

33 OH)D was associated with lower mean residual forced vital capacity and forced expiratory volume in 1

34 We observed a modest reduction in forced vital capacity and forced expiratory volume in on

35 Forced vital capacity and mid-expiratory flow did not si

36 The rate of progression of the forced vital capacity and of the ALS Functional Rating S

37 ated with increased airflow limitation (FEV1/forced vital capacity and residual volume/total lung cap

38 ation was associated with a decrease in FVC (forced vital capacity) and FEV1 (forced expiratory volum

39 diagnosis, gender, smoking history, baseline forced vital capacity, and 6-month change in forced vita

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

41 second, forced expiratory volume in 1 second/forced vital capacity, and diffusing capacity.

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

43 EV1, forced expiratory flow at 25% to 75% of forced vital capacity, and FEV1/forced vital capacity (a

44 t predicted FEV1 [ppFEV1], percent predicted forced vital capacity, and FEV1/forced vital capacity ra

45 otein cholesterol, forced expiratory volume, forced vital capacity, and height.

46 is inadequate and functional rating scales, forced vital capacity, and patient survival have been th

47 ced expiratory volume in 1 second (FEV1) and forced vital capacity, and the 10-year incidence of coro

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

49 The primary endpoint, change in forced vital capacity as a percentage of the predicted n

50 ith forced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted

51 of forced expiratory volume in 1 second and forced vital capacity as the percentage of the predicted

52 For example, the decrease in forced vital capacity associated with a 70-ppb/month gre

53 in forced expiratory volume in 1 second and forced vital capacity associated with a decrease of 1 st

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

55 ebo group had a decline in percent predicted forced vital capacity at 48 weeks (p=0.0373).

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

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

58 ose with initial mRSS >14) or an increase in forced vital capacity by more than 10%.

59 airways obstruction (FEV1 as a percentage of forced vital capacity) compared with women who did not.

60 related myopathies by analysing longitudinal forced vital capacity data in a large international coho

61 a statistically significant increase in ALS-forced vital capacity decline in SOD1(A4V) compared with

62 lity were similar in all 3 groups, while the forced vital capacity decreased significantly in the rel

63 >25% increase in mRSS or decrease of >10% in forced vital capacity) despite treatment with cyclophosp

64 ate pregnancy was negatively associated with forced vital capacity (difference in standard deviation

65 disease activity, pulmonary function tests (forced vital capacity, diffusing capacity for carbon mon

66 and lung involvement in SSc, as well as the forced vital capacity, diffusing capacity for carbon mon

67 ere examined together with 6-month change in forced vital capacity, diffusing capacity for carbon mon

68 B with survival was independent of age, sex, forced vital capacity, diffusing capacity of carbon mono

69 rkers of disease severity, including a lower forced vital capacity, diffusion capacity for carbon mon

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

71 of forced expiratory volume in one second to forced vital capacity (FEB1/FVC) and the forced expirato

72 d expiratory flow between 25% and 75% of the forced vital capacity (FEF(25-75)) (-16.2%, 95% confiden

73 orced expiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), -5.5%, 95% CI: -10.5

74 ed midexpiratory flow between 25% and 75% of forced vital capacity (FEF(25-75)), 48%; total airway re

75 d lower forced expiratory flow at 75% of the forced vital capacity (FEF(75)) (-8.3%, 95% confidence i

76 ed midexpiratory flow between 25% and 75% of forced vital capacity (FEF25-75) was associated with the

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

78 n the first second (FEV(1)) and its ratio to forced vital capacity (FEV(1)/FVC), an indicator of airf

79 e second (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC).

