ライフサイエンスコーパス: COPD

1 COPD affected 34.2% of donors.

2 COPD AMs also increased basal mROS expression, but they

3 COPD AMs had elevated levels of Mcl-1, an antiapoptotic

4 COPD can be diagnosed early using spirometry, but spirom

5 COPD is associated with several comorbidities (multimorb

6 COPD is characterised by poorly reversible airflow obstr

7 COPD is characterized by chronic airway inflammation and

8 COPD lung macrophages include distinct subpopulations; S

9 COPD lung tissue displayed significantly elevated CCR2 l

10 COPD patients had six-fold greater baseline retrograde

11 COPD patients performed this intervention a second time

12 COPD was defined as FEV1/forced vital capacity (FVC) of

13 f subjects with (n = 11) or without (n = 11) COPD was collected for tissue fibrocyte detection.

14 ighted prevalence of asthma alone was 13.5%, COPD alone 4.1%, and ACOS 2.9%.

15 h immunostaining and autoradiography (n = 6, COPD) with (64)Cu-DOTA-ECL1i.

16 xacerbation in the previous 12 months, and a COPD Assessment Test total score of at least 10.

17 the role of childhood lung function in adult COPD phenotypes.

18 h ICS/LABA therapy in patients with advanced COPD.

19 For this analysis, COPD was spirometrically defined as a post-bronchodilato

20 16.3; 95% confidence interval, 4.7-55.9) and COPD (odds ratio, 5.76; 95% confidence interval, 1.9-17.

21 ains the association between albuminuria and COPD, (2) CS-induced albuminuria is linked to increases

22 here is an association between Asp358Ala and COPD or asthma risk, and to explore the role of the Asp3

23 nce for an association between Asp358Ala and COPD.

24 d investigators with expertise in asthma and COPD.

25 often easy to distinguish between asthma and COPD.

26 ed with nonaccidental, CVD, lung cancer, and COPD mortality in China.

27 fect that could exacerbate disease in CF and COPD patients.

28 c pleiotropy between nicotine dependence and COPD or lung function.

29 sets of smoking behavior, lung function and COPD, and addressed two questions, (1) whether the genet

30 in cigarette smoke-induced inflammation and COPD.

31 mmatory M1s in the small airways of NLFS and COPD compared to controls with a reciprocal decrease in

32 wed a dominant M2 phenotype in both NLFS and COPD subjects.

33 ated and nuclear translocated in smokers and COPD, and their expression is closely related to both EM

34 with chronic inflammatory diseases, such as COPD, in patients with hemoptysis, TAE of the BAA and of

35 Asthma-COPD overlap syndrome (ACOS) was defined as the coexiste

36 nowledge gaps in our understanding of asthma-COPD overlap and identified strategies and research prio

37 he workshop, current understanding of asthma-COPD overlap was discussed among clinicians, pathologist

38 Some studies suggest that asthma-COPD overlap syndrome (ACOS) is associated with worse ou

39 Individuals with undiagnosed, asymptomatic COPD had an increased risk of exacerbations and pneumoni

40 n individuals with undiagnosed, asymptomatic COPD.

41 As in other common diseases, genes at COPD GWAS loci were not differentially expressed; howeve

42 To examine the association between COPD readmissions and other quality measures.

43 also identified genetic correlation between COPD and asthma.

44 There were significant correlations between COPD readmission rates and all patient experience measur

45 There were modest correlations between COPD readmission rates and readmission rates for other m

46 contrast, we found low correlations between COPD readmission rates and readmission rates for surgica

47 ccuracy of the model to discriminate between COPD cases and non-cases by calculating area under the r

48 potential regions of genetic overlap between COPD and other respiratory diseases.

49 ACOS) was defined as the coexistence of both COPD and current asthma.

50 ibroblasts from COPD patients and induced by COPD-related stimuli, such as TGF-beta, cigarette smoke

51 A five-item questionnaire, CAPTURE (COPD Assessment in Primary Care to Identify Undiagnosed

52 oding RNA (lncRNAs) have been shown to cause COPD.

