ライフサイエンスコーパス: expiratory

1 respiratory rate, 40; FIO2, 0.6; inspiratory:expiratory, 1:2; and positive end-expiratory pressure, 3

2 rticles by healthy humans performing various expiratory activities while wearing different types of m

3 ion and regulates the formation of abdominal expiratory activity during active expiration.

4 but interacting populations for controlling expiratory activity during hypoxia.

5 Its expiratory activity seems to preserve lung volume and to

6 he BotC caused opposing effects on abdominal expiratory activity, suggesting complex inhibitory circu

7 se (COPD), but studies on the progression of expiratory air trapping in smokers are scarce.

8 red the CT extent of mosaic attenuation, end-expiratory air trapping, and tracheal shape.

9 We aimed to compare maximal expiratory airflow in these individuals during late adol

10 d chronic pulmonary disease, moderate-severe expiratory airflow limitation and radiologically determi

11 is characterized by incompletely reversible expiratory airflow limitation.

12 Maximal expiratory airflow peaks early in the third decade of li

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

14 PET/ex (a method that calculates a range of expiratory amplitudes from the lowest one to the highest

15 tances preserves the positive effects of the expiratory brake while minimizing expiratory diaphragmat

16 Subjects underwent inspiratory and expiratory chest CT and spirometry at baseline and 5-yea

17 8,034 subjects with complete inspiratory and expiratory computed tomographic data participating in th

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

19 ires, spirometry, volumetric inspiratory and expiratory computed tomography, and longitudinal follow-

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

21 The loss of diaphragmatic expiratory contraction during mechanical ventilation and

22 The inspiratory and end-expiratory cross-sectional areas of the trachea were mea

23 d at baseline, quantitative inspiratory, and expiratory CT and at 5 years.

24 was quantified by using mean lung density at expiratory CT and CT-measured functional residual capaci

25 volume with attenuation less than -856 HU at expiratory CT as a measure of air trapping.

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

27 EF(50) and FEF(25-75) obtained from the same expiratory curves were prespecified secondary outcomes.

28 During spontaneous breathing, expiratory diaphragmatic contraction counteracts tidal-E

29 er external expiratory resistances 1) affect expiratory diaphragmatic contraction during spontaneous

30 cts of the expiratory brake while minimizing expiratory diaphragmatic contraction.

31 We analyzed expiratory diaphragmatic electric activity and respirato

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

33 However, although associated with reduced expiratory duration and increased respiratory frequency,

34 of coughing and sneezing, which are dramatic expiratory events that yield both easily visible droplet

35 e anaerobic threshold (0.28 L/min), the peak expiratory flow (11%), and the extensor muscle exercise

36 lag 2) were associated with lower mid-forced expiratory flow (FEF(25%-75%) ) and FEV(1) /FVC ratio (C

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

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

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

40 interval [CI]: -0.92, -0.28; P < .001), mean expiratory flow 25% (r = 0.78; 95% CI: -0.95, -0.39; P <

41 -0.03 [-0.06 to -0.00]) but not with forced expiratory flow after exhaling 75% of FVC or asthma.

42 tion during spontaneous breathing, 2) reduce expiratory flow and make lung compartments more homogene

43 bronchodilator and postbronchodilator forced expiratory flow at 25% to 75% of vital capacity growth w

44 prebronchodilator/postbronchodilator forced expiratory flow at 25% to 75% of vital capacity over 1 y

45 capacity [FVC], FEV(1)/FVC ratio, and forced expiratory flow at 25-75% of FVC [FEF(25-75%)]) were con

46 1)), forced vital capacity (FVC), and forced expiratory flow at 25-75% of the pulmonary volume (FEF(2

47 total expiratory time (tptef/te) and maximal expiratory flow at FRC (VmaxFRC)-have been linked to inc

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

49 the work of breathing (W(b) ) and alleviate expiratory flow limitation (EFL); (ii) through an inspir

50 Rationale: Tidal expiratory flow limitation (tidal-EFL) is not completely

51 atory constraint (i.e. work of breathing and expiratory flow limitation) than their male counterparts

52 Control of the expiratory flow may provide a novel option for lung-prot

53 ith or without a spacer, variability in peak expiratory flow of more than 20% (measured over 7 days),

54 d acrophase were comparable to those of peak expiratory flow or serum cortisol.

