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1                                              FEV(0.5) and Feno values were significantly associated w
2                                              FEV(1) and MRI ventilation defects, quantified as ventil
3                                              FEV(1) decline in sustained former smokers and current s
4                                              FEV(1) decrease was -25.7 mL/y in the overall population
5                                              FEV(1) was the driver of control-level assignment in 30%
6                                              FEV(1), FVC, fractional exhaled nitric oxide, symptom sc
7 8 [1.18], -0.25 [-0.40 to -0.10], p=0.0012), FEV(1)/FVC ratio (0.14 [1.10] vs -0.64 [1.35], -0.74 [-0
8 < .0001), forced vital capacity (P = .0017), FEV(1) (P = .037), and total lung capacity (P = .013) bu
9 ower post-bronchodilator FEV(1) (P = 0.007), FEV(1)/FVC (P = 0.003), and greater computed tomography-
10       Neither signal associated with FEV(1), FEV(1)/forced vital capacity, atopy, and age of asthma o
11 severe COPD (forced expiratory volume in 1s (FEV(1) ) +/- SEM = 0.9 +/- 0.1 l, 30% of predicted) and
12 expressing the transcription factors NKX2.2, FEV, GATA2 and LMX1B in combination with ASCL1 and NGN2
13 er a median follow-up of 7 years (IQR 3-20), FEV(1) decline at the median age (57 years) was 31.01 mL
14 ] yr; 55% male; body mass index, 24 [21-29]; FEV(1)% predicted, 37 [29-45]; and BODE [body mass index
15                                      Year 30 FEV(1) and FVC were lower in the highest level of TLR5 c
16  the hazard ratios (HR) markedly, e.g. for a FEV(1)/FVC below 0.7 from 1.55 [95% confidence-interval
17 stment, former smokers showed an accelerated FEV(1) decline of 1.82 mL per year (95% CI 1.24-2.40) co
18       Compared to never-smokers, accelerated FEV(1) decline was observed in former smokers for decade
19  eosinophils was associated with accelerated FEV(1) decrease.
20              Minimal overlap was seen across FEV(1) and asthma control day predictors, suggesting dis
21  and models were fit with and without adding FEV(1) as a predictor.
22                   Mepolizumab did not affect FEV(1), FVC, and fractional exhaled nitric oxide, neithe
23       HFEV(1) asthmatics had larger airways (FEV(1) z-scores 1.12 vs -2.37; P < .05), greater lung vo
24 f 0.70 or less after bronchodilators (and an FEV(1) of 70% or less of predicted), and a documented hi
25 th a reduced FEV(1) percent predicted and an FEV(1)-to-forced vital capacity ratio at age 50 years (-
26 ren, whom when clinically stable can have an FEV(1) >100% of predicted, but during an acute bronchosp
27 L], FVC -0.012L [95% CI -0.060 to 0.036] and FEV(1)/FVC ratio -0.0012 [95% CI -0.0072 to 0.0047L]).
28 related with FEV(1) (r = -0.35; P = .04) and FEV(1)/forced vital capacity ratio (r = -0.41; P = .01).
29 9586 = -0.31, placebo = -0.17, P = .058) and FEV(1) (GSK679586 = -0.01, placebo = 0.03, P = .276).
30 walls correlated with FEV(1) (r = -0.60) and FEV(1)/FVC ratio (r = -0.60) (P < .001).
31 d-forced expiratory flow (FEF(25%-75%) ) and FEV(1) /FVC ratio (Coef.
32 body mass index-Z of 0.66 (-2.4 to 1.9), and FEV(1)% predicted of 102 (39-122).
33 R (2) = 0.80; P < .01), but PC(20), age, and FEV(1) did not (R (2) = 0.63; P = .15).
34 strictive and adrenal permissive alleles and FEV(1)PP in patients with (GC) and without (noGC) daily
35 s no association between gene expression and FEV(1)/FVC.
36                                     Feno and FEV(0.5) values returned to baseline levels within 10 da
37 n to influence lung development with FVC and FEV(1)/FVC.
38 nd (FEV(1)), Forced Vital Capacity (FVC) and FEV(1)/FVC).