53 We compared COPD readmission rates to other risk-adjusted measures o

54 After controlling for covariates, COPD was not found to be associated with poor transplant

55 y, such as emphysema measured by CT density, COPD assessment test scores, Body-mass index, airflow Ob

56 bular phenotype of emphysematous destruction COPD is driven by a Th1 response activated by infiltrati

57 t identifying patients at risk of developing COPD.

58 All individuals with physician-diagnosed COPD between the ages 40 and 55 years from 2009 and 2011

59 ssessment may not be reliable for diagnosing COPD in patients with mild to moderate airflow obstructi

60 Chronic obstructive pulmonary disease (COPD) affects over 65 million individuals worldwide, whe

61 with chronic obstructive pulmonary disease (COPD) and asthma compared to controls and more TRAP acti

62 e how chronic obstructive pulmonary disease (COPD) and mechanical ventilation time affect corneal don

63 a and chronic obstructive pulmonary disease (COPD) are highly prevalent chronic obstructive lung dise

64 with chronic obstructive pulmonary disease (COPD) are limited.

65 with chronic obstructive pulmonary disease (COPD) by using free-breathing dynamic fluorinated (fluor

66 Chronic obstructive pulmonary disease (COPD) comprises chronic bronchitis and emphysema, and is

67 ts on chronic obstructive pulmonary disease (COPD) development, while long noncoding RNA (lncRNAs) ha

68 ) for chronic obstructive pulmonary disease (COPD) exacerbations, helium/oxygen (heliox) reduces the

69 with chronic obstructive pulmonary disease (COPD) frequently have albuminuria (indicative of renal e

70 ch as chronic obstructive pulmonary disease (COPD) has not been investigated.

71 with chronic obstructive pulmonary disease (COPD) has not been reported.

72 um in chronic obstructive pulmonary disease (COPD) have been associated with increased frequency of e

73 NALE: Chronic obstructive pulmonary disease (COPD) is a chronic, progressive disease, and reversal of

74 Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease, both at th

75 NALE: Chronic obstructive pulmonary disease (COPD) is characterized by impaired clearance of pulmonar

76 Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is t

77 ce of chronic obstructive pulmonary disease (COPD) is increasing faster among women than among men.

78 en of chronic obstructive pulmonary disease (COPD) is increasing, yet there are limited data on early

79 NALE: Chronic obstructive pulmonary disease (COPD) is often unrecognized and untreated.

80 Chronic obstructive pulmonary disease (COPD) is regarded as a disease of accelerated lung aging

81 duced chronic obstructive pulmonary disease (COPD) is the primary testing methodology for drug therap

82 es in chronic obstructive pulmonary disease (COPD) is unknown.

83 f the Chronic Obstructive Pulmonary Disease (COPD) patients engaged in exercise-based muscle rehabili

84 with chronic obstructive pulmonary disease (COPD) rely on a history of two or more events in the pre

85 sk of chronic obstructive pulmonary disease (COPD) require external validation in order to assess the

86 ry of chronic obstructive pulmonary disease (COPD) that has developed from airway remodeling due to a

87 with chronic obstructive pulmonary disease (COPD) who were undergoing lung transplantation (n = 16)

88 with chronic obstructive pulmonary disease (COPD) with an eosinophilic phenotype may benefit from tr

89 CVD), chronic obstructive pulmonary disease (COPD), and lung-cancer mortality.

90 with chronic obstructive pulmonary disease (COPD), but their clinical and pathophysiologic implicati

91 NALE: Chronic obstructive pulmonary disease (COPD), in particular emphysema, is characterized by loss

92 E: In chronic obstructive pulmonary disease (COPD), the benefits of pulmonary rehabilitation (PR) ten

93 with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution

94 from chronic obstructive pulmonary disease (COPD), who presented with non-massive hemoptysis.

95 with chronic obstructive pulmonary disease (COPD).

96 ng in chronic obstructive pulmonary disease (COPD).

97 nt of chronic obstructive pulmonary disease (COPD).

98 ys in chronic obstructive pulmonary disease (COPD).