55 Studies were eligible if they reported on expiratory flow rates beyond 16 years of age in individu

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

57 s associated with reduced time to peak tidal expiratory flow to expiratory time (beta = -0.004; P = 0

58 particularly vulnerable (time to peak tidal expiratory flow to expiratory time: beta = -0.003, P = 0

59 ng the ratio of the time to reach peak tidal expiratory flow to the total expiratory time (tptef/te)

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

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

62 Individual participant data on expiratory flow variables (FEV(1), forced vital capacity

63 sed during spontaneous breathing by >10%, 2) expiratory flow was reduced and the expiratory time cons

64 Seven of 12 studies reported reduced peak expiratory flow, and 16 of 21 studies reported increased

65 (25% versus 15%), anaerobic threshold, peak expiratory flow, and muscular exercise capacity.

66 ontrolled ventilation", providing a constant expiratory flow, has been suggested as a new lung-protec

67 ) had lower FEV(1)/FVC (P = 0.02) and forced expiratory flow, midexpiratory phase (P = 0.009).

68 and growth rates of FVC, FEV(1), and forced expiratory flow, midexpiratory phase in both sexes (e.g.

69 levels and growth rates of FEV(1) and forced expiratory flow, midexpiratory phase only in boys and lo

70 Area under expiratory flow-volume curve (AEX) has been proposed rec

71 AZD9412 improved lung function (morning peak expiratory flow; mPEF) by 19.7 L/min.

72 emental vitamin C would have improved forced expiratory flows (FEFs) at 3 months of age compared with

73 ion of emphysema, airway wall thickness, and expiratory gas trapping.

74 mutual connections with the pFRG, providing expiratory inhibition during the first stage of expirati

75 GABAergic and glycinergic synapses, provides expiratory inhibition that restrains the expiratory osci

76 rom sequential recruitment of muscles in the expiratory, inspiratory, and postinspiratory (post-I) ph

77 We evaluated the results of paired expiratory/inspiratory computed tomography in a cohort o

78 luate elastic registration of inspiratory-to-expiratory lung MRI for the assessment of pulmonary fibr

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

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

81 m cigarette smoke and forced oscillation and expiratory measurements were recorded.

82 In contrast, shedding of non-expiratory micron-scale particulates from friable cellul

83 t increasing hyperinflation.Conclusions: The expiratory modulation induced by external expiratory res

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

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

86 usion Elastic registration of inspiratory-to-expiratory MRI shows less lung base respiratory deformat

87 eases ventilation through the recruitment of expiratory muscles.

88 f juvenile rats, we recorded the activity of expiratory neurons and performed pharmacological manipul

89 The expiratory neurons of the Botzinger complex (BotC) provi

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

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

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

93 End-expiratory occlusion increased cardiac index estimated b

94 luid responsiveness was predicted by the end-expiratory occlusion induced percent change in cardiac i

95 gnostic threshold is higher than if only end-expiratory occlusion induced percent changes in cardiac

96 successive end-inspiratory occlusion and end-expiratory occlusion maneuvers is greater than 9%, it is

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

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

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

100 15-second end-inspiratory occlusion and end-expiratory occlusion, separated by 1 minute.

101 gated how the BotC neurons interact with the expiratory oscillator located in the parafacial respirat

102 tory pattern requires the recruitment of the expiratory oscillator located on the ventral surface of

103 des expiratory inhibition that restrains the expiratory oscillator under resting condition and regula

104 important source of inhibitory drive to the expiratory oscillator.

105 PPTg projections may simultaneously activate expiratory output from the pFRG, we speculate that choli

106 determination of their efficacy at reducing expiratory particle emission.