39 o 3 months after birth, on FEV(1) , FVC, and FEV(1) /FVC ratio at 12 and 18 years.
40 ) were evaluated with PFTs (FEV(1), FVC, and FEV(1)/FVC) in meta-analyses across seven cohorts from t
41  attenuated associations between the GRS and FEV(1)/FVC by 100% and 60% in MESA and SPIROMICS, respec
42 xacerbations, Transition Dyspnoea Index, and FEV(1), with former smokers being more corticosteroid re
43 ations, asthma control, quality of life, and FEV(1) ) at follow-up and the course of FEV(1) between s
44 by the expression of Ascl1, Foxa2, Lmx1b and FEV.
45 hma Quality of Life Questionnaire scores and FEV(1), and number of clinical asthma exacerbations duri
46  binomial model using age, sex, smoking, and FEV(1) % predicted as clinical covariates.
47 e asthma symptoms, rescue albuterol use, and FEV(1) reversal (P < 0.001, 0.03, and 0.03, respectively
48  specific fungal exact sequence variants and FEV(1), fraction of exhaled nitric oxide values, BAL flu
49  more exacerbations in the previous year and FEV(1) percent predicted values, whereas chronic sinusit
50                    Early COPD was defined as FEV(1)/FVC less than the lower limit of normal in indivi
51 t individuals with normal maximally attained FEV(1) had an increased risk of nonmalignant respiratory
52 ine of FEV(1) from normal maximally attained FEV(1) in early adulthood (normal maximally attained FEV
53  developed through normal maximally attained FEV(1) trajectory is associated with an increased risk o
54 n early adulthood (normal maximally attained FEV(1) trajectory) but also through a trajectory with FE
55 l in early adulthood (low maximally attained FEV(1) trajectory).Objectives: To test whether the long-
56 loped COPD through normal maximally attained FEV(1) trajectory, 65 had developed COPD through low max
57 eveloped COPD through low maximally attained FEV(1) trajectory, and 1,026 did not have COPD.Measureme
58 OPD developed through low maximally attained FEV(1) trajectory.
59 with individuals with low maximally attained FEV(1).Conclusions: COPD developed through normal maxima
60          All patients should have a baseline FEV(1) and DL(CO) measured, and predicted postoperative
61 se, C-reactive protein at baseline, baseline FEV(1) percentage of predicted, SGRQ total score, and Ps
62 f boys and two thirds of girls with baseline FEV(1)/FVC ratios of 90% or greater were in remission at
63 ment period, changes from baseline in pre-BD FEV(1) and asthma control (5-item asthma control questio
64                     Across subgroups, pre-BD FEV(1) improved by 0.18-0.22 L/0.19-0.24 L (all P < .05)
65 g (MZ; n = 74) had lower post-bronchodilator FEV(1) (P = 0.007), FEV(1)/FVC (P = 0.003), and greater
66 limitation (defined as a post-bronchodilator FEV(1)/forced vital capacity [FVC] ratio <=0.70) and a s
67 I -0.086 to -0.0009) and post-bronchodilator FEV(1)/FVC ratio (adj.
68  relates to the ratio of post-bronchodilator FEV(1)/FVC, but only among those with atopic sensitizati
69 users were compared with matched controls by FEV(1)% predicted rate of decline and rates of intraveno
70 iratory volume in 1 s/forced vital capacity (FEV(1)/FVC) but not FVC was related to mortality after a
71 he ratio of FEV(1) to forced vital capacity (FEV(1)/FVC: r(g) = 0.137, p = 2.0 x 10(-12)).
72 either alpha-T or gamma-T with mid-childhood FEV(1) or FVC.
73 evel (per 10 muM) had a higher mid-childhood FEV(1) percent predicted (beta = 3.09; 95% CI = 0.58-5.5
74 d with lung function parameters in children (FEV(1) FVC(%pred) and FEF(25-75%pred) ), thus lower sEV-
75        Results were independently confirmed: FEV(1)PP for homozygous adrenal restrictive genotype in
76 ; or COPD Assessment Test score, >=10) COPD (FEV(1), 30-60% predicted).
77                       Fifteen men with COPD (FEV(1) = 32.2 +/- 12.0% predicted; FEV(1)/FVC = 31.6 +/-
78 he concentration of methacholine to decrease FEV(1) by 20% (PC(20)) was greater in FEV(1)-irreversibl
79                                 Differential FEV(1) decline was also evaluated according to duration
80 as associated (P = .048) with a differential FEV(1) response favoring LABA over ICS step-up therapy,
81 ginally (P = .053) related to a differential FEV(1) response favoring LTRA over LABA step-up therapy.
82 % of predicted, while others have diminished FEV(1) .
83 fects linear regression was used to estimate FEV(1) and FVC from age 11 to 15 years in 2,120 adolesce
84                  Medications, exacerbations, FEV(1) (76% predicted vs 76% predicted; P = .91), and VD
85 eported ever diagnosed asthma were excluded (FEV(1) -0.011L, [95% CI -0.05 to 0.028L], FVC -0.012L [9
86 zebrafish revealed a role for the ETS factor FEV in endothelial identity downstream of ETV2 (Etsrp in
87  previously implicated in ASD including FEV (FEV transcription factor, ETS family member), which enco
88 ed 55 genes, of which 36 (16 for FVC, 19 for FEV(1)/FVC, and one for both) had not been identified in
89 s for birth weight were stronger in boys for FEV(1) (boys: 0.31 L, 95% confidence interval (CI) 0.24
90 8) and the regression estimates (95% CI) for FEV(1) % predicted varied from 0.6 (-3.5 to 4.6) to -9.9
91 garette consumption, the effect estimate for FEV(1) decline in current smokers consuming less than fi
92 ry preterm or very low birthweight group for FEV(1) (-0.06 [SD 1.03] vs -0.81 [1.33], mean difference
93            Similar results were observed for FEV(1), Transition Dyspnoea Index, and SGRQ total score;
94 ter 4 had a significant lower lung function (FEV(1) , FVC), higher FeNO and higher risk of sensitizat
95    Cleaners overall had lower lung function (FEV(1) , FVC; P < .05).
96 tage in both subtypes correlated with future FEV(1)/FVC decline (r = -0.16 [P < 0.001] in the Tissue-
97  with higher levels and growth rates of FVC, FEV(1), and forced expiratory flow, midexpiratory phase
98 nical and lung function biomarkers (PEF, FVC,FEV(1)), we estimated this loss of adaptive capacity (AC
99 iables (FEV(1), forced vital capacity [FVC], FEV(1)/FVC ratio, and forced expiratory flow at 25-75% o
100 CI], 0.86-4.76%; P = 0.0047), 11.02% greater FEV(1)/FVC decline (95% CI, 4.43-17.62%; P = 0.0011), an
101 sformed albuminuria, there was 2.81% greater FEV(1) decline (95% confidence interval [CI], 0.86-4.76%
102 ange, 38-73 ppb]) with significantly greater FEV(1)% (mean, 88.2 +/- 16.4 vs. 74.1 +/- 20.9; P < 0.01
103                      Mean changes in 4-10 h %FEV(1) were as follows: -21.08 (placebo), -14.30 (VI), -
104 s of inhaled tobramycin and azithromycin had FEV(1)% predicted per-year decline of -0.16 versus nonus
105 d fat mass index were associated with higher FEV(1) (z-score difference [95% confidence interval (CI)
106 egnancy (p=0.030) was associated with higher FEV(1)%.
107 ions in pulmonary exacerbations and improved FEV(1).
108 choline, positive reversibility (a change in FEV(1) >=12% and >=200 mL within 30 min) after treatment
109 dichotomized by postbronchodilator change in FEV(1) at follow-up, and differences between reversible
110                                    Change in FEV(1) over time did not differ significantly across clu
111                       The relative change in FEV(1) was a deterioration of 0.87% predicted value (-2.
112  was used to associate miRNAs with change in FEV(1)% (prebronchodilator FEV(1) as a percent predicted
113 re exacerbations, quality of life, change in FEV(1), 6-min walk distance, mortality, adherence to tre
114 piratory Questionnaire (SGRQ), and change in FEV(1).
115                               The changes in FEV(1) % during the first year predicted the results at
116                 When adjusted for changes in FEV(1), corresponding numbers were -2.2 (95% CI: -3.0, -
117  stages 2-4 were accounted for by changes in FEV(1).
118 he early allergic response (21.4% decline in FEV(1) area under the curve, P = 0.03).
119 th lower lung function and faster decline in FEV(1) over 10 years, in a threshold manner, providing n
120 e (mean +/- SD, 23.7% +/- 13.2%) decrease in FEV(1) and an increase in sputum eosinophil counts 24 ho
121 hood was associated with large decrements in FEV(1) among participants with a mean age of 66 years (-
122 fectiveness outcomes included: difference in FEV(1) responder rates, target lobe volume reduction, hy
123                           A relative drop in FEV(1) >=10% in chronic obstructive pulmonary disease (C
124 s (HR 2.1; CI 1.1-3.9), and relative drop in FEV(1) >=30% over 12 months (HR 1.7; CI 1.0-2.8) increas
125 crease FEV(1) by 20% (PC(20)) was greater in FEV(1)-irreversible participants at follow-up (P = .01).
126 associated with a significant improvement in FEV(1) (67 mL at 1 year, -22 to 112; p=0.14).
127 uced by 30%, we estimated a 4.4% increase in FEV(1) growth (95% CI, 2.8-5.9) and a 7.1% increase in F
128  0.58 L (95% CI -0.80 to -0.37), increase in FEV(1) of 15.87% (95% CI 12.27 to 19.47), improvement in
129 st 7 days was associated with a reduction in FEV(1) (-15.5 mL; 95% CI: -27.6, -3.3 per doubling of po
130 s not previously implicated in ASD including FEV (FEV transcription factor, ETS family member), which
131 nical predictors of exacerbations, including FEV(1)% predicted and history of exacerbations.
132 ted with decreased odds of asthma, increased FEV(1) in children and adults, and increased FVC in adul
133  acculturation was associated with increased FEV(1) compared with low language acculturation (P = .02
134 ities remained at 1994 to 1997 NO(2) levels, FEV(1) and FVC growth were estimated to have been reduce
135                                          Low FEV(1)% predicted and FVC% predicted were also associate
136 erence [95% CI], 0.07 [0.03 to 0.10]), lower FEV(1)/FVC (z-score difference [95% CI], -0.05 [-0.09 to
137 tics without sensitization including a lower FEV(1) /FVC ratio (p < .05).
138     Ever smoking was associated with a lower FEV(1)% predicted (-14.3%; P = 0.0092) and a lower FEV(1
139 % predicted (-14.3%; P = 0.0092) and a lower FEV(1)/FVC ratio (-0.075; P = 0.0041) in SZ-AATD.
140 tibody deficiency, antibiotic allergy, lower FEV(1), radiographic sinus disease severity, nasal polyp
141 qual to 100 cells/muL (P < .0001), and lower FEV(1) (P = .026).
142 reased asthma severity (P = 0.02), and lower FEV(1)/FVC ratio (P = 0.01).
143 ce [95% CI], 0.07 [0.04 to 0.10]), and lower FEV(1)/FVC ratio (z-score difference [95% CI], -0.07 [-0
144 stant asthma, EPA was characterized by lower FEV(1) and a higher prevalence of obesity, hypertension,
145 nd heterozygotes (ZS/ZV(R); n = 7) had lower FEV(1)/FVC (P = 0.02) and forced expiratory flow, midexp
146  the adrenal restrictive genotype have lower FEV(1)PP compared with noGC patients (54.3% vs. 75.1%; P
147  as a whole, atopy was associated with lower FEV(1) (adjusted difference -0.068L, 95% confidence inte
148 o tobacco exposure was associated with lower FEV(1) and FVC compared with those with no in utero toba
149 l in utero tobacco was associated with lower FEV(1) and FVC longitudinally from 6 to 24 years (mean d
150 he first trimester was associated with lower FEV(1)% predicted (-0.826; 95% confidence interval [CI],
151 =0.030) exposures were associated with lower FEV(1)%, and inverse distance to nearest road during pre
152 stnatal exposures were associated with lower FEV(1)%: copper (p=0.041), ethyl-paraben (p=0.029), five
153 o full-term birth) was associated with lower FEV(1)/FVC and FEF(25-75%).
154 y higher female ratio and numerically lower %FEV(1) than the asymptomatic group.
155 ption factor ETS-5, an ortholog of mammalian FEV/Pet1, controls satiety-induced quiescence.
156                                         Mean FEV(1) showed statistically significant improvements bet
157 en (median age 8.1 years, IQR 6.5-9.0), mean FEV(1)% was 98.8% (SD 13.2).
158 duced bronchodilator response (6% vs 9% mean FEV(1) -%-predicted change, P < .05) compared to asthma
159 s, median albuminuria was 5.6 mg/g, and mean FEV(1) decline was 31.5 ml/yr.
160         Sixty-seven patients with COPD (mean FEV(1), 1.05 L [41.6% predicted]; aged 40-80 yr; body ma
161  no statistically significant change in mean FEV(1) % predicted (FEV(1) %) from baseline to the 25-ye
162  efficacy outcome was the difference in mean FEV(1) from baseline to 6 months.
163 0.3 years, 90.5% of patients were male, mean FEV(1) was 49%, 71.6% of patients were treated with ICS,
164 impaired on all spirometric parameters (mean FEV(1) z-score, -1.08 SD [95% confidence interval, -1.40
165 o, the late change (4-10 h) in weighted mean FEV(1) was -0.466 l (-0.589; -0.343) and -0.298 l (-0.41
166  and 196 were randomized (51% female, median FEV(1%) predicted, 36 [interquartile range, 27-48]).
167 ce of GSK2190915 vs. placebo for the minimum FEV(1) EAR was 0.408 L (0.205, 0.611).
168 us adrenal permissive genotype, there was no FEV(1)PP difference in GC vs. noGC patients (73.4% vs. 7
169                                       Normal FEV(1) % at the end of the first year predicted normal F
170 r predicted normal FEV(1) , and below-normal FEV(1) % at 1 year predicted below-normal FEV(1) % at 25
171 al FEV(1) % at 1 year predicted below-normal FEV(1) % at 25 years.
172 ure, the HFEV(1) group could generate normal FEV(1) due to proportionally enlarged airways and reduce
173                    The combination of normal FEV(1)/FVC ratio, airways responsiveness, and serum eosi
174 t the end of the first year predicted normal FEV(1) , and below-normal FEV(1) % at 1 year predicted b
175                      As previously observed, FEV(1) increased after lebrikizumab treatment.
176  ACO was associated with severe obstruction (FEV(1) %, <50; 31.6% of ACO vs 10.9% of COPD alone) and
177  and FEV(1) ) at follow-up and the course of FEV(1) between seven cluster-based asthma phenotypes ide
178 ctory dominated by an accelerated decline of FEV(1) from normal maximally attained FEV(1) in early ad
179                       The 10-year decline of FEV(1) was faster in the highest level of CCR1 as compar
180                                The degree of FEV(1)/forced vital capacity (FVC) ratio impairment was
181          In adult-onset asthma, the level of FEV(1) reached during the first treatment year seems to
182 atory phase only in boys and lower levels of FEV(1)/FVC in both sexes.
183 ciated with lower levels and growth rates of FEV(1) and forced expiratory flow, midexpiratory phase o
184  = 0.098, p = 2.3 x 10(-8)) and the ratio of FEV(1) to forced vital capacity (FEV(1)/FVC: r(g) = 0.13
185  < .001; MRI: r = -0.70, P < .001), ratio of FEV(1) to forced vital capacity (model: r = -0.73, P < .
186 llen exposure up to 3 months after birth, on FEV(1) , FVC, and FEV(1) /FVC ratio at 12 and 18 years.
187    A genome-wide interaction study (GWIS) on FEV(1)/FVC was performed for individuals with FEV(1)/FVC
188 ossible causal effect for DNA methylation on FEV(1) at 18 CpGs (p < 1.2 x 10(-4)).
189 not clearly mediate the effect of smoking on FEV(1), although DNA methylation at some sites might inf
190 ethylation mediates the effect of smoking on FEV(1).
191 ith FEV(1)/FVC, and the effect of smoking on FEV(1)/FVC differs among the associated genotypes.
192 ts interacting with pack-years of smoking on FEV(1)/FVC ratios in individuals with normal lung functi
193 aenoic acid [DHA]) were evaluated with PFTs (FEV(1), FVC, and FEV(1)/FVC) in meta-analyses across sev
194                           Postbronchodilator FEV(1) was also dependent on exacerbations, age of onset
195                         A postbronchodilator FEV(1)-FVC ratio less than 0.70 is required for a diagno
196  in prebronchodilator and postbronchodilator FEV(1) growth were as follows: 107 mL/y (95% CI, 37-177
197        We defined COPD as postbronchodilator FEV(1)/forced vital capacity ratio below the lower limit
198 nd no association between postbronchodilator FEV(1) and annual residential pollutant attributions.
199 were generated to explain postbronchodilator FEV(1) reversibility at follow-up.
200 86 (0.71-1.04) for 30 mg; postbronchodilator FEV(1) of less than 40% had RRs of 0.76 (0.64-0.91) for
201  age, 67 [7.4]; mean [SD] postbronchodilator FEV(1), 65% [21%]; mean [SD] COPD Assessment Test score
202             At follow-up, postbronchodilator FEV(1) was not reversible in six of 11 participants; the
203 hilia was associated with postbronchodilator FEV(1) in asthmatic patients.
204 DL(CO) measured, and predicted postoperative FEV(1) and DL(CO) calculated to assist with risk predict
205                            Prebronchodilator FEV(1) values remained stable between years 1 and 5 afte
206 As with change in FEV(1)% (prebronchodilator FEV(1) as a percent predicted) over the 4-year treatment
207  with greater increases in prebronchodilator FEV(1) and prebronchodilator/postbronchodilator forced e
208 ciated with an increase in prebronchodilator FEV(1) of 131 mL/y (95% CI, 97-166 mL/y).
209 ciated with an increase in prebronchodilator FEV(1) of 238 mL/y (95% CI, 177-299 mL/y), whereas less
210 as associated with reduced prebronchodilator FEV(1)/forced vital capacity (beta coefficient, -0.10; 9
211  mug/g), and the mean (SD) prebronchodilator FEV(1)/forced vital capacity ratio was 80.2% (9.0%).
212 t = 0.50; P = 0.001) independently predicted FEV(1) (R(2) = 0.27; P = 0.003) and, in a separate model
213 status, and baseline percentage of predicted FEV(1) (2.17, 1.33-3.57; p=0.0021), whereas those with n
214 ificantly lower mean percentage of predicted FEV(1) at baseline than did children without small-colon
215 acebo, resulted in a percentage of predicted FEV(1) that was 13.8 points higher at 4 weeks and 14.3 p
216  significantly lower percentage of predicted FEV(1) throughout the study in regression models, both i
217  included adult age group, percent predicted FEV(1) (ppFEV(1)) less than 40%, and numbers of intraven
218 ls had significantly lower percent predicted FEV(1) and weight and height z-scores than the isolated
219 tations (n = 34) had lower percent predicted FEV(1) and weight and height z-scores than those with DN
220 up) and clinical features (percent predicted FEV(1) and weight and height z-scores).
221     For the entire cohort, percent predicted FEV(1) decline was heterogeneous with a mean (SE) declin
222 res showed strong correlation with predicted FEV(1) (R = -0.62 to -0.66, P < .001) and weak to modera
223 gnificant change in mean FEV(1) % predicted (FEV(1) %) from baseline to the 25-year control.
224 ith COPD (FEV(1) = 32.2 +/- 12.0% predicted; FEV(1)/FVC = 31.6 +/- 7.1%; exercise oxygen saturation a
225 pared with the BDP/FF group, week 26 predose FEV(1) improved in the BDP/FF/G group by 57 mL (95% CI 1
226                      Subjects with preserved FEV(1)-to-forced vital capacity ratio and reduced FEV(1)
227 among current and former smokers with PRISm (FEV(1)/FVC >= 0.7 and FEV1 < 80%) in COPDGene was used t
228 hildhood were also associated with a reduced FEV(1) percent predicted and an FEV(1)-to-forced vital c
229 )-to-forced vital capacity ratio and reduced FEV(1) percentage predicted were categorized as having p
230 domization analyses demonstrate that reduced FEV(1) increases squamous cell carcinoma risk (odds rati
231 fidence intervals: 1.21-1.88), while reduced FEV(1)/FVC increases the risk of adenocarcinoma (OR = 1.
232 piratory reasons was associated with reduced FEV(1) and midexpiratory flow at 18 years (interaction b
233  relative to the degree of volume reduction: FEV(1) (r(2)=0.86; p<0.0001), 6MWT (r(2)=0.77; p<0.0001)
234 re pre-dose forced expiratory volume in 1 s (FEV(1)) at week 26 and rate of moderate and severe exace
235 nchodilator forced expiratory volume in 1 s (FEV(1)) in a subset of subjects with uncontrolled asthma
236 ted CpGs on forced expiratory volume in 1 s (FEV(1)) in UK Biobank (n = 321,047) by using two-sample
237  in minimum forced expiratory volume in 1 s (FEV(1)) of -1.091 l (95% CI: -1.344; -0.837) following p
238  a ratio of forced expiratory volume in 1 s (FEV(1)) to forced vital capacity of 0.70 or less after b
239 nchodilator forced expiratory volume in 1 s (FEV(1), primary outcome), forced vital capacity (FVC), a
240 e predicted forced expiratory volume in 1 s (FEV(1)PP).
241 f predicted forced expiratory volume in 1 s [FEV(1)] and frequency of respiratory exacerbations) were
242 ith participants with asthma (-1.61 z scores FEV(1); 95% CI, -1.48 to -1.75) or COPD alone (-0.94 z s
243 uction in forced expiratory volume in 1 sec (FEV(1)) or forced vital capacity (FVC), or both, after a
244 re-BD) forced expiratory volume in 1 second (FEV(1) ) and quality of life measures, and it was genera
245 n have forced expiratory volume in 1 second (FEV(1) ) values >=100% of predicted, while others have d
246 d with forced expiratory volume in 1 second (FEV(1)) (model: r = -0.65, P < .001; MRI: r = -0.70, P <
247 d with forced expiratory volume in 1 second (FEV(1)) (r = 0.65, P < .001), the FEV(1)-to-forced vital
248 ges in forced expiratory volume in 1 second (FEV(1)) and CT-quantified emphysema and air trapping in
249 dicted forced expiratory volume in 1 second (FEV(1)) at week 4.
250 ilator forced expiratory volume in 1 second (FEV(1)) reversibility Materials and Methods Spirometry a
251 e mean forced expiratory volume in 1 second (FEV(1)) was 41.1+/-16.3% of the predicted value.
252 ABLE), forced expiratory volume in 1 second (FEV(1)), and risk of respiratory exacerbations were eval
253 t with forced expiratory volume in 1 second (FEV(1)), forced vital capacity (FVC), and forced expirat
254 tio of forced expiratory volume in 1 second (FEV(1))-to-functional vital capacity (FVC) ratio (-1.7 v
255 orced expiratory volume during first second (FEV(1)) or carbon monoxide diffusing capacity (DL(CO)),
256 orced expiratory volume in the first second (FEV(1), %) and forced vital capacity (FVC, %) values.
257 ar's forced expiratory volume in one second (FEV(1) ) predicts the long-term prognosis.
258  the Forced Expiratory Volume in one second (FEV(1)) can be inferred, and the pulmonologist is able t
259 ilar forced expiratory volume in one second (FEV(1)) measurements.
260 ion (Forced Expiratory Volume in one second (FEV(1)), Forced Vital Capacity (FVC) and FEV(1)/FVC).
261 uced forced expiratory volume in one second (FEV(1): r(g) = 0.098, p = 2.3 x 10(-8)) and the ratio of
262 eas forced expiratory volume at 0.5 seconds (FEV(0.5)) significantly decreased compared with baseline
263                              Cross-sectional FEV(1)% predicted measurements were plotted by age at wh
264 lly relevant improvements in cross-sectional FEV(1)% predicted over a range of ages (6-82 yr).
265 ation used minimization to balance age, sex, FEV(1) % predicted, frailty, transport availability, and
266 fixed effects models adjusting for age, sex, FEV(1), and trial.
267 ssion showed, even after adjustment for sex, FEV(1)% predicted, body mass index (z-score), age at CPE
268  1 second (FEV(1)) (r = 0.65, P < .001), the FEV(1)-to-forced vital capacity ratio (r = 0.81, P < .00
269 n ratio values correlated inversely with the FEV(1) (%) and FVC (%) values.
270 ars (1991-2008) were examined in relation to FEV(1)% predicted and FVC% predicted at ages 8 (n = 5,27
271 gnificantly diminished in the FE trajectory (FEV(1) /FVC, mean [95%CI]: 89.9% [89.3-90.5] vs. 88.1% [
272 ntained throughout the study for both trough FEV(1) and St.
273 I 10 to 70) and 60 mL (20 to 100) for trough FEV(1), -0.01 (-0.68 to 0.66) and 0.30 (-0.37 to 0.97) f
274 erbations and change from baseline in trough FEV(1) and St.
275 We modelled differences at week 52 in trough FEV(1), St George's Respiratory Questionnaire (SGRQ) tot
276 tory volume in 1 s percent predicted values (FEV(1)%).
277 rticipant data on expiratory flow variables (FEV(1), forced vital capacity [FVC], FEV(1)/FVC ratio, a
278       Primary outcomes were residual volume, FEV(1), St George's Respiratory Questionnaire (SGRQ), an
279  DPA and DHA were positively associated with FEV(1) and FVC (P < 0.025), with evidence for effect mod
280 ic inflammation in sputum is associated with FEV(1) decrease in patients with severe asthma and wheth
281 ified 7 miRNAs significantly associated with FEV(1)% change (P <= 0.05) and 15 miRNAs with significan
282               Neither signal associated with FEV(1), FEV(1)/forced vital capacity, atopy, and age of
283  SNPs on the 6p21 region are associated with FEV(1)/FVC, and the effect of smoking on FEV(1)/FVC diff
284              DHEA-sulfate is associated with FEV(1)PP and is suppressed with GC treatment.
285 availability and tested for association with FEV(1) % predicted and exacerbation frequency.
286 in three groups of children: asthmatics with FEV(1) >=100% (HFEV(1) ; n = 13), asthmatics with FEV(1)
287 ) >=100% (HFEV(1) ; n = 13), asthmatics with FEV(1) <=80% (LFEV(1) ; n = 14) and non-asthmatic contro
288                          VDP correlated with FEV(1) (r = -0.35; P = .04) and FEV(1)/forced vital capa
289 th thickened bronchial walls correlated with FEV(1) (r = -0.60) and FEV(1)/FVC ratio (r = -0.60) (P <
290 bnormal ADC) were negatively correlated with FEV(1) (r = -0.65 and -0.42, respectively; P < .001) and
291 EV(1)/FVC was performed for individuals with FEV(1)/FVC ratio >= 70 in the Korea Associated Resource
292 tum percent solids correlated inversely with FEV(1) and positively with bronchiectasis extent, as mea
293 ssess the association of alpha-T levels with FEV(1) and forced vital capacity (FVC) percent predicted
294  total score; however, the relationship with FEV(1) was less marked.
295 ajectory) but also through a trajectory with FEV(1) below normal in early adulthood (low maximally at
296 of CD4(+) T cells expressing CRTh2 and worse FEV(1) during exacerbation compared with the follow-up.
297      Twenty-four patients (mean age 48 year, FEV(1) 84%, ACQ 1.67) received 4 weeks run-in with a con
298 asurements and Main Results: Across 3 years, FEV(1)% predicted per-year decline was nearly 40% less i
299                              At age 8 years, FEV(1) /FVC was significantly lower and FeNO significant
300 % female; mean +/- SD: age, 63.7 +/- 6.8 yr; FEV(1), 41.6 +/- 7.3% predicted; modified Medical Resear

 
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