ライフサイエンスコーパス: expiratory

1 Its expiratory activity seems to preserve lung volume and to

2 expiratory/inspiratory ratio, a CT marker of expiratory air trapping (R = 0.77, P < .0001 for ADCs at

3 ables, such as inspiratory airway dimension, expiratory air trapping, and registration-based lung def

4 hange and changes in airway dynamics impairs expiratory airflow and leads to progressive air trapping

5 produced active expiration and reduced early expiratory airflow but only during wake.

6 Expiratory airflow was measured at 8 years of age, and v

7 00 mm Hg with at least 8 cm H2O positive end-expiratory airway pressure (PEEP), and bilateral infiltr

8 Lung volume was decreased by lowering end-expiratory airway pressure in a stepwise manner.

9 iguus motor pools located at positions where expiratory and laryngeal motor neurons reside.

10 nterneurons onto which both central efferent expiratory and locomotor drives converge, presumably fac

11 aled the ratio of the difference between end-expiratory and minimum-inspiratory diameter over the end

12 than 50% of luminal area during exhalation (expiratory central airway collapse [ECAC]) is associated

13 ragmatic contraction delayed and reduced the expiratory collapse and increased lung aeration compared

14 8,034 subjects with complete inspiratory and expiratory computed tomographic data participating in th

15 We analyzed paired inspiratory-expiratory computed tomography images at baseline of 680

16 Analysis of paired inspiratory-expiratory computed tomography images from a large multi

17 e, 0.4-0.53) yielding a mean inspiratory and expiratory concentrations of 0.79% (SD, 0.24) and 0.76%

18 The loss of diaphragmatic expiratory contraction during mechanical ventilation and

19 g (PRM), a technique pairing inspiratory and expiratory CT images to define emphysema (PRM(emph)) and

20 ponse mapping analysis of paired inspiratory/expiratory CTs to identify functional small airway abnor

21 spiratory interneurons, including seven BotC expiratory-decrementing and 11 preBotC preinspiratory ne

22 nd minimum-inspiratory diameter over the end-expiratory diameter.

23 We hypothesized the occurrence of an expiratory diaphragmatic contraction directed at stabili

24 Whether there is an expiratory diaphragmatic contraction that preserves lung

25 they are both mute and unable to produce the expiratory drive required for vocalization.

26 = .03) and airway obstruction: 50% of forced expiratory flow (abeta coefficient, -0.13 L/s; 95% CI, -

27 dilator FEV1, FVC, FEV1/FVC, and maximum mid-expiratory flow (MMEF).

28 ished a series of diary events based on peak expiratory flow (P), reliever use (R), symptoms (S), awa

29 The difference in peak expiratory flow (PEF) (DeltaPEF, l/min) after 16 weeks o

30 To determine if fluctuations in peak expiratory flow (PEF) are predictive of subsequent treat

31 data included PAQLQ (primary outcome), peak expiratory flow (PEF) monitoring, diurnal peak flow vari

32 fied the smallest set of questions plus peak expiratory flow (PEF) with optimal sensitivity (SN) and

33 y worsening of respiratory symptoms and peak expiratory flow (PEF), and when stable underwent spirome

34 ith reduced MEF240% (i.e., the ratio of Mean Expiratory Flow after 240s of hypertonic saline inhalati

35 chodilator FEV1 and prebronchodilator forced expiratory flow at 25% to 75% of forced vital capacity.