99 uding chronic obstructive pulmonary disease (COPD).

100 im in chronic obstructive pulmonary disease (COPD).

101 evere chronic obstructive pulmonary disease (COPD).

102 id in chronic obstructive pulmonary disease (COPD).

103 cy in chronic obstructive pulmonary disease (COPD).

104 es in chronic obstructive pulmonary disease (COPD).

105 than chronic obstructive pulmonary disease (COPD).

106 ch as chronic obstructive pulmonary disease (COPD).

107 with chronic obstructive pulmonary disease (COPD).

108 ) and chronic obstructive pulmonary disease (COPD; P = 0.015).

109 gy of Chronic Obstructive Pulmonary Disease [COPD]; non-Hispanic white and African American), ECLIPSE

110 tential as a therapeutic target in emphysema/COPD.

111 n or qCT, but were increased in eosinophilic COPD.

112 g function loss in subjects with established COPD, particularly those with mild disease.

113 piratory events in those without established COPD) as acute respiratory symptoms requiring either ant

114 ession was reduced in human and experimental COPD lung tissues as well as in primary human ATII cells

115 y which RAGE influences COPD in experimental COPD models, we investigated the efficacy of the RAGE-sp

116 parable cigarette smoke-induced experimental COPD mouse model was assessed for relevant mRNA profiles

117 rs, patients with COPD, and two experimental COPD models by quantitative reverse transcriptase-polyme

118 activity in lungs of mice with experimental COPD or asthma.

119 2.9 years, 712 (8%) individuals had a first COPD hospitalization, 964 (11%) a first respiratory-rela

120 a compared to those without were as follows: COPD (adjusted odds ratio [aOR] 5.65, 95% CI 5.52-5.79),

121 The gene module most highly associated for COPD in Weighted Gene Co-Expression Network Analysis (WG

122 hils alone were not a reliable biomarker for COPD severity or exacerbations, or for sputum eosinophil

123 s for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabol

124 about the role of atopy as a risk factor for COPD.

125 anisms may open therapeutic perspectives for COPD patients with systemic inflammation who are unrespo

126 uals were regarded as being at high risk for COPD (defined as individuals aged 40 years or older, wit

127 nical trials of corticosteroid treatment for COPD have shown that the blood eosinophil count is assoc

128 hospital contact, nor medical treatment for COPD, was registered.

129 Data from the French COPD cohort 'INITIATIVES BronchoPneumopathie Chronique O

130 s increased in primary lung fibroblasts from COPD patients and induced by COPD-related stimuli, such

131 uiring ICU admission resulted primarily from COPD or obesity.

132 assessed in patients enrolled in the German COPD and Systemic Consequences-Comorbidities Network coh

133 itiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and ag

134 1843 patients had COPD, of which 1105 patients had 3 years of complete, pr

135 sed, controlled trial, eligible patients had COPD, post-bronchodilator forced expiratory volume in 1

136 and 32 518 (34%) were at high risk of having COPD.

137 reduce COPD readmissions, it is unclear how COPD readmission rates are related to other measures of

138 However, COPD is still diagnosed and treated according to simple

139 posttranslationally modified WNT-5A in human COPD tissue specimens.

140 g NIV failure (25-15%) in severe hypercapnic COPD exacerbations.

141 ve interactors of the first three identified COPD GWAS genes IREB2, HHIP, and FAM13A, based on gene s

142 to devise strategies to promote adherence in COPD.

143 hase of intracellular bacterial clearance in COPD.

144 The defect in COPD AM intracellular killing was associated with a redu

145 re the onset of emphysematous destruction in COPD.

146 )), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest

147 f eosinophils to the mechanism of disease in COPD and to identify their association with levels of cl

148 irculating populations of fibrocyte exist in COPD, with distinct clinical associations, but are not p

149 acrophages showed lower marker expression in COPD current compared to ex-smokers.

150 to enumerate blood and tissue fibrocytes in COPD and determine the association of blood fibrocytes w

151 rials targeting eosinophilic inflammation in COPD should consider assessing sputum eosinophils.