107 lish the efficacy of cloth masks at blocking expiratory particles for speech and coughing at varied i

108 s emitted up to two orders of magnitude more expiratory particles via coughing than average.

109 sting conditions and contribute to abdominal expiratory pattern formation during active expiration ob

110 The emergence of this active expiratory pattern requires the recruitment of the expir

111 Respiratory motion and expiratory phase chest CT with the second intervention d

112 Baseline incidence of motion artifacts and expiratory phase scanning in chest CT was 35% (292/826).

113 reduce the frequency of motion artifacts and expiratory phase scanning in chest CT.

114 can reduce frequency of motion artifacts and expiratory phase scanning in chest CT.

115 Presence of motion artifacts and expiratory phase scanning was assessed.

116 piratory, postinspiratory (post-I), and late-expiratory phases.

117 additional criterion for stopping was if end-expiratory pleural pressure was lower than -20 cm H(2)O

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

119 intraoperative higher level of positive end-expiratory positive pressure (PEEP) with alveolar recrui

120 ontomedullary respiratory network, including expiratory premotor neurons in the caudal ventral respir

121 200 mm Hg received helmet NIV (positive end-expiratory pressure >= 10 cm H(2)O, pressure support = 1

122 ml/kg predicted body weight and positive end-expiratory pressure >=8 cm H(2)O.

123 .001), required higher level of positive end-expiratory pressure (15 vs 8 cm H2O in controls; p < 0.0

124 ical tidal volume (7 mL/kg) and positive end-expiratory pressure (9 cm H2O) after inducing acute resp

125 alating/de-escalating (dynamic) positive end-expiratory pressure (DynPEEP; n = 26).

126 ting for Pa(O(2))/Fi(O(2)), and positive end-expiratory pressure (odds ratio, 1.51; P = 0.024) and af

127 All patients received positive end-expiratory pressure (PEEP) at 5 cm H2O.

128 Rationale: Response to positive end-expiratory pressure (PEEP) in acute respiratory distress

129 asive ventilation can use lower positive end-expiratory pressure (PEEP) in critically ill patients wi

130 Adjusting positive end-expiratory pressure (PEEP) to offset pleural pressure mi

131 The median positive end-expiratory pressure (PEEP) was 14 (IQR, 12-16) cm H2O, a

132 .850; p = 0.032) but not higher positive end-expiratory pressure (r = 0.018; p = 0.972).

133 end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H2O, 3) spontaneous breathing

134 end-expiratory pressure = best-positive end-expiratory pressure + 4 cm H2O, 4) spontaneous breathing

135 end-expiratory pressure = best-positive end-expiratory pressure - 4 cm H2O, 2) no spontaneous breath

136 end-expiratory pressure = best-positive end-expiratory pressure - 4 cm H2O.

137 3%; radius, 0.35 +/- 0.08 mm at positive end-expiratory pressure 12) at baseline and five of 32 (15.6

138 47.5 x 47.5 mum voxel size, at positive end-expiratory pressure 12, 9, 6, 3, and 0 cm H2O.

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

140 ng ultrasound were performed at positive end-expiratory pressure 5 cm H2O.

141 kg/m, PaO2/FIO2 147 +/- 42, and positive end-expiratory pressure 9.3 +/- 1.4 cm H2O) were enrolled.

142 ntaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory press

143 ntaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory press

144 ntaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory press

145 ntaneous breathing activity and positive end-expiratory pressure = best-positive end-expiratory press

146 nal inspired oxygen <27 kPa and positive end-expiratory pressure [PEEP] >=8 cm H(2)O) in five univers

147 red oxygen of <150 mm Hg with a positive end-expiratory pressure [PEEP] of >=8 cm of water) to a 48-h

148 three groups: 1) nonprotective (positive end-expiratory pressure [PEEP], 5 cm H(2)O; Vt, 10 ml/kg; re