80 o of forced expiratory volume in 1 second to forced vital capacity (FEV(1):FVC ratio; pulmonary), hem

81 olume in 1 s (FEV1) and the ratio of FEV1 to forced vital capacity (FEV1/FVC) in the general populati

82 teria, based on the forced expiratory volume/forced vital capacity (FEV1/FVC) ratio and then using th

83 s at V2 was negatively correlated with FEV1, forced vital capacity, FEV1/forced vital capacity ratio,

84 percentile) was associated with deficits in forced vital capacity for both boys and girls and with d

85 Asian values for forced vital capacity, forced expiratory volume in 1 s (

86 Pulmonary parameters of response included forced vital capacity, forced expiratory volume in 1 sec

87 nt from baseline to 12 months in measures of forced vital capacity, functional residual capacity, ser

88 Patients were at least 5 yr old with a forced vital capacity (FVC) > or = 35% of predicted and

89 d for 10 pack-years or more, and had an FEV1/forced vital capacity (FVC) <0.7.

90 that correlated with the absolute change in forced vital capacity (FVC) (% predicted values) and the

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

92 concentrations were associated with maximum forced vital capacity (FVC) (P </= 0.01) and forced expi

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

94 with DPT demonstrated significantly reduced forced vital capacity (FVC) (p = 0.002) and diffusing ca

95 point required 12% or greater improvement in forced vital capacity (FVC) and 1 point or greater decre

96 1) Serial measurement of forced vital capacity (FVC) and carbon monoxide diffusin

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

98 y, there was a significant decline in median forced vital capacity (FVC) and diffusing capacity of ca

99 etermined by the pulmonary function tests of forced vital capacity (FVC) and diffusion capacity for c

100 gain between 3 and 7 years of age and higher forced vital capacity (FVC) and FEV1 values at age 15 ye

101 n of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genom

102 as characterized by the spirometric measures forced vital capacity (FVC) and forced expiratory volume

103 ns had significantly lower percent predicted forced vital capacity (FVC) and forced expiratory volume

104 We assessed lung function by measuring forced vital capacity (FVC) and forced expiratory volume

105 Forced vital capacity (FVC) and total lung capacity (TLC

106 y volume in 1 second (FEV1) and its ratio to forced vital capacity (FVC) are used in the diagnosis an

107 The primary outcome was estimated change in forced vital capacity (FVC) at 30 weeks (mean follow-up)

108 endpoint was change in percentage predicted forced vital capacity (FVC) at week 72.

109 Similar associations were seen for forced vital capacity (FVC) but not for the FEV(1):FVC r

110 year, was defined as a decrease in predicted forced vital capacity (FVC) by 10% or more, a decrease i

111 CNV association (discovery P = 0.0007) with Forced Vital Capacity (FVC) downstream of BANP on chromo

112 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) during that period (referred

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

114 ance was negatively associated with FEV1 and forced vital capacity (FVC) in adolescents with and with

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

116 ancestry is associated with lower FEV(1) and forced vital capacity (FVC) in Puerto Rican children ind

117 e in 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC) in the SpiroMeta consortium

118 statistically significant difference between forced vital capacity (FVC) in the standing versus sitti

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

120 EV1) increased by 118+/-330 ml (P=0.06), the forced vital capacity (FVC) increased by 390+/-570 ml (P

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

122 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) measurements.

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

124 alue, a ratio of post-bronchodilator FEV1 to forced vital capacity (FVC) of 0.70 or less, a smoking h

125 xacerbation, lung transplant, or decrease in forced vital capacity (FVC) of 10% or greater or decreas

126 ter bronchodilation and a ratio of FEV(1) to forced vital capacity (FVC) of 70% or less.

127 rced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.70 as assesse

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

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

130 e progression, as measured by the decline in forced vital capacity (FVC) or vital capacity, in patien

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

132 ed with PEA showed a lower decrease in their forced vital capacity (FVC) over time as compared with u

133 bject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC

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

135 ), although the correlation between the FEV1/forced vital capacity (FVC) ratio and 129Xe VDP (r=-0.95

136 The FEV1/forced vital capacity (FVC) ratio is used as a criterion

137 orced expiratory volume in 1 second (FEV(1))/forced vital capacity (FVC) ratio with increasing age wa

138 unger gestational age had a lower FEV1, FEV1/forced vital capacity (FVC) ratio, and forced expiratory

139 ed expiratory volume in 1 second (FEV(1)) to forced vital capacity (FVC) ratio, those with chronic ob

140 -related decrease in FEV(1) and its ratio to forced vital capacity (FVC) stratified a priori by asthm