36 lung function as measured by average maximal expiratory flow at functional residual capacity during i

37 EV1, forced vital capacity [FVC], and forced expiratory flow between 25% and 75% [FEF25-75]) and frac

38 Percent predicted forced expiratory flow between the 25th and 75th percentile of

39 dance with non-level A recommendations (peak expiratory flow measurement and timeliness) decreased at

40 essure, which increased the ratio of the end-expiratory flow rate (EEFR) to the peak expiratory flow

41 end-expiratory flow rate (EEFR) to the peak expiratory flow rate (PEFR; from 10% to 25% to 50% to 75

42 pacity ratio (percent predicted), and forced expiratory flow rate from 25% to 75% of expired volume (

43 Sex and peak expiratory flow rate were associated with retinal thickn

44 surgery, ocular perfusion pressure, and peak expiratory flow rate were associated with retinal thickn

45 ine treatment in the newborn period improves expiratory flow rates in midchildhood, which seems to be

46 Hospital in Melbourne at 11 years of age had expiratory flow rates measured according to the standard

47 Peak expiratory flow significantly improved to a similar degr

48 ide [FeNO] >/=35 parts per billion, and peak expiratory flow variability >20%).

49 bility, and FeNO at follow-up; data for peak expiratory flow variability were not available.

50 was associated with increased FEV240 (Forced Expiratory Flow Volume after 240s of hypertonic saline i

51 ctivity-symptom diary and measured PEF (peak expiratory flow) using peak flow meters.

52 ed expiratory volume in 1 s and morning peak expiratory flow), Asthma Control Questionnaire (ACQ-5),

53 capacity) and lesser flows (FEV1 and forced expiratory flow, midexpiratory phase), and with indicato

54 smokers, and lung function test (Maximum Mid-Expiratory Flow, MMEF25-75%), AFP and CEA for never smok

55 A total of 142 children had expiratory flows measured.

56 Expiratory flows were better in the caffeine group, by a

57 By matching inspiratory and expiratory images voxel by voxel using image registratio

58 trapping measured based on mean lung density expiratory/inspiratory ratio was significantly increased

59 rrelated strongly with the mean lung density expiratory/inspiratory ratio, a CT marker of expiratory

60 per lobe from the change in inspiratory and expiratory lobar volumes.

61 al airways and preventing or reducing cyclic expiratory lung collapse.

62 c compliance, tidal impedance variation, end-expiratory lung impedance, and their respective regional

63 ceded by a recruitment maneuver restored end-expiratory lung volume (30.4 +/- 9.1 mL/kg ideal body we

64 d and predicted on the basis of expected end-expiratory lung volume and static compliance of the resp

65 uring expiration increased by decreasing end-expiratory lung volume during spontaneous breathing.

66 sity and four complex traits: height, forced expiratory lung volume in one second, general cognitive

67 H (P = 0.27 and P = 0.23, respectively); end-expiratory lung volume increased (P < 0.001), and tidal

68 During the recruitment procedure, end-expiratory lung volume measured by respiratory inductive

69 enation improved (p < 0.001 vs no-Sigh), end-expiratory lung volume of nondependent and dependent reg

70 End-expiratory lung volume progressively increased during th

71 inspiratory effort, minute ventilation, end-expiratory lung volume, dynamic compliance, and ventilat

72 -expiratory pressure titration increased end-expiratory lung volumes (Delta11 +/- 7 mL/kg; p < 0.01)

73 ry pressure were effective at increasing end-expiratory lung volumes while decreasing end-inspiratory

74 mulation, the activity of both thoracolumbar expiratory motoneurons and interneurons is rhythmically

75 evealed that this locomotor-related drive to expiratory motoneurons is solely dependent on propriospi

76 -free survival and Tw Pdi and maximal static expiratory mouth pressure for absolute survival.

77 c pressure (Tw Pdi), age, and maximal static expiratory mouth pressure were significant predictors of

78 vity, whereas patients with COPD had greater expiratory muscle activity.

79 n motor neurons that innervate laryngeal and expiratory muscles, but the brain center that coordinate

80 t2a with particular reference to glycinergic/expiratory neurons in the Botzinger Complex (BotC) and N

81 tions generated by brainstem inspiratory and expiratory neurons.

82 onsiveness with similar reliability than end-expiratory occlusion alone but with a higher threshold,

83 f echocardiography than that obtained by end-expiratory occlusion alone.

