ライフサイエンスコーパス: COPD

1 COPD is frequently punctuated by acute exacerbations tha

2 COPD was assessed from the Danish national registries on

3 COPD, chronic bronchitis (CB) and active smoking have al

4 mer smokers [32 subjects without COPD and 39 COPD subjects].

5 117 patients were screened and 60 COPD patients entered a 1-month run-in period on low-dos

6 or raised C-reactive protein 14 days after a COPD exacerbation, an additional course of ciprofloxacin

7 Subjects were recruited into a COPD (emphysema versus airway disease [EvA]) or asthma c

8 -smoking interactions are expected to affect COPD onset.

9 Although, COPD-derived ALI cultures preserved some features known

10 3.30-9.02), CAD (IRR range, 2.77-10.7), and COPD (IRR range, 5.89-8.78) and tapered with age.

11 e to vitamin D supplementation in asthma and COPD associated with reduced molar ratios of 25(OH)D(3)-

12 ter analysis by airway ecology of asthma and COPD in stable state identified two subgroups differenti

13 ssociated with the development of asthma and COPD later in life, and exacerbations of these diseases

14 We focus on asthma and COPD, two chronic respiratory diseases that have been lo

15 of clinical trials of IFN-beta in asthma and COPD.

16 IgE was increased in eosinophilic asthma and COPD.

17 sequence (WGS) analysis of lung function and COPD in a multi-ethnic sample of 11,497 participants fro

18 iators of the interactions between GSDMB and COPD-associated genes.

19 ly observed cell trajectories in healthy and COPD-affected scenarios.

20 n participants with asthma (20.9 nmol/L) and COPD (21.5 nmol/L) was lower than in control subjects (3

21 d NK cell function is altered in smokers and COPD.

22 ostsupplementation in 93 adults with asthma, COPD, or neither condition, and metabolite-to-parent com

23 Increased Tfh-cell induction by COPD cDC2s correlated with increased presence of Tfh-lik

24 e assigned 1:1 to receive either usual care (COPD discharge bundle including PR information leaflet)

25 ed by normal distal airway progenitor cells, COPD lungs were inundated by three variant progenitors e

26 tients and 3,479 controls from the COPDGene (COPD Genetic Epidemiology) study to identify subtypes of

27 vidence for HIV and the presence of a cough, COPD, ischemic heart disease, pregnancy-related mortalit

28 e (CS) is the leading risk factor to develop COPD.

29 attained FEV(1) trajectory, 65 had developed COPD through low maximally attained FEV(1) trajectory, a

30 sent analyses, 79 participants had developed COPD through normal maximally attained FEV(1) trajectory

31 -matching included age, BMI, race, diabetes, COPD, OR time>2 hours, immunosuppressants, smoking, acti

32 ing chronic respiratory obstructive disease (COPD), asthma, apnea, and others for timely and objectiv

33 Chronic obstructive pulmonary disease (COPD) and asthma remain prevalent human lung diseases.

34 with chronic obstructive pulmonary disease (COPD) and chronic severe daytime hypoxemia.

35 iated chronic obstructive pulmonary disease (COPD) and from mice chronically exposed to cigarette smo

36 es in chronic obstructive pulmonary disease (COPD) and hypercapnia is uncertain.

37 with chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD).Methods: The m

38 with chronic obstructive pulmonary disease (COPD) are poorly understood.

39 with chronic obstructive pulmonary disease (COPD) are susceptible to bacterial infections, which wor

40 g the Chronic Obstructive Pulmonary Disease (COPD) Assessment Test and St.

41 with chronic obstructive pulmonary disease (COPD) at risk of future exacerbations.

42 with chronic obstructive pulmonary disease (COPD) by all major COPD clinical practice guidelines.

43 ce of chronic obstructive pulmonary disease (COPD) by current diagnostic criteria is, to the knowledg

44 nale: Chronic obstructive pulmonary disease (COPD) can develop not only through a lung function traje

45 oping chronic obstructive pulmonary disease (COPD) could lead to implementation of preventive measure

46 is of chronic obstructive pulmonary disease (COPD) each year, and it is the fourth leading cause of d

47 thout chronic obstructive pulmonary disease (COPD) enrolled in the prospective Genetic Epidemiology o

48 nale: Chronic obstructive pulmonary disease (COPD) exacerbations are prone to nonrecovery, but there

49 auses chronic obstructive pulmonary disease (COPD) exacerbations.