141 I < 22.5) and obese (BMI > or = 30) men, but forced vital capacity (FVC) tended to decrease with incr

142 expiratory volume in 1 second (FEV(1)) and a forced vital capacity (FVC) that were significantly high

143 n forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) under the lower limit of nor

144 Forced vital capacity (FVC) was highly correlated with b

145 , 398.4; p < 0.001) and the average adjusted forced vital capacity (FVC) was reduced by 287.8 ml (95%

146 truction phenotype (A Trpg) was defined as a forced vital capacity (FVC) z score of less than -1.64 o

147 Forced vital capacity (FVC), a spirometric measure of pu

148 ding forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), airway responsiveness as in

149 nge in volume between 50% and 75% of expired forced vital capacity (FVC), and (2) the fraction of the

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

151 enome-wide association study (GWAS) of FEV1, forced vital capacity (FVC), and FEV1/FVC in 1144 Hutter

152 de polymorphisms in 15 genes with TEW, FEV1, forced vital capacity (FVC), and FEV1/FVC ratio was stud

153 were forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and forced expiratory flow

154 icantly correlated with vital capacity (VC), forced vital capacity (FVC), and forced expiratory volum

155 rced expiratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and ratio of FEV(1) to FVC.

156 on, body mass index, percentage of predicted forced vital capacity (FVC), and the ratio of forced exp

157 Exploratory efficacy measurements included forced vital capacity (FVC), carbon monoxide diffusing c

158 ratory volume in the first second (FEV1) and forced vital capacity (FVC), even after adjustment for a

159 ditional associations with percent predicted forced vital capacity (FVC), FEV(1)/FVC ratio, and PC(20

160 with forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC, and diffusing cap

161 Forced vital capacity (FVC), forced expiratory volume fo

162 of exposure to refractory ceramic fibers on forced vital capacity (FVC), forced expiratory volume in

163 We measured forced vital capacity (FVC), forced expiratory volume in

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

165 ced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), obtained by spirometry, wer

166 orced expiratory volume in 1 sec (FEV(1)) or forced vital capacity (FVC), or both, after administrati

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

168 Eligible patients, stratified by baseline forced vital capacity (FVC), serum LOXL2 (sLOXL2) concen

169 Forced vital capacity (FVC), the forced expiratory flow

170 d expiratory volume in one-second (FEV1) and forced vital capacity (FVC).

171 e at 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC).

172 xpiratory volume (FEV) after 1 second (FEV1)/forced vital capacity (FVC).

173 tion, measured using percentage of predicted forced vital capacity (FVC).

174 end point was the annual rate of decline in forced vital capacity (FVC).

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

176 eased forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC)] was associated with an incr

177 [forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC)] was measured at 2 and up to

178 irst year, and the primary end point was the forced vital capacity (FVC, expressed as a percentage of

179 of forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] <70%, bronchodilator reversi

180 e in 1 s [FEV(1)] 46.8% of predicted, FEV(1)/forced vital capacity [FVC] 54.6%, and postsalbutamol re

181 Spirometry (forced vital capacity [FVC] and forced expiratory volume

182 es, and physiologic parameters of breathing (forced vital capacity [FVC] and single-breath diffusing

183 or forced expiratory volume in 1 s [FEV1] to forced vital capacity [FVC] ratio <0.7 in patients with

184 have the greatest decline in lung function (forced vital capacity [FVC]% predicted) in the early yea

185 ratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wav

186 n 1 second [FEV(1)], percentage of predicted forced vital capacity [FVC]) results were compared by us

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

188 forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and peak expiratory flow ra

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

190 We conclude that a 6-month change in forced vital capacity gives additional prognostic inform

191 ary fibrosis (defined as death or decline in forced vital capacity >10% at 12 months after study enro

192 ations with the GI scale, and changes in the forced vital capacity had an excellent correlation with

193 ither ALS Functional Rating Scale-Revised or forced vital capacity, having at least 25% improvement a

194 of DM, including rash, alopecia, and reduced forced vital capacity, improved markedly in patients wit

195 o of forced expiratory volume in 1 second to forced vital capacity in 48,201 individuals of European

196 01) whereas the relationship between age and forced vital capacity in patients with Bethlem myopathy

197 d expiratory volume in 1 second (FEV(1)) and forced vital capacity in the CARDIA cohort.