84 15-second end-inspiratory occlusion and end-expiratory occlusion and after fluid administration.

85 A 15-second end-expiratory occlusion and end-inspiratory occlusion, sepa

86 onsecutive end-inspiratory occlusion and end-expiratory occlusion change velocity-time integral is gr

87 End-expiratory occlusion increased velocity-time integral mo

88 veness is predicted by the effects of an end-expiratory occlusion on the velocity-time integral of th

89 f an end-inspiratory occlusion and of an end-expiratory occlusion on velocity-time integral can predi

90 variation, central venous pressure, and end-expiratory occlusion test obtained during tidal volume 6

91 The end-expiratory occlusion test was performed at tidal volumes

92 luid responsiveness was predicted by the end-expiratory occlusion-induced change in velocity-time int

93 e difference between end-inspiratory and end-expiratory pauses.

94 1 preBotC neurons influences the inspiratory-expiratory phase transition during respiratory rhythmoge

95 ic mechanisms also contribute to inspiratory-expiratory phase transition is unknown.

96 s respiration, in particular the inspiratory/expiratory phase transition.

97 hort-term synaptic depression in inspiratory-expiratory phase transition.

98 thout altering inspiratory duration, whereas expiratory-phase photoinhibition shortened the latency u

99 prematurely terminated inspiration, whereas expiratory-phase photostimulation delayed the onset of t

100 irway pressure of 24 (IQR, 22-26) cm H2O, an expiratory positive airway pressure of 4 (IQR, 4-5) cm H

101 olled inspiratory pressure support on top of expiratory positive airway pressure.

102 .045) despite of using a higher positive end-expiratory pressure (17.4 +/- 0.7 vs 9.5 +/- 2.4 cm H2O;

103 tes) and conditional for higher positive end-expiratory pressure (moderate confidence in effect estim

104 pendent regions with decreasing positive end-expiratory pressure (p < 0.001) and suggest that overdis

105 mL/kg and progressively higher positive end-expiratory pressure (PEEP) (5, 10, 16, 20, and 24 cm H2O

106 study, we examined whether (1) positive end-expiratory pressure (PEEP) has a protective effect on th

107 Positive end-expiratory pressure (PEEP) has been used during mechanic

108 tidal volume or high levels of positive end-expiratory pressure (PEEP) improve outcomes for patients

109 RATIONALE: Optimal positive end-expiratory pressure (PEEP) is unknown in patients with s

110 ts of recruitment maneuvers and positive end-expiratory pressure (PEEP) titration on clinical outcome

111 nd pressure support of 10 above positive end-expiratory pressure 5 cm H2O, as well as 5 and 60 minute

112 predicted bodyweight [PBW], and positive end-expiratory pressure [PEEP] expressed as cm H2O), develop

113 itment maneuver and decremental positive end-expiratory pressure and corresponded to a positive (2.1

114 echanical ventilation using low positive end-expiratory pressure and high inspiratory pressures.

115 These motor neurons control expiratory pressure and laryngeal tension, respectively,

116 ion applying the optimum global positive end-expiratory pressure and the optimum-selective positive e

117 mal mice in respiration without positive end expiratory pressure as 58 +/- 14 (mean +/- s.d.) mum on

118 Commonly used positive end-expiratory pressure by clinicians is inadequate for opti

119 reported that high Vt with zero positive end-expiratory pressure caused overwhelming lung injury, sub

120 To test whether positive end-expiratory pressure consistent with an open lung approac

121 In this experimental setting, positive end-expiratory pressure consistent with the open lung approa

122 The positive end-expiratory pressure corresponding to maximum dynamic com

123 End expiratory pressure dependent changes in airway caliber

124 nal hypertension and changes in positive end-expiratory pressure during different models of lung path

125 ve Frecruited values of zero at positive end-expiratory pressure greater than or equal to 3 cm H2O.

