ライフサイエンスコーパス: emphysema

1 ly history of lung cancer; and self-reported emphysema.

2 that EBVs are also effective in homogeneous emphysema.

3 d lung proteins during tobacco smoke-induced emphysema.

4 increased feature sizes related to pulmonary emphysema.

5 orrelated with both PRM gas trapping and PRM emphysema.

6 aimed at reducing hyperinflation in advanced emphysema.

7 lly related to both PRM gas trapping and PRM emphysema.

8 the first second, pack-years of smoking, and emphysema.

9 may represent a novel treatment strategy for emphysema.

10 disrupted rhythms of pulmonary function, and emphysema.

11 ognized as idiopathic pulmonary fibrosis and emphysema.

12 ive effects on neutrophilic inflammation and emphysema.

13 cause of sterile inflammation and pulmonary emphysema.

14 lls and low BMI may temporize progression of emphysema.

15 , and those who met NLST criteria and/or had emphysema.

16 potential treatment for patients with severe emphysema.

17 in particular, PH appears to be unrelated to emphysema.

18 ssion of SERPINE2, a susceptibility gene for emphysema.

19 tter clarify these associations with percent emphysema.

20 after LVRS in patients with severe COPD and emphysema.

21 the evidence for using it as a biomarker for emphysema.

22 of which is associated with the presence of emphysema.

23 's susceptibility to cigarette smoke-induced emphysema.

24 s AAT replacement therapy is therapeutic for emphysema.

25 explored the role of the microRNA miR-22 in emphysema.

26 ritis, atherosclerosis, aortic aneurism, and emphysema.

27 agment, extraconal emphysema, and intraconal emphysema.

28 ories, and presence of diabetes mellitus and emphysema.

29 s of mice and observed tobacco smoke induced emphysema.

30 cathepsin E mice and found that they develop emphysema.

31 n/apoptosis in the pathogenesis of pulmonary emphysema.

32 ys; ZZ-AT) is a well-known genetic cause for emphysema.

33 evealed independent associations for percent emphysema.

34 inhibited cathepsin E-induced apoptosis and emphysema.

35 cted murine lungs from developing CS-induced emphysema.

36 pulations including smokers and persons with emphysema.

37 cs, smoking history, and computed tomography emphysema.

38 exposure produces predominantly right-sided emphysema.

39 demonstrated benefit in severe heterogeneous emphysema.

40 lid nodules, and more nodule spiculation and emphysema.

41 months, Mmp28(-/-) mice were protected from emphysema.

42 levels in sera is responsible for pulmonary emphysema.

43 linical improvement for patients with severe emphysema.

44 n and gene coexpression in bronchiolitis and emphysema.

45 was inversely correlated with the extent of emphysema.

46 ing progressive small airway remodelling and emphysema.

47 PD, but it was otherwise not associated with emphysema (0.89 [0.60-1.32]) or gas trapping (1.15 [0.92

48 m]), bronchodilator reversibility (2.7%), % emphysema (0.9%), % gas trapping (10.7%), and square roo

49 40), 5.18 (4.29-6.27), and 6.21 (5.06-7.62); emphysema-4.86 (3.16-7.47), 6.41 (4.09-10.05), and 17.79

50 ondria was also observed in mouse lungs with emphysema (6 months CS exposure, 100 mg TPM/m(3)) as wel

51 sity (ND) by traditional thresholds for mild emphysema (-910 Hounsfield units) and gas trapping (-856

52 PMBF was reduced with greater percentage emphysema-950HU and radiologist-defined emphysema, parti

53 rse health outcomes in nonsmokers, including emphysema (a chronic obstructive pulmonary disease).

54 f interest in relation to smoking-associated emphysema, a component of chronic obstructive pulmonary

55 Cigarette smoking causes emphysema, a fatal disease involving extensive structura

56 ified A1PI augmentation slows progression of emphysema, a finding that could not be substantiated by

57 , and greater airway-wall thickening without emphysema according to HRCT than did asymptomatic curren

58 ase-null mice, short telomeres predispose to emphysema after chronic cigarette smoke exposure.

59 uated T(H)17 responses and failed to develop emphysema after exposure to smoke or nCB.

60 The final decision tree used four variables: emphysema, airway abnormality, the percentage of ground

61 s, the identified genes are also involved in emphysema, airway obstruction, and bronchial inflammatio

62 a, particularly panlobular and centrilobular emphysema (all P </= 0.01).

63 Whole-lung quantitative CT percentage emphysema also showed statistically significant correlat

64 We randomly assigned patients with severe emphysema and a confirmed absence of collateral ventilat

65 ed trial in patients with both heterogeneous emphysema and a target lobe with intact interlobar fissu

66 f Zephyr EBVs in patients with heterogeneous emphysema and absence of collateral ventilation.

67 QCT density measures for emphysema and air trapping were significantly higher in

68 duced development of cigarette smoke-induced emphysema and airspace enlargement, with concurrent redu

69 eloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice ex

70 nd lobar quantitative CT-derived metrics for emphysema and bronchial wall thickness were calculated.

71 obstructive pulmonary disease includes both emphysema and chronic bronchitis, and in the case of chr

72 This generic term encompasses emphysema and chronic bronchitis, two common conditions,

73 erbations and clinical subphenotypes such as emphysema and chronic bronchitis.

74 130(F/F) genetic mouse model for spontaneous emphysema and cigarette smoke-induced emphysema models.