149 imal lung recruitment, titrated positive end expiratory pressure and further Vt limitation, or contro

150 ompletely avoidable by applying positive end-expiratory pressure and may cause respiratory and hemody

151 data suggest that the "higher" positive end-expiratory pressure approach in patients with severe acu

152 mpared a "lower" and a "higher" positive end-expiratory pressure approach, respectively, according to

153 d lung injury (with low Vt/high positive end-expiratory pressure as the main pillars), in selected po

154 ver design to find the level of positive end-expiratory pressure associated with: 1) positive end-exp

155 with higher compared with lower positive end-expiratory pressure both without spontaneous breathing a

156 ion-perfusion mismatch at lower positive end-expiratory pressure by electrical impedance tomography.

157 l volume, respiratory rate, and positive end-expiratory pressure can guide mechanical ventilation.

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

159 End expiratory pressure dependent changes in airway caliber

160 aily positive fluid balance and positive end-expiratory pressure greater than or equal to 7 cm H2O (a

161 n, absence of bowel sounds, and positive end-expiratory pressure greater than or equal to 7 cm H2O we

162 ared the physiologic effects of positive end-expiratory pressure guided by electrical impedance tomog

163 es exist to select personalized positive end-expiratory pressure in patients affected by the acute re

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

165 Each positive end-expiratory pressure level was maintained for 20 minutes,

166 At each positive end-expiratory pressure level, we assessed arterial blood ga

167 g hyperinflation.Methods: Three positive end-expiratory pressure levels and four external expiratory

168 Personalized positive end-expiratory pressure levels selected by electrical impeda

169 respiratory distress syndrome, positive end-expiratory pressure levels that stabilize dependent lung

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

171 At both positive end-expiratory pressure levels, pulmonary acute respiratory

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

173 recruitment, gas exchange, and positive end-expiratory pressure response.

174 Higher positive end-expiratory pressure resulted in a more homogeneous distr

175 mpedance tomography could guide positive end-expiratory pressure selection based on optimal homogenei

176 stress syndrome network and the positive end-expiratory pressure setting in adults with acute respira

177 ly ventilated patients to guide positive end-expiratory pressure setting, assess the efficacy of trea

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

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

180 omography monitor underwent two positive end-expiratory pressure titration trials by randomized cross

181 avoid volutrauma, together with positive end-expiratory pressure to increase the fraction of open lun

182 VEOLI [Assessment of Low Vt and Elevated End-Expiratory Pressure to Obviate Lung Injury], and FACTT [

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

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

185 We performed a two-step positive end-expiratory pressure trial with change of 10 cm H2O in ra

186 Positive end-expiratory pressure was increased from 9 +/- 3.5 to 17.7

187 ilation with low tidal volumes, positive end-expiratory pressure was set 4 cm H2O above the level to

188 ain viable oxygenation at lower positive end-expiratory pressure was significantly correlated with th

189 Positive end-expiratory pressure was varied between 0 and 20 cm H2O t

190 lungs prone to collapse (at low positive end-expiratory pressure), 1) the expiratory transdiaphragmat

191 regions at end-expiration (best-positive end-expiratory pressure).

192 nspiratory:expiratory, 1:2; and positive end-expiratory pressure, 3 cm H2O) at baseline.

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

194 ould be re-inflated by applying positive end expiratory pressure, although at the expense of decrease

195 tidal cycle (plateau pressure, positive end-expiratory pressure, and their difference [driving press

196 eak airway pressures, intrinsic positive end-expiratory pressure, and use of vasopressors.

197 tricted cubic spline), baseline positive end-expiratory pressure, baseline tidal volume, and hospital

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

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

200 At higher positive end-expiratory pressure, respiratory mechanics did not chang

201 ered ventilation increased with positive end-expiratory pressure, without affecting intrathoracic pre

202 and low pressure 5 cm H2O (low positive end-expiratory pressure-high driving pressure); and 3) high

203 and low pressure 5 cm H2O (low positive end-expiratory pressure-low driving pressure).