50 ng of chronic obstructive pulmonary disease (COPD) has focused on CT or MRI measurements, but these h

51 ns of chronic obstructive pulmonary disease (COPD) improves exercise capacity and health-related qual

52 s and chronic obstructive pulmonary disease (COPD) increase patients' susceptibility to infections, b

53 Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous syndrome.

54 Chronic obstructive pulmonary disease (COPD) is a progressive condition of chronic bronchitis,

55 Chronic obstructive pulmonary disease (COPD) is characterized by frequent exacerbations.

56 Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptom

57 with chronic obstructive pulmonary disease (COPD) is not known.

58 Chronic obstructive pulmonary disease (COPD) is the most common noninfectious pulmonary disease

59 Chronic Obstructive Pulmonary Disease (COPD) is the third leading cause of death worldwide.

60 a and chronic obstructive pulmonary disease (COPD) management, metabolic rate measurement, capnograph

61 on in chronic obstructive pulmonary disease (COPD) patients.

62 s) in chronic obstructive pulmonary disease (COPD) progression.

63 on of chronic obstructive pulmonary disease (COPD) renders identifying different trajectories of dise

64 thout chronic obstructive pulmonary disease (COPD) using blood samples from the COPDGene enrollment v

65 on of chronic obstructive pulmonary disease (COPD) was associated with improved survival, although th

66 nt of chronic obstructive pulmonary disease (COPD) with inhaled corticosteroids (ICS) is controversia

67 RDS), chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis (PF).

68 nt of chronic obstructive pulmonary disease (COPD), asthma, or urinary incontinence.

69 on in chronic obstructive pulmonary disease (COPD), but few large longitudinal cohort studies exist.

70 erlap chronic obstructive pulmonary disease (COPD), but studies on the progression of expiratory air

71 with chronic obstructive pulmonary disease (COPD), increased activity of neck inspiratory muscles ha

72 with chronic obstructive pulmonary disease (COPD), when compared to healthy controls.

73 with chronic obstructive pulmonary disease (COPD), with mounting evidence supporting an important ro

74 r for chronic obstructive pulmonary disease (COPD), yet much of COPD risk remains unexplained.

75 a and chronic obstructive pulmonary disease (COPD).

76 , and chronic obstructive pulmonary disease (COPD).

77 with chronic obstructive pulmonary disease (COPD).

78 with chronic obstructive pulmonary disease (COPD).

79 s had chronic obstructive pulmonary disease (COPD).

80 s and chronic obstructive pulmonary disease (COPD).

81 , and chronic obstructive pulmonary disease (COPD).

82 r for chronic obstructive pulmonary disease (COPD); however, more than 25% of COPD patients are non-s

83 igher chronic obstructive pulmonary disease [COPD] prevalence, maternal sepsis, higher risk of anemia

84 Early COPD was defined as FEV(1)/FVC less than the lower limit

85 f tobacco consumption, 1,175 (15%) had early COPD, of whom 58% were current smokers.

86 hanges, suggesting a new biomarker of "early COPD."

87 al population, 15% fulfill criteria of early COPD.

88 h individuals without COPD, those with early COPD had multivariable adjusted hazard ratios of 6.42 (9

89 ics, and prognosis of individuals with early COPD in the general population.Methods: We investigated

90 Individuals with early COPD more often had chronic respiratory symptoms, severe

91 Individuals with early COPD more often have chronic respiratory symptoms and se

92 esting imaging changes consistent with early COPD.

93 s defined as no recorded diagnosis of either COPD or asthma.

94 ciated with mortality in models adjusted for COPD status, age, sex, current smoking status, and pack-

95 d 2011 who did not meet current criteria for COPD (defined as Global Initiative for Obstructive Lung

96 The main risk factor for COPD is tobacco smoke, but other environmental exposures

97 vice Medicare beneficiaries hospitalized for COPD in 2014, at 4446 acute care hospitals in the US.

98 vice Medicare beneficiaries hospitalized for COPD, initiation of pulmonary rehabilitation within 3 mo

99 nce exists that any existing medications for COPD modify mortality.