152 lar macrophage CD206 expression was lower in COPD patients compared to smokers.

153 lations and Intermediate Outcome Measures in COPD Study (SPIROMICS) cohort, we analysed patients aged

154 lations and Intermediate Outcome Measures in COPD Study (SPIROMICS) using questionnaires administered

155 ations and Intermediate Outcomes Measures in COPD Study) (n = 1,544) and COPDGene (Genetic Epidemiolo

156 lations and Intermediate Outcome Measures in COPD Study) cohort.

157 hrough a small airway-dependent mechanism in COPD.

158 ty and to move towards precision medicine in COPD, we need to integrate (bioinformatics) and interpre

159 imed to: (1) assess the prevalence of PAD in COPD compared with distinct control groups; and (2) stud

160 al dysregulation of macrophage phenotypes in COPD pathogenesis through integrated study of human smal

161 ine manipulation of macrophage phenotypes in COPD.

162 ticularly macrophage-derived proteinases, in COPD pathogenesis.

163 1 (WNT)/beta-catenin signaling is reduced in COPD; however, the mechanisms thereof, specifically the

164 gnaling is linked to impaired lung repair in COPD; however, the factors responsible for attenuating t

165 hibition has an essential protective role in COPD.

166 with marked cytoplasmic to nuclear shift in COPD (P < 0.01).

167 Models of integrated working in COPD could include: services triggered by troublesome sy

168 disposition of nicotine dependence influence COPD risk and lung function; and (2) the genetic pleiotr

169 molecular mechanism by which RAGE influences COPD in experimental COPD models, we investigated the ef

170 as HMGB1, which interacts with AGER, a known COPD GWAS gene.

171 jects were persons with no COPD or with mild COPD (FEV1 >/=60% predicted, no exacerbation in the past

172 Whether exacerbations in subjects with mild COPD or similar acute respiratory events in smokers with

173 a spirometric diagnosis of mild or moderate COPD is subject to variability and potential error.

174 ghlight another potential target to modulate COPD.

175 Control subjects were persons with no COPD or with mild COPD (FEV1 >/=60% predicted, no exacer

176 spectively, for distinguishing cases from no-COPD control subjects.

177 P of 67.8% for differentiating cases from no-COPD control subjects.

178 %, respectively) and for all cases versus no-COPD control subjects (89.7% and 93.1%, respectively).

179 itching in both mucosal and luminal areas of COPD patients, that strongly associated with cytokine ba

180 NALE: Evidence supporting the association of COPD or airflow obstruction with use of solid fuels is c

181 The unpredictable course of COPD and the difficulty of predicting survival are barri

182 ong-term consequences for the development of COPD and ACOS by middle age.

183 The effect of COPD on alveolar macrophage (AM) microbicidal responses

184 1,544) and COPDGene (Genetic Epidemiology of COPD) (n = 602) cohorts had 90 plasma or serum candidate

185 nd African American), ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate End

186 percapnia following an acute exacerbation of COPD, adding home noninvasive ventilation to home oxygen

187 Exacerbations of COPD were an additional predefined endpoint.

188 ischaemic heart disease and exacerbations of COPD.

189 One main pathological feature of COPD is the loss of functional alveolar tissue without a

190 acerbations (p=0.35) or the other indices of COPD severity, such as emphysema measured by CT density,

191 the alveolar spaces and lung interstitium of COPD patients and controls.

192 (and opportunities) in existing knowledge of COPD pathobiology, how systems biology and network medic

193 dicator of clinically meaningful measures of COPD.

194 data indicated that a viable mouse model of COPD can be established by combining the results from wh

195 The mouse-model of COPD showed similar increase in mRNA for M2 markers.

196 t of 71 patients, an in vivo murine model of COPD, and primary human bronchial epithelial cells.

197 ge (BAL) and an experimental murine model of COPD.

198 nonical WNT-5A in two experimental models of COPD and increased posttranslationally modified WNT-5A i

199 elastase, as well as in CS-induced models of COPD.