198 A reduced forced vital capacity is prevalent in patients with adul

199 ren with asthma and airway obstruction (FEV1/forced vital capacity < 0.85 and FEV1 < 100% predicted)

200 Moderate/severe airflow obstruction (FEV1/forced vital capacity <0.70 and FEV1 < 80% of predicted

201 mortality: age > or =65 years at enrollment, forced vital capacity <50% predicted, clinically signifi

202 orced expiratory volume in 1 second (FEV(1))/forced vital capacity <70% and FEV(1 )<80% predicted.

203 vel (> or = 106 micromol/L [1.2 mg/dL]), low forced vital capacity (< or = 2.06 mL), aortic stenosis

204 ng active therapy, as assessed by either the forced vital capacity (mean change IFNalpha -8.2 versus

205 P=.36) and forced expiratory flow at 50% of forced vital capacity (mean z score for cases vs control

206 A total of 486 forced vital capacity measurements obtained in 145 patie

207 e noted in other outcome measures, including forced vital capacity, measures of oral aperture and han

208 Secondary outcomes were forced vital capacity, number of pulmonary exacerbations

209 levels below 85% of those predicted for both forced vital capacity (odds ratio (OR) = 3.10, 95% CI: 1

210 pulmonary fibrosis on chest radiograph and a forced vital capacity of <55% of predicted; 4) in the GI

211 forced expiratory volume in 1 s (FEV(1)) to forced vital capacity of 0.70 or less after bronchodilat

212 mediate patients had a cumulative decline in forced vital capacity of 2.3% per year (P < 0.0001) wher

213 on, and demonstrated a cumulative decline in forced vital capacity of 2.6% per year (P < 0.0001).

214 been diagnosed in the past 48 months, had a forced vital capacity of 55-90% of the predicted value,

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

216 EV1] of less than 80% and a ratio of FEV1 to forced vital capacity of less than 70%), and had a smoki

217 monary fibrosis was independent of age, sex, forced vital capacity, or diffusing capacity of carbon m

218 -0.797, P <.001) and the ratio of FEV(1) to forced vital capacity, or FVC, (r = -0.930, P <.001).

219 ty for forced expiratory volume in 1 second, forced vital capacity, or the forced expiratory volume i

220 as <5% and >/=10% decline, respectively, in forced vital capacity over the preceding 6-month period.

221 f cytokine mRNA had a significant decline in forced vital capacity over time after the BAL, whereas p

222 roup was characterized by considerably lower forced vital capacity (P < .001) and higher S(cond) (P =

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

224 n the ratio of maximal midexpiratory flow to forced vital capacity (p = 0.02), whereas exposure to oz

225 with a lower value for the percent predicted forced vital capacity (P<0.0001).

226 ted that improvements in mRSS (p<0.0001) and forced vital capacity (p<0.03) persisted.

227 of dysphagia (OR=10.67; p=0.03) and reduced forced vital capacity (p=0.005).

228 l volume (P=0.007), a lower ratio of FEV1 to forced vital capacity (P=0.03), and a reduced carbon mon

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

230 om -5.1% to -1.2%/month percentage predicted forced vital capacity, P < .04 and from -1.2 to 0.6 ALS

231 Pseudomonas aeruginosa infection, FEV1/FVC (forced vital capacity), PA:A greater than 1, and previou

232 luding forced expiratory volume in 1 second, forced vital capacity, peak expiratory flow, diffusing c

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

234 iated with acute care visits, decreased FEV1/forced vital capacity percentage values, fraction of exh

235 Mean peak VO2 and forced vital capacity (% Pred) were significantly reduce

236 t contributors to AQLQ(S) score were R20 and forced vital capacity (% pred.).