100 The mainstay of treatment for COPD is inhaled bronchodilators, whereas the role of inh

101 PD, a 50-pack-year smoking history, frequent COPD exacerbations, and recurrent pneumonia.

102 cal phenomenon that results in more frequent COPD exacerbation events, contributing to disease progre

103 ily-based studies, and 8499 individuals from COPD-enriched studies in the NHLBI Trans-Omics for Preci

104 cultures preserved some features known from COPD patients, CS-induced effects were similarly pronoun

105 elative to lung size associated with greater COPD risk.

106 d iron were elevated in participants who had COPD exacerbations, with a 2-fold increase in BALF ferri

107 ed FEV(1) trajectory, and 1,026 did not have COPD.Measurements and Main Results: From 2001 until 2018

108 ose in the lowest had a significantly higher COPD incidence (9.8 vs 1.2 cases per 1000 person-years;

109 for patients with chronic stable hypercapnic COPD (conditional recommendation, moderate certainty); 2

110 hat patients with chronic stable hypercapnic COPD undergo screening for obstructive sleep apnea befor

111 in patients with chronic stable hypercapnic COPD who are initiating NIV (conditional recommendation,

112 on of Pa(CO(2)) in patients with hypercapnic COPD on long-term NIV (conditional recommendation, low c

113 However, newly identified COPD susceptibility genes are already providing novel in

114 dentification of this activity might improve COPD management after a severe exacerbation.

115 r understanding of the role of miR-145-5p in COPD and suggests that reduced expression of miR-145-5p

116 tum neutrophil counts and more severe AHR in COPD patients.

117 rrelates with airway neutrophilia and AHR in COPD patients.

118 otect against airway neutrophilia and AHR in COPD.

119 ilia and airway hyperresponsiveness (AHR) in COPD patients.

120 gene expression from bronchial brushings in COPD and asthma.

121 the major constraint to exercise capacity in COPD, allowing maximal muscle function to be attained an

122 associated with lower diffusion capacity in COPD.

123 with increased presence of Tfh-like cells in COPD lungs as compared with those in control lungs, and

124 Skeletal muscle wasting is also common in COPD, but less is known about its contribution to LV siz

125 uction by control lung cDC2s.Conclusions: In COPD lungs, we found lung EBI2(+) (Epstein-Barr virus-in

126 is no consensus on how MIF levels differ in COPD compared to control conditions and there are no rep

127 Low lnc-IL7R expression in COPD may augment TLR2/4-mediated inflammation and be ass

128 y implicated in lymphoid organ formation, in COPD.Methods: Myeloid cell heterogeneity and phenotype w

129 , little understanding of immune function in COPD exacerbations exists.

130 Toll-like receptor 4 (TLR4) is implicated in COPD.

131 Finally, this signature was increased in COPD patients compared to controls in nasal, bronchial a

132 nflation contributes to dyspnea intensity in COPD.

133 lations and InteRmediate Outcome Measures In COPD (SPIROMICS) bronchoscopy sub-study (n = 195).

134 lations and Intermediate Outcome Measures in COPD Study (SPIROMICS), which involved 2726 participants

135 the impaired epithelial repair mechanisms in COPD, which is still a high medical need.

136 ced inflammatory cell phenotypes observed in COPD positively related to virus load and illness severi

137 mucosal eosinophils and neutrophils only in COPD and CD8(+) T lymphocytes in patients with COPD and

138 with clinical and inflammatory phenotypes in COPD.

139 n concert to drive pathological processes in COPD.

140 distinct patterns of disease progression in COPD using SuStaIn, likely representing different endoty

141 d two trajectories of disease progression in COPD: a "Tissue->Airway" subtype (n = 2,354, 70.4%), in

142 pulated by switch genes, all up-regulated in COPD cases and related to the regulation of immune respo

143 ntative module genes, both down-regulated in COPD cases.

144 immune signature genes, all up-regulated in COPD cases; one where the GWAS genes AGER and CAVIN1 are

145 trophilic inflammation, and fibrosis seen in COPD.

146 ity of SuStaIn for patient stratification in COPD.Methods: We applied SuStaIn to cross-sectional comp

147 of immune cell activation leading to TLOs in COPD remain to be defined.Objectives: To examine the rol

148 ed corticosteroids (ICSs) are widely used in COPD, but the extent to which these therapies protect or

149 thout prevalent COPD, 98 (4.3%) had incident COPD at a median of 6.2 years.