75 etylcystein significantly improved pulmonary emphysema and dysfunction.

76 s, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in s

77 The relationship between emphysema and fibrosis extents and change in pulmonary f

78 vestigated the relationship between baseline emphysema and fibrosis extents, as well as pulmonary fun

79 /=200 ml), and computed tomography-diagnosed emphysema and gas trapping (>5% and >15% of lung, respec

80 sphingomyelins are strongly associated with emphysema and glycosphingolipids are associated with COP

81 onsistently up-regulated in human lungs with emphysema and in mouse emphysema models; however, the me

82 nchial valves in patients with heterogeneous emphysema and intact interlobar fissures produces signif

83 Genes increased in both emphysema and IPF relative to control were enriched for

84 entify convergent transcriptomic pathways in emphysema and IPF.

85 m both genotypes showed disseminated foci of emphysema and large areas of goblet cell metaplasia in b

86 d evidence of an association between percent emphysema and long-term pollution concentrations in an a

87 a rare nonsynonymous variant in PTPRO, with emphysema and obstruction was demonstrated in all non-Hi

88 s, bone mineral density reduction, pulmonary emphysema and senile atrophy of skin.

89 ical trial conducted among 315 patients with emphysema and severe air trapping recruited from 21 Nort

90 Among patients with emphysema and severe hyperinflation treated for 12 month

91 ise tolerance, and symptoms in patients with emphysema and severe lung hyperinflation.

92 ing generation, the mother died of pulmonary emphysema and she was blind after the age of 50.

93 sease on CT and gas trapping largely because emphysema and small airways disease occurred in differen

94 Thus, miR-22 is a critical regulator of both emphysema and T(H)17 responses.

95 We performed a GWAS on two quantitative emphysema and two quantitative airway imaging phenotypes

96 oduced in a group of patients with incipient emphysema and when patients with emphysema were matched

97 easured percentage of lung with emphysema (% emphysema) and gas trapping (% gas trapping), and small

98 FEV1, FEV1/FVC, low-attenuation area/visual emphysema, and diffusing capacity in SCCOR participants,

99 nked sRAGE to COPD, and more specifically to emphysema, and evidence is accumulating that this link i

100 ated in remodeling processes, development of emphysema, and fibrosis.

101 Lung tissues from patients with emphysema, and from spontaneous and cigarette smoke-indu

102 flow obstruction, respiratory symptoms, more emphysema, and gas trapping in men and women.

103 ord length (MACL), a quantitative measure of emphysema, and gene-by-environment interactions were exa

104 improves survival in selected patients with emphysema, and has generated interest in bronchoscopic a

105 by optic canal fracture fragment, extraconal emphysema, and intraconal emphysema.

106 ease (COPD) comprises chronic bronchitis and emphysema, and is a leading cause of morbidity and morta

107 omorbidities include pulmonary hypertension, emphysema, and lung cancer, while non-pulmonary conditio

108 , including in regions of lung without frank emphysema, and may represent a distinct pathological pro

109 ground glass-reticular (GGR), honeycombing, emphysema, and normal lung densities were measured by AM

110 inflammatory lung diseases including asthma, emphysema, and pulmonary fibrosis.

111 mice were also resistant to elastase-induced emphysema, and this resistance was reversed by coadminis

112 one, those with computed tomography-detected emphysema, and those who met NLST criteria and/or had em

113 VDP, ADC, and PRM gas trapping and emphysema (ANOVA, P < .001) measurements were significan

114 assessed functional small airway disease and emphysema are associated with FEV1 decline, but the asso

115 Therapeutic options for severe emphysema are limited.

116 eatment effect of A1PI on the progression of emphysema as assessed by the loss of lung density in rel

117 Emphysema assessed based on lung density measured by usi

118 emphysema development and appeared to reduce emphysema-associated lung volume expansion in mice expos

119 R imaging showed correlation with percentage emphysema at lobar quantitative CT (r = -0.32, P < .001

120 ters of airway remodeling, air trapping, and emphysema between asthmatic patients and patients with C

121 ly increased risk of airflow obstruction and emphysema but the risk of chronic obstructive pulmonary

122 We observed that in emphysema (but not in bronchiolitis) (1) up-regulated ge

123 id mediators might reduce the development of emphysema by controlling chronic inflammation.

124 merase mutations are a risk factor for human emphysema by examining their frequency in smokers with c

125 of circulating Z alpha1-antitrypsin lead to emphysema by loss of inhibition of neutrophil elastase.

126 , more frequent exacerbations, and increased emphysema by QCT.

127 ns-signaling antagonist sgp130Fc ameliorated emphysema by suppressing augmented alveolar type II cell

128 but who have visual evidence of centriacinar emphysema (CAE) on CT.

129 uction of lung parenchyma and development of emphysema, caused by low AAT levels and a high neutrophi

130 nd exercise capacity in patients with severe emphysema characterized by an absence of interlobar coll

131 and PDGFA occurred more frequently in IPF or emphysema compared with control and validated these find

132 resistant to chronic cigarette smoke-induced emphysema compared with Fam13a(+/+) mice.

133 nto its potential as a therapeutic target in emphysema/COPD.

134 Unlike quantification of emphysema, CT measurement of airway remodeling correlate

135 than 50 (two generations) had also a severe emphysema, despite no history of smoking or asthma.

136 jects meeting either NLST criteria or having emphysema detected most cancers (88% and