204 w pressure 20 cm H2O (very high positive end-expiratory pressure-very low driving pressure); 2) high

205 increasing respiratory rate and positive end-expiratory pressure.

206 ificantly reduced by increasing positive end-expiratory pressure.

207 ce between mechanical power and positive end-expiratory pressure.

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

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

210 y an "atypical" response to the positive end-expiratory pressure.

211 r management included levels of positive end expiratory pressures and timing of introduction of enter

212 apnea, vocal fold adduction, swallowing, and expiratory reflexes.

213 l-EFL.Objectives: To assess whether external expiratory resistances 1) affect expiratory diaphragmati

214 External expiratory resistances optimize lung mechanics and limit

215 he expiratory modulation induced by external expiratory resistances preserves the positive effects of

216 controlled mechanical ventilation, external expiratory resistances reduce tidal-EFL.Objectives: To a

217 expiratory pressure levels and four external expiratory resistances were tested in 10 pigs after lung

218 Results: Consequently to additional external expiratory resistances, and mainly in lungs prone to col

219 mall conducting airways, and the addition of expiratory scans has enabled measurement of small airway

220 limited (three-location) inspiratory and end-expiratory thoracic CT before and after surgery, with co

221 educed time to peak tidal expiratory flow to expiratory time (beta = -0.004; P = 0.01), increased res

222 each peak tidal expiratory flow to the total expiratory time (tptef/te) and maximal expiratory flow a

223 >10%, 2) expiratory flow was reduced and the expiratory time constants became more homogeneous, and 3

224 partments more homogeneous with more similar expiratory time constants, and 3) reduce tidal atelectas

225 rable (time to peak tidal expiratory flow to expiratory time: beta = -0.003, P = 0.05; respiratory ra

226 xtent change (r(s) = 0.46, P = .001) and end-expiratory tracheal shape change (r(s) = 0.40, P = .01).

227 ow positive end-expiratory pressure), 1) the expiratory transdiaphragmatic pressure decreased during

228 ry pressure associated with: 1) positive end-expiratory transpulmonary pressure (PEEPPL) and 2) propo

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

230 The positive end-expiratory transpulmonary pressure strategy aims to coun

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

232 ted participants but similar 1-second forced expiratory volume (FEV1), especially in those with limit

233 All patients completed pre-operative forced expiratory volume capacity (FEV1), diffusing capacity of

234 ients completed tests of preoperative forced expiratory volume capacity in 1 s (FEV1) and diffusing c

235 ls (BDP/FF/G vs BDP/FF) were pre-dose forced expiratory volume in 1 s (FEV(1)) at week 26 and rate of

236 cts of 474 smoking-associated CpGs on forced expiratory volume in 1 s (FEV(1)) in UK Biobank (n = 321

237 and lung function: postbronchodilator forced expiratory volume in 1 s (FEV(1), primary outcome), forc

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

239 sessed by the percentage of predicted forced expiratory volume in 1 s (FEV1%).

240 ease, and with a percentage predicted forced expiratory volume in 1 s (ppFEV(1)) of 40-90%, inclusive

241 ung function (percentage of predicted forced expiratory volume in 1 s [FEV(1)] and frequency of respi

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

243 applied to test the association with forced expiratory volume in 1 s percent predicted values (FEV(1

244 Forced expiratory volume in 1 s/forced vital capacity (FEV(1)/F

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

246 , improved prebronchodilator (pre-BD) forced expiratory volume in 1 second (FEV(1) ) and quality of l

247 h severe persistent disease, can have forced expiratory volume in 1 second (FEV(1) ) values >=100% of

248 HP (3)He MRI VDP were correlated with forced expiratory volume in 1 second (FEV(1)) (model: r = -0.65

249 ments were positively correlated with forced expiratory volume in 1 second (FEV(1)) (r = 0.65, P < .0

250 nship between longitudinal changes in forced expiratory volume in 1 second (FEV(1)) and CT-quantified

251 m baseline in percentage of predicted forced expiratory volume in 1 second (FEV(1)) at week 4.