237 r layer thickness positively correlated with forced vital capacity % predicted and forced expiratory

238 rced expiratory volume in 1 second (FEV1) to forced vital capacity (r = 0.63, r = 0.67, and r = -0.60

239 V values of patients with CF correlated with forced vital capacity (r = 0.7; 95% confidence interval

240 ed expiratory volume in 1 second (r = 0.70), forced vital capacity (r = 0.84), and %VV (r = 0.56).

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

242 een the C-C and C-UC groups, except for FEV1/forced vital capacity ratio (86% vs 82%, respectively; P

243 el was associated with a 5% decrease in FEV1/forced vital capacity ratio (beta = -0.05; 95% CI, -0.08

244 , and IL4R were associated with reduced FEV1/forced vital capacity ratio (beta = -0.11, -0.08, and -0

245 12-4.01; P = 0.021), as did a decreased FEV1/forced vital capacity ratio (FEV1 response increased 0.3

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

247 l Test score, FEV1 (percent predicted), FEV1/forced vital capacity ratio (percent predicted), and for

248 or the forced expiratory volume in 1 second/forced vital capacity ratio among white, African-America

249 A lower postbronchodilator FEV1/forced vital capacity ratio and a higher number of cigar

250 ry forced expiratory volume in 1 s (FEV1) to forced vital capacity ratio of less than 0.7, without an

251 s (FEV(1), forced vital capacity, and FEV(1)/forced vital capacity ratio) are proposed as core outcom

252 nt predicted forced vital capacity, and FEV1/forced vital capacity ratio) were performed in 4 white p

253 9% of baseline for every 1% decrease in FEV1/forced vital capacity ratio).

254 lated with FEV1, forced vital capacity, FEV1/forced vital capacity ratio, transfer lung capacity of c

255 associated with the forced expiratory volume/forced vital capacity ratio.

256 er prevalence of asthma and decreased FEV(1)/forced vital capacity ratio.

257 ange in forced vital capacity, a decrease in forced vital capacity remained an independent risk facto

258 Forced expiratory volume in 1 second and forced vital capacity remained unchanged after BEP but i

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

260 ices for assessment of physical fitness were forced vital capacity, resting heart rate, hand grip str

261 o of forced expiratory volume in 1 second to forced vital capacity (rs=-0.72; 95% CI: -0.92, -0.52; P

262 s who could be reviewed after 4 weeks, FEV1, forced vital capacity, S(acin), and S(cond) values showe

263 iratory volume in 1 second normalized to the forced vital capacity (standardized coefficients [betaS]

264 atory volume in 1 s and percentage predicted forced vital capacity than did those consuming the high-

265 Pulmonary function tests (PFTs) included forced vital capacity, total lung capacity, forced expir

266 ntedanib prevent about 50% of the decline in forced vital capacity typically seen in this disease; fu

267 ith forced expiratory volume in 1 second and forced vital capacity using data collected from 1996 to

268 significant improvement from baseline, while forced vital capacity values declined from baseline.

269 ator forced expiratory volume in 0.5 seconds/forced vital capacity values than did boys (mean differe

270 uced forced expiratory volume in 0.5 seconds/forced vital capacity values than did girls of equivalen

271 o of forced expiratory volume in 1 second to forced vital capacity was -0.75 (95% confidence interval

272 flow between the 25th and 75th percentile of forced vital capacity was also inversely associated with

273 lationship between maximal motor ability and forced vital capacity was highly significant (P < 0.0001

274 iffusing capacity for carbon monoxide or the forced vital capacity was increased > or = 10%, worse if

275 with usual interstitial pneumonia, change in forced vital capacity was the best physiologic predictor

276 (>/=200 mL and >/=12% increase in FEV(1) or forced vital capacity) was present in 20 (9.0%) particip

277 ), forced expiratory volume in 1 second, and forced vital capacity were performed systematically befo

278 Age at diagnosis and most recent forced vital capacity were significant predictors of mor

279 ume in 1 second) and 23% improvement in FVC (forced vital capacity) were seen after lung volume reduc

280 tional hazards models were used for FEV1 and forced vital capacity, with gender-specific lung functio

281 uiring a chest tube, P = .006) and FEV1/FVC (forced vital capacity) (x100) (45% vs 66%, P = .001).