126 Tidal volume and positive end-expiratory pressure had no impact on mortality.

127 The two methods of evaluating positive end-expiratory pressure identified similar optimal positive

128 cruitment maneuver, and at best positive end-expiratory pressure identified through a best decrementa

129 nd-expiratory pressure, at best positive end-expiratory pressure identified through esophageal pressu

130 f randomized clinical trials of positive end-expiratory pressure in ARDS that support this hypothesis

131 The approach to applying positive end-expiratory pressure in morbidly obese patients is not we

132 nce tomography-derived maps and positive end-expiratory pressure indicate that, expectedly, tidal rec

133 ateau pressure and the level of positive end-expiratory pressure is not known.

134 lung recruitment identified the positive end-expiratory pressure level (17.4 +/- 2.1 cm H2O) needed t

135 The positive end-expiratory pressure level resulting in highest complianc

136 sure identified similar optimal positive end-expiratory pressure levels (20.7 +/- 4.0 vs 21.3 +/- 3.8

137 short-time scales in all tested positive end-expiratory pressure levels and despite stable pressure c

138 n multivariate analysis, higher positive end-expiratory pressure levels during the first 3 days of ex

139 Even for positive end-expiratory pressure levels minimizing global elastance a

140 The positive end-expiratory pressure levels set by the clinicians (11.6 +

141 Thereafter, three positive end-expiratory pressure levels were applied in a random orde

142 gh FiO2 concentration, and high positive end-expiratory pressure levels.

143 me severity at standardized low positive end-expiratory pressure may improve the association between

144 possible VAP with daily minimum positive end-expiratory pressure of </=5 cm H2O and fraction of inspi

145 chanical ventilation, with mean positive end-expiratory pressure of 14 cm H2O at the onset of critica

146 6 were placed on FIO2 of 0.50, positive end-expiratory pressure of 5 cm H2O, and pressure support.

147 ry pressure with optimum global positive end-expiratory pressure on regional collapse and aeration di

148 Ventilation at lowest elastance positive end-expiratory pressure preceded by a recruitment maneuver r

149 1 kg/m), 21.7 +/- 3.7 cm H2O of positive end-expiratory pressure resulted in the lowest elastance of

150 proximately 3 mL/kg and 1) high positive end-expiratory pressure set above the level where dynamic co

151 s were obtained at the baseline positive end-expiratory pressure set by the clinicians, at zero posit

152 s compared with higher or lower positive end-expiratory pressure settings.

153 animals underwent a decremental positive end-expiratory pressure titration (steps of 2 cm H2O startin

154 both trials were done utilizing positive end-expiratory pressure titration and recruitment maneuvers

155 End-expiratory pressure titration increased end-expiratory l

156 A recruitment maneuver followed by end-expiratory pressure titration was found to significantly

157 e trial (volutrauma); or 2) low positive end-expiratory pressure to achieve driving pressure comparab

158 e increased more than 5% during positive end-expiratory pressure trial (volutrauma); or 2) low positi

159 compliance during a decremental positive end-expiratory pressure trial after lung recruitment was det

160 y the benefits of a decremental positive end-expiratory pressure trial preceded by a recruitment mane

161 A decremental positive end-expiratory pressure trial preceded by a recruitment mane

162 t of atelectasis, a decremental positive end-expiratory pressure trial preceded by lung recruitment i

163 ung recruitment and decremental positive end-expiratory pressure trial, animals were randomly assigne

164 fied through a best decremental positive end-expiratory pressure trial.

165 pplication of optimum-selective positive end-expiratory pressure values for the dependent and nondepe

166 titration of optimum-selective positive end-expiratory pressure values for the dependent and the non

167 ment maneuvers and titration of positive end-expiratory pressure were both necessary to improve lung

168 maneuvers followed by titrated positive end-expiratory pressure were effective at increasing end-exp

169 ung recruitability and clinical positive end-expiratory pressure were higher than in patients who rem

170 y distress syndrome at clinical positive end-expiratory pressure were reclassified to either moderate

171 he effects of optimum-selective positive end-expiratory pressure with optimum global positive end-exp

172 efined globally (optimum global positive end-expiratory pressure) and for each individual lung (optim

173 y, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (oblitera

174 ressure (plateau pressure minus positive end-expiratory pressure) has been suggested as the major det

175 eau pressure, tidal volume, and positive end-expiratory pressure) on ICU mortality using multivariabl

176 ividual lung (optimum-selective positive end-expiratory pressure).