252 tudinal changes in postbronchodilator forced expiratory volume in 1 second (FEV(1)) reversibility Mat

253 tients was 65.0+/-7.8 years; the mean forced expiratory volume in 1 second (FEV(1)) was 41.1+/-16.3%

254 prognostic scores (Liou and CF-ABLE), forced expiratory volume in 1 second (FEV(1)), and risk of resp

255 of prematurity and birth weight with forced expiratory volume in 1 second (FEV(1)), forced vital cap

256 ruction with lower values of ratio of forced expiratory volume in 1 second (FEV(1))-to-functional vit

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

258 Forced expiratory volume in 1 second (FEV1) and forced vital ca

259 Forced expiratory volume in 1 second (FEV1) values obtained 6 m

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

261 line in lung function, as measured by forced expiratory volume in 1 second (FEV1), forced vital capac

262 Forced expiratory volume in 1 second (FEV1), forced vital capac

263 A priori determined covariates were forced expiratory volume in 1 second and diffusion capacity of

264 er improvement relative to placebo in forced expiratory volume in 1 second at Day 28 (102 mL [95% CI:

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

266 lan-Meier curves showed patients with forced expiratory volume in 1 second decline >=5% and >=10% at

267 requirement >2 L/min at diagnosis and forced expiratory volume in 1 second decline >=5% postinfection

268 Forced expiratory volume in 1 second is an important predictor

269 Forced expiratory volume in 1 second just before ECP was associ

270 associated with a greater decline in forced expiratory volume in 1 second per 10 years (baseline: 13

271 -0.80; P < .001) and correlated with forced expiratory volume in 1 second percentage predicted (r, -

272 T2-weighted VIP were associated with forced expiratory volume in 1 second percentage predicted (rho

273 ay obstruction, defined by a ratio of forced expiratory volume in 1 second to the forced vital capaci

274 interval (CI): -198, -7) mL, and for forced expiratory volume in 1 second was -90 (95% CI: -170, -11

275 Greater effects on forced expiratory volume in 1 second were observed in the high

276 2% for forced vital capacity, 93% for forced expiratory volume in 1 second, 116% for total lung capac

277 nterval [CI], 67-345 mL; P = .004 and forced expiratory volume in 1 second, 143 mL higher; 95% CI, 11

278 Safety, pharmacokinetics, forced expiratory volume in 1 second, asthma control questionna

279 ) correlated with obstruction markers forced expiratory volume in 1 second-to-forced vital capacity r

280 t percentage were correlated with the forced expiratory volume in 1 second.

281 related with the percentage predicted forced expiratory volume in 1 second.

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

283 failure, asthma control days, and the forced expiratory volume in 1 second; a two-sided P value of le

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

285 ) in eight patients with severe COPD (forced expiratory volume in 1s (FEV(1) ) +/- SEM = 0.9 +/- 0.1

286 nd whether the first treatment year's forced expiratory volume in one second (FEV(1) ) predicts the l

287 e Forced Vital Capacity (FVC) and the Forced Expiratory Volume in one second (FEV(1)) can be inferred

288 e found to be associated with similar forced expiratory volume in one second (FEV(1)) measurements.

289 of these six genes and lung function (Forced Expiratory Volume in one second (FEV(1)), Forced Vital C

290 s genetically correlated with reduced forced expiratory volume in one second (FEV(1): r(g) = 0.098, p

291 Forced expiratory volume in one second accounted for less than

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

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

294 values correlated positively with the forced expiratory volume in the first second (FEV(1), %) and fo

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

296 isease (COPD) requires a ratio of the forced expiratory volume in the first second to the forced vita

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

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

299 n dynamic transpulmonary pressure (DeltaPl), expiratory Vt, and respiratory rate were recorded on adm

300 epitation on palpation of the anterior neck, expiratory wheezes, and crackles heard at auscultation o