200 S exposure in building their mouse models of COPD.

201 how RAGE is involved in the pathogenesis of COPD.

202 has been shown to improve the phenotyping of COPD by allowing for the visualization and quantificatio

203 d transplant suitability but the presence of COPD did not.

204 smaller sex difference in the prevalence of COPD, especially in countries where smoking patterns hav

205 rrent smoking patients with a broad range of COPD severity, high concentrations of sputum eosinophils

206 hronic, progressive disease, and reversal of COPD diagnosis is thought to be uncommon.

207 of nsv823469 significantly decreased risk of COPD compared with normal (2-copy) (OR = 0.77, 95% CI =

208 inophil count is associated with the risk of COPD exacerbations, mortality, decline in FEV1, and resp

209 t vs. lowest quintile) increased the risk of COPD.

210 mplexes were associated with the severity of COPD evaluated by using the composite Global Initiative

211 tomatic smokers, even though early stages of COPD can be asymptomatic.

212 s paper discusses a possible new taxonomy of COPD, the role of endotypes and associated biomarkers an

213 iatives for early diagnosis and treatment of COPD are needed.

214 indicating an airway predominant variety of COPD with significant biomass exposure.

215 ionwide that had publically reported data on COPD readmissions.

216 l Glycopyronium vs Fluticasone Salmeterol on COPD Exacerbations) study, which compared once-daily lon

217 ed a previous model for predicting new onset COPD in a different database.

218 Stimuli related to asthma and/or COPD were tested for their capacity to induce TRAP.

219 deling due to asthma, as compared with other COPD phenotypes.

220 accharides (LPS) inhalation, in building our COPD mouse model.

221 considered undiagnosed if neither a previous COPD hospital contact, nor medical treatment for COPD, w

222 2 months adjusted for the number of previous COPD admissions, previous use of long-term oxygen, age,

223 is (mortality) are not different from 'pure' COPD patients.

224 Compared to 'pure' COPD patients, patients with ACOS exhibit lower cumulati

225 us (St. George's Respiratory Questionnaire), COPD Assessment Test, and EuroQol-5-Dimensions were asse

226 Despite growing pressure to reduce COPD readmissions, it is unclear how COPD readmission ra

227 sputum or blood are associated with a severe COPD phenotype, including greater exacerbation frequency

228 e of HRCT in quantifying emphysema in severe COPD patients and to study the variations in the pattern

229 dysfunction in patients with moderate-severe COPD, and (2) to test whether low flow oxygen administra

230 including 143 patients with moderate-severe COPD, with 3 years of PR maintenance following an 8-week

231 l apoptosis in patients with moderate-severe COPD.

232 dysfunction in patients with moderate-severe COPD.

233 ss than 50%, at least one moderate-to-severe COPD exacerbation in the previous 12 months, and a COPD

234 The primary endpoint was moderate-to-severe COPD exacerbation rate.

235 rmation is increased in patients with severe COPD and associated with more frequent exacerbations and

236 her in current or former smokers with severe COPD than in controls who had never smoked (3166+/-402 v

237 5AC in current or former smokers with severe COPD were approximately 3 times as high and 10 times as

238 ected lung tissues from subjects with severe COPD.

239 cell (MDSC)-like fibrocytes] cells in stable COPD (n = 41) and control (n = 29) subjects.

240 N: Individuals with undiagnosed, symptomatic COPD had an increased risk of exacerbations, pneumonia,

241 in individuals with undiagnosed, symptomatic COPD.

242 with tiotropium in patients with symptomatic COPD, FEV1 of less than 50%, and a history of exacerbati

243 We characterized the COPD status of 917 participants from the Subpopulations

244 s. 5.9% in patients with GOLD stage 0 in the COPD and Systemic Consequences-Comorbidities Network) ha

245 3699 (11%) of these participants met the COPD criteria and 2903 (78%) were undiagnosed, of whom 2

246 es and FEV1, symptoms evaluated by using the COPD assessment test, and higher levels of NET complexes

247 Material/A total of thirty COPD patients and a control group of the same size, matc

248 ecific loci associated with lung function to COPD, and identify potential regions of genetic overlap

249 th asymptomatic and symptomatic, undiagnosed COPD in the general population in Denmark.