177 linical, 5 cm H2O, or 15 cm H2O positive end-expiratory pressure).

178 lume, 2) appropriate setting of positive end-expiratory pressure, 3) oxygen weaning, and 4) head-of-b

179 ure support level, 5-15 cm H2O; positive end-expiratory pressure, 5-10 cm H2O; fraction of inspired o

180 set by the clinicians, at zero positive end-expiratory pressure, at best positive end-expiratory pre

181 ics (peak inspiratory pressure, positive end-expiratory pressure, DeltaP [PIP minus PEEP], tidal volu

182 urs, peak inspiratory pressure, positive end-expiratory pressure, DeltaP were higher, and Cdyn and Pa

183 Peak inspiratory pressure, positive end-expiratory pressure, DeltaP, tidal volume, Cdyn, and PaO

184 struction, higher preextubation positive end-expiratory pressure, higher postextubation pressure rate

185 d on quantiles of tidal volume, positive end-expiratory pressure, plateau pressure, and driving press

186 who recruit lung in response to positive end-expiratory pressure, recruitment maneuvers, and prone po

187 0.01 for all) in tidal volume, positive end-expiratory pressure, respiratory rate, oxygen administra

188 volume, or plateau pressure and positive end-expiratory pressure, V(RM) remained independently associ

189 ived maps were computed at each positive end-expiratory pressure-titration step, and whole-lung CT ta

190 s with differential response to positive end-expiratory pressure.

191 ssure and the optimum-selective positive end-expiratory pressure.

192 linical, 5 cm H2O, or 15 cm H2O positive end-expiratory pressure.

193 g pressures, and high levels of positive end-expiratory pressure.

194 luated two methods of titrating positive end-expiratory pressure; both trials were done utilizing pos

195 hyperaerated regions at higher positive end-expiratory pressures (r >/= 0.72; p < 0.003).

196 ith nonaerated regions at lower positive end-expiratory pressures and with hyperaerated regions at hi

197 s compared with higher or lower positive end-expiratory pressures in experimental acute respiratory d

198 increases both at high and low positive end-expiratory pressures in nondependent regions (p < 0.027)

199 ses in respiratory rate, higher positive end-expiratory pressures in patients who recruit lung in res

200 The use of higher positive end-expiratory pressures in the open lung approach strategy

201 ontrast synchrotron imaging, at positive end-expiratory pressures of 12, 9, 6, 3, and 0 cm H2O before

202 iratory activity, and when present, reducing expiratory-related abdominal activity.

203 ila allatostatin receptors, for the enhanced expiratory-related oscillations in sympathetic activity

204 t they are not involved in the enhanced late-expiratory-related sympathetic activity triggered by act

205 ast, hypercapnia or hypoxia-induced enhanced expiratory-related sympathetic oscillations were unaffec

206 alities (inspiratory scans) and trapped air (expiratory scans).

207 The expiratory time constants of regional airflows in the se

208 with low strain rates had an inspiratory-to-expiratory time ratio of 1:2-1:3.

209 h strain rates had much lower inspiratory-to-expiratory time ratios (down to 1:9).

210 derecruitment occurred when the positive end-expiratory transpulmonary pressure decreased below 2-4 c

211 onded to a positive (2.1 +/- 2.2 cm H2O) end-expiratory transpulmonary pressure.