150 associated with adverse outcomes, including COPD.

151 mg/L initiated 14 (+/-3) days after an index COPD exacerbation.

152 wing experimental rhinovirus (RV)-16-induced COPD exacerbations and its relationship to disease sever

153 with COPD and in mice with elastase-induced COPD-like changes.

154 study, using a murine model of smoke-induced COPD, we demonstrate that lung and circulating hepcidin

155 al inflammation and ameliorate virus-induced COPD exacerbations.

156 However, incident cancers, injuries, COPD, and pneumonia were most common in HICs and least c

157 es are already providing novel insights into COPD pathogenesis.

158 Investigating COPD trends may help healthcare providers to forecast fu

159 Chronic Obstructive Lung Disease stage II-IV COPD and persistent symptoms and/or serum C-reactive pro

160 or Chronic Obstructive Lung Disease stage IV COPD lungs with TLOs.Measurements and Main Results: Sing

161 ork modules related to complex diseases like COPD.

162 uctive pulmonary disease (COPD) by all major COPD clinical practice guidelines.

163 y changes were 2.5 times more likely to meet COPD diagnostic criteria at follow-up.Conclusions: We de

164 (GOLD) stage (GOLD 0, no COPD; GOLD 1, mild COPD; GOLD 2, moderate COPD; GOLD 3, severe COPD; GOLD 4

165 no COPD; GOLD 1, mild COPD; GOLD 2, moderate COPD; GOLD 3, severe COPD; GOLD 4, very severe COPD).

166 uctive Lung Disease (GOLD) stage (GOLD 0, no COPD; GOLD 1, mild COPD; GOLD 2, moderate COPD; GOLD 3,

167 between eosinophilic versus noneosinophilic COPD cases.

168 ry disease (COPD); however, more than 25% of COPD patients are non-smokers, and gene-by-smoking inter

169 decoding the complex genetic architecture of COPD.

170 eroids (ICS) affect this important aspect of COPD pathophysiology.

171 osis was replicated in bronchial biopsies of COPD patients.

172 BD)), which is the primary characteristic of COPD.

173 conditions, and those with a codiagnosis of COPD and asthma.

174 ymptoms in young children and development of COPD.

175 ess than 0.70 is required for a diagnosis of COPD.

176 se among adults with a recorded diagnosis of COPD.

177 d in the prospective Genetic Epidemiology of COPD (COPDGene) study (ClinicalTrials.gov identifier: NC

178 spective analysis of Genetic Epidemiology of COPD (COPDGene) study participants enrolled between 2007

179 s of the prospective Genetic Epidemiology of COPD study evaluated current or former smokers enrolled

180 set of the COPDGene (Genetic Epidemiology of COPD) study, representing 101 deaths among 667 current a

181 ession patterns using ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate End

182 individuals from the ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate End

183 2 participants enrolled in the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End

184 n adults with mild to severe exacerbation of COPD.

185 018, we observed 139 severe exacerbations of COPD and 215 deaths, of which 55 were due to nonmalignan

186 e the pathologic and progressive features of COPD when expanded to high numbers.

187 he expression of already well-known genes of COPD and IPF across multiple experiments and the results

188 wer AGER and TLR4 expression irrespective of COPD status, possibly reflecting negative feedback regul

189 /or TLR4 gene deficiency in a mouse model of COPD and also determined whether expression of these rec

190 uctive pulmonary disease (COPD), yet much of COPD risk remains unexplained.

191 pective studies from infancy to the onset of COPD.

192 F may be contributing to the pathogenesis of COPD, as SNPs that influence MIF expression are also ass

193 into the potential immune pathophysiology of COPD exacerbations, and indicate that NK cell phenotypin

194 ociates with distinct clinical phenotypes of COPD, including increased exacerbation susceptibility, i

195 er-smokers demonstrated no increased risk of COPD, regardless of AAT concentration.

196 tes, 2010-2018), and a case-control study of COPD: the Subpopulations and Intermediate Outcome Measur

197 tality differs between these two subtypes of COPD.Methods: The cohort included 1,170 young adults enr

198 ression are also associated with symptoms of COPD.

199 s colocalized with Tfh-like cells in TLOs of COPD lungs.

200 ons regarding the pharmacologic treatment of COPD based on currently available evidence.

201 into novel therapeutics for the treatment of COPD.

202 year, differed between those with asthma or COPD versus control subjects.

203 cal samples taken from adults with asthma or COPD versus control subjects.Measurements and Main Resul

204 vitamin D metabolism is altered in asthma or COPD.Methods: We conducted a longitudinal study in 186 a

205 asthma, chronic kidney disease, diabetes, or COPD in the 12 months before and after diagnosis and for

206 poorly correlate with the presence of GCH or COPD.

207 and biologically relevant marker to predict COPD exacerbations.

208 The smaller cluster was predominantly COPD and was characterized by dominance of Haemophilus a

209 37 of 2531 participants (9.4%) had prevalent COPD, the mean (SD) airway to lung ratio was 0.033 (0.00

210 294 MESA Lung participants without prevalent COPD, 98 (4.3%) had incident COPD at a median of 6.2 yea

211 es: To assess whether incompletely recovered COPD exacerbations benefit from additional treatment wit

212 y the underlying mechanisms of viral-related COPD and asthma and to develop appropriate therapies.

213 he p53 class mediator, which is a replicable COPD gene expression signature in the upper and lower ai

214 with ciprofloxacin for incompletely resolved COPD exacerbations prolonged the time until the next eve

215 eath and death associated with the patient's COPD.Conclusions: In this secondary analysis of an effic

216 COPD; GOLD 2, moderate COPD; GOLD 3, severe COPD; GOLD 4, very severe COPD).

217 eatment improves RV/TLC% predicted in severe COPD.

218 epithelial gene-expression profile in severe COPD.

219 er diversity was associated with more severe COPD according to the Global Initiative for Chronic Obst

220 thma and 78 subjects with moderate-to-severe COPD in a prospective single centre trial.

221 PD; GOLD 3, severe COPD; GOLD 4, very severe COPD).

222 hermodilution) in eight patients with severe COPD (forced expiratory volume in 1s (FEV(1) ) +/- SEM =

223 In patients with severe COPD and activity-matched controls, muscle oxygen transp

224 , reflect on the care of a woman with severe COPD, a 50-pack-year smoking history, frequent COPD exac

225 rformed on sputum from 253 clinically stable COPD patients (4-year median follow-up).

226 were adjusted for demographics and standard COPD risk factors (primary and secondhand tobacco smoke

227 versus UMEC/VI in patients with symptomatic COPD and a history of exacerbations.

228 ions that present with respiratory symptoms (COPD, heart failure, asthma) and declined afterward.

229 lysis of 60 SZ individuals demonstrated that COPD at baseline, but not former smoking or AAT concentr

230 The COPD incidence in the lowest airway to lung quartile was

231 Our aim was to investigate the COPD sputum microbiome and its association with inflamma

232 Consistently, we found that the COPD correlation network built by SWIM consists of three

233 C/VI 62.5/25 mug following a run-in on their COPD therapies.

234 ors dictate the limits of tolerance in these COPD patients.

235 ng cells from three healthy donors and three COPD patients, cultured under ALI (air-liquid interface)

236 patterns of lung function growth leading to COPD in children with asthma and additionally increases

237 mphysema, and higher rates of progression to COPD at 5 years (36% versus 17%; p < 0.001) relative to

238 espiratory exacerbations, (3) progression to COPD at 5 years, and (4) all-cause mortality.

239 trapping, exacerbations, and progression to COPD.

240 Primary outcome was COPD defined by postbronchodilator ratio of forced expir

241 a VE in community-dwelling older adults with COPD in Ontario, Canada using health administrative data

242 ervational studies that enrolled adults with COPD with hypercapnia who used home NIPPV for more than

243 ted hospitalizations among older adults with COPD.

244 dysanapsis was significantly associated with COPD, with lower airway tree caliber relative to lung si

245 ly, multiple genomic regions associated with COPD-related phenotypes, such as quantitative emphysema

246 a A/H1N1 and A/H3N2, and against deaths with COPD as the underlying cause.

247 Participants hospitalized with COPD exacerbations were assigned 1:1 to receive either u

248 In participants with COPD (1655 participants, 40%), those with visual presenc

249 nd ferritin were higher in participants with COPD and in smokers without COPD when compared to non-sm

250 ed from chest CT images in participants with COPD and then to determine the clinical relevance of the

251 of an historical cohort of 201 patients with COPD (Global Initiative for Chronic Obstructive Lung Dis

252 s needed, including studies in patients with COPD 80 years of age and older, those with multiple chro

253 enance oral corticosteroids in patients with COPD and a history of severe and frequent exacerbations;

254 long-acting bronchodilators in patients with COPD and blood eosinophilia, except for those patients w

255 s addressing the use of NIV in patients with COPD and chronic stable hypercapnic respiratory failure.

256 phages and lymphocytes in both patients with COPD and control subjects.

257 dual therapy with LABA/LAMA in patients with COPD and dyspnea or exercise intolerance who have experi

258 er LABA or LAMA monotherapy in patients with COPD and dyspnea or exercise intolerance; 2) a condition

259 In this meta-analysis of patients with COPD and hypercapnia, home BPAP, compared with no device

260 epithelial cell cultures from patients with COPD and in mice with elastase-induced COPD-like changes

261 m healthy control subjects and patients with COPD and infected with influenza virus either prior to o

262 hilia and neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both p

263 PD and CD8(+) T lymphocytes in patients with COPD and nonsmokers.

264 itochondria were diminished in patients with COPD compared to control subjects.

265 l blood mononuclear cells from patients with COPD compared with those from normal controls, and the l

266 and neutrophil inflammation in patients with COPD experiencing naturally occurring exacerbations.

267 ndation for ICS withdrawal for patients with COPD receiving triple therapy (ICS/LABA/LAMA) if the pat

268 uscle activity during sleep in patients with COPD recovering from severe exacerbations (i.e., requiri

269 ared sputum ACE2 expression in patients with COPD stratified according to use or nonuse of ICS.

270 rease the risk of pneumonia in patients with COPD treated with ICS.

271 -induced inflammatory cells in patients with COPD were positively associated with virus load, illness

272 activity occurs frequently in patients with COPD who are recovering from a severe exacerbation and s

273 on for opioid-based therapy in patients with COPD who experience advanced refractory dyspnea despite

274 domized trial to determine, in patients with COPD who have nocturnal arterial oxygen desaturation wit

275 ck-muscle EMG was performed in patients with COPD who were recovering from a severe exacerbation.

276 Compared with ICS nonusers, patients with COPD who were taking ICSs also had reduced sputum expres

277 tives: To identify subtypes of patients with COPD with distinct longitudinal progression patterns usi

278 py is limited.Target Audience: Patients with COPD, clinicians who care for them, and policy makers.Me

279 In patients with COPD, we compared an interval exercise (IE) protocol (al

280 pithelial cells (HSAEpCs) from patients with COPD.

281 t, diagnosis, and treatment of patients with COPD.

282 to long-term oxygen therapy in patients with COPD.

283 n healthy control subjects and patients with COPD.

284 tality and quality of life for patients with COPD.

285 study to identify subtypes of patients with COPD.

286 , and the risk of pneumonia in patients with COPD.Methods: This was a post hoc long-term observationa

287 a-associated hospitalizations in people with COPD.

288 tructive Lung Disease stage II subjects with COPD and as controls 20 smokers and 11 nonsmokers with n

289 ine, compared with nonsmokers, subjects with COPD and smokers had increased numbers of bronchial muco

290 AMs from smokers and subjects with COPD display increased expression of ferroportin as well

291 -cause mortality in smokers with and without COPD.

292 to lung tissue of patients with and without COPD.

293 gene expression in patients with and without COPD.

294 Compared with individuals without COPD, those with early COPD had multivariable adjusted h

295 ) measurements in ex-smokers with or without COPD by using volume-matched CT and hyperpolarized heliu

296 For participants without COPD, those with visual presence of mild and moderate em

297 Ex-smokers without COPD had a larger fraction of normal mPRM voxels (60% vs

298 articipants with COPD and in smokers without COPD when compared to non-smoker control participants bu

299 of which were present in ex-smokers without COPD.

300 rrent or former smokers [32 subjects without COPD and 39 COPD subjects].