250 S-ZM1 administration in in vivo and in vitro COPD models.

251 of asthma was significantly associated with COPD and respiratory-related hospitalizations (hazard ra

252 A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk s

253 findings highlight new loci associated with COPD, demonstrate the importance of specific loci associ

254 018), but no evidence of an association with COPD exacerbations (p=0.35) or the other indices of COPD

255 ed two previously reported associations with COPD susceptibility (4q31 near HHIP and 15q25 near CHRNA

256 ificance, including 13 new associations with COPD.

257 ontrol study, and was further confirmed with COPD and pulmonary function-based family analyses, respe

258 Donors with COPD and donors who were mechanically ventilated exhibit

259 Donors with COPD and donors who were mechanically ventilated had red

260 m 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited

261 Participants with COPD reported more cough (odds ratio [OR] 1.95, 95% CI 0

262 A total of 2,088 patients with COPD (61.1% male; mean [SD] age, 65.3 [8.2] years, GOLD

263 Patients with COPD (n = 244) were recruited.

264 eline ACT scores were worse in patients with COPD (P = 0.004).

265 aseline data from SPIROMICS in patients with COPD aged 40-80 years who had a smoking history of at le

266 confidence interval, 34-69) in patients with COPD and 81% (95% confidence interval, 54-96) in patient

267 acerbations than placebo among patients with COPD and an eosinophilic phenotype.

268 Cases were patients with COPD and at least one exacerbation in the past year or F

269 lavage from healthy donors or patients with COPD and challenged with opsonized serotype 14 Streptoco

270 iated with disease severity in patients with COPD and how they are associated with microbiota composi

271 Patients with COPD and/or CS-exposed mice have pulmonary and renal end

272 ratification, and treatment of patients with COPD can occur on the basis of their pathobiological mec

273 hout airflow limitation and in patients with COPD compared with never-smokers.

274 soluble sputum and serum from patients with COPD during periods of disease stability and during exac

275 A cohort of 2,614 patients with COPD recruited outside the hospital setting was examined

276 on in vivo and in vitro and in patients with COPD was assessed by immunofluorescence staining, Wester

277 every 4 weeks for 52 weeks in patients with COPD who had a history of moderate or severe exacerbatio

278 CAPTURE with PEF can identify patients with COPD who would benefit from currently available therapy

279 In 26 patients with COPD, 24 ever-smokers without COPD, 32 nonsmokers who un

280 Among 9053 patients with COPD, 2717 (30%) had a history of asthma.

281 choscopic airway biopsies from patients with COPD, and in smoking and non-smoking controls.

282 lls of never-smokers, smokers, patients with COPD, and two experimental COPD models by quantitative r

283 s, tissues, and circulation of patients with COPD, during both stable disease and exacerbations.

284 In patients with COPD, the AL classification based on z-score predicts wo

285 wice-daily ICS/LABA therapy in patients with COPD.

286 rt-term effects on outcomes in patients with COPD.

287 primary human ATII cells from patients with COPD.

288 and safety of the treatment of patients with COPD.

289 phils with soluble sputum from patients with COPD.

290 ified in a real-life cohort of patients with COPD.

291 metabolic equivalents [METs]) by people with COPD.

292 sity physical activity levels in people with COPD.

293 mm in diameter) from 50 former smokers with COPD and 39 control subjects.

294 hout airflow limitation, and 12 smokers with COPD.

295 In subjects with COPD, exacerbations were associated with excess FEV1 dec

296 , we analysed patients aged 40-80 years with COPD for whom 3 years of prospective data were available

297 Compared with individuals without COPD, the age and sex adjusted hazard ratio (HR) was 5.0

298 Patients without COPD were primarily obese.

299 fidence interval, 54-96) in patients without COPD.

300 patients with COPD, 24 ever-smokers without COPD, 32 nonsmokers who underwent a renal biopsy or neph