212 airflow limitation (ratio of FEV1 to forced expiratory volume [FEV1/FVC] less than 70% plus FEV1 % p

213 orced vital capacity (FVC) ratio, and forced expiratory volume after exhaling 75% of vital capacity (

214 and lung parameters such as decreased forced expiratory volume and increased residual volume compared

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

216 The neonatal forced expiratory volume at 0.5 seconds was inversely associate

217 re is a fall in total lung volume and forced expiratory volume at 100 ms.

218 Girls had higher prebronchodilator forced expiratory volume in 0.5 seconds/forced vital capacity v

219 as change from baseline at week 12 in forced expiratory volume in 1 s (FEV1 in L) in patients with ba

220 were on-treatment rate of decline in forced expiratory volume in 1 s (FEV1) and a composite of cardi

221 tive Aging Study whose lung function [forced expiratory volume in 1 s (FEV1) and forced vital capacit

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

223 ary endpoints were pre-bronchodilator forced expiratory volume in 1 s (FEV1) and total asthma symptom

224 dary endpoints were prebronchodilator forced expiratory volume in 1 s (FEV1) and total asthma symptom

225 per lobe-predominant emphysema with a forced expiratory volume in 1 s (FEV1) between 20% and 45%, sub

226 0 years and had a post-bronchodilator forced expiratory volume in 1 s (FEV1) between 50% and 70% of t

227 , from the middle and extremes of the forced expiratory volume in 1 s (FEV1) distribution among heavy

228 ugh documents have traditionally used forced expiratory volume in 1 s (FEV1) for staging, clinical pa

229 ssociated with accelerated decline in forced expiratory volume in 1 s (FEV1) in patients with chronic

230 ly assigned (1:1) adults with COPD, a forced expiratory volume in 1 s (FEV1) less than 50% predicted,

231 of cystic fibrosis, percent predicted forced expiratory volume in 1 s (FEV1) of 70 or more, and lung

232 a postbronchodilator reversibility in forced expiratory volume in 1 s (FEV1) of at least 12% at scree

233 structive pulmonary disease who had a forced expiratory volume in 1 s (FEV1) of less than 50% predict

234 atients had COPD, post-bronchodilator forced expiratory volume in 1 s (FEV1) of less than 50%, at lea

235 nts with COPD had post-bronchodilator forced expiratory volume in 1 s (FEV1) of lower than 50%, one o

236 ed asthma and a postbronchodilatatory forced expiratory volume in 1 s (FEV1) to forced vital capacity

237 p by questionnaires until age 5, when forced expiratory volume in 1 s (FEV1) was measured by spiromet

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

239 usted for sex, body-mass index (BMI), forced expiratory volume in 1 s (FEV1), and PA:A greater than 1

240 endpoints included prebronchodilator forced expiratory volume in 1 s (FEV1), Asthma Control Question

241 we studied genome-wide association of forced expiratory volume in 1 s (FEV1), forced vital capacity (

242 nctional volumes were correlated with forced expiratory volume in 1 s (FEV1), forced vital capacity (

243 monary function levels, including the forced expiratory volume in 1 s (FEV1), in general population s

244 year (defined as post-bronchodilator forced expiratory volume in 1 s [FEV1] to forced vital capacity

245 ction measures sequentially (ratio of forced expiratory volume in 1 s [FEV1] to forced vital capacity

246 ther outcomes included lung function (forced expiratory volume in 1 s and morning peak expiratory flo

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

248 FVC (forced vital capacity) and FEV1 (forced expiratory volume in 1 s) of 0.03 L [95% confidence inte

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

250 was the only measure associated with forced expiratory volume in 1 sec (FEV1) decline, with each 10-

251 function [average reduction in FEV1 (forced expiratory volume in 1 sec) for a 10% increase in CO was

252 forced vital capacity % predicted and forced expiratory volume in 1 second % predicted (P < 0.05).

253 4.0 percentage points lower predicted forced expiratory volume in 1 second (95% CI, -6.6 to -1.5; P =

254 , r = -0.8; 95% CI: -0.94, 0.42), and forced expiratory volume in 1 second (airway obstruction, r = 0

255 ine in lung function measurements for forced expiratory volume in 1 second (FEV1) (388 mL), forced vi

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

257 of age, measured as the increases in forced expiratory volume in 1 second (FEV1) and forced vital ca

258 change in the percentage of predicted forced expiratory volume in 1 second (FEV1) from the baseline v

259 e study was to compare the changes in forced expiratory volume in 1 second (FEV1) of omalizumab respo

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

261 ge in the percentage of the predicted forced expiratory volume in 1 second (FEV1) through week 24 (ca

262 ry disease (COPD) requires a ratio of forced expiratory volume in 1 second (FEV1) to forced vital cap

263 derately correlated with the ratio of forced expiratory volume in 1 second (FEV1) to forced vital cap

264 ion by spirometry, using the ratio of forced expiratory volume in 1 second (FEV1) to forced volume ca

265 < .0001) with percentage predicted of forced expiratory volume in 1 second (FEV1) was observed; corre

266 mittent culture positivity and higher forced expiratory volume in 1 second (FEV1) were most likely to

267 of either benralizumab regimen on the forced expiratory volume in 1 second (FEV1), as compared with p

268 changes from baseline to 6 months in forced expiratory volume in 1 second (FEV1), forced vital capac

269 ecline on the basis of graphs showing forced expiratory volume in 1 second (FEV1), representing spiro

270 w-frequency reactance area (ALX), and forced expiratory volume in 1 second (FEV1).

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

272 correlation (P < .01) with changes in forced expiratory volume in 1 second (r = 0.70), forced vital c

273 asthma hospitalization in prior year, forced expiratory volume in 1 second [FEV1 ; FEV1 <65% vs >/=65

274 ry of lung cancer, and lung function (forced expiratory volume in 1 second [FEV1]).

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

276 Forced expiratory volume in 1 second and forced vital capacity

277 The prebronchodilator forced expiratory volume in 1 second at week 52 was higher in a

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

279 The decline in forced expiratory volume in 1 second during the reference perio

280 that predicted PRM gas trapping, the forced expiratory volume in 1 second normalized to the forced v

281 ence in the z scores for the ratio of forced expiratory volume in 1 second to forced vital capacity w

282 the lungs for carbon monoxide (DLCO), forced expiratory volume in 1 second, and forced vital capacity

283 re use and lung function, measured by forced expiratory volume in 1 second.

284 mated glomerular filtration rate, and forced expiratory volume in 1 second.

285 ing day was associated with a reduced forced expiratory volume in 8-yr-olds; -32.4 ml; 95% CI: -50.6

286 kUA /L) (n = 418) and lung function [forced expiratory volume in one second (FEV1 ) and forced vital

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

288 ults from a standard spirometry test, forced expiratory volume in one-second percent (FEV1 %), and qu

289 primary outcome measure was change in forced expiratory volume in the first second (FEV1) at 24 weeks

290 Questionnaire (MCID, 4) and change in forced expiratory volume in the first second (FEV1; MCID, 10%).

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

292 I of 21.6 [IQR, 18.2-26.1], mean [SD] forced expiratory volume in the first second of expiration of 0

293 I, 0.03 L to infinity) (P = .002) for forced expiratory volume in the first second, +21 m (95% CI, -4

294 for age, sex, race, body mass index, forced expiratory volume in the first second, pack-years of smo

295 ensity lipoprotein (HDL) cholesterol, forced expiratory volume, grip strength, HbA1c, longevity, obes

296 secondary outcomes included change in forced expiratory volume, Mini Asthma Quality of Life Questionn

297 Lower forced expiratory volume, PA:A>1, and hyperinflation correlated

298 s been previously associated with the forced expiratory volume/forced vital capacity ratio.

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

300 defined by episodic shortness of breath with expiratory wheezing and cough, is a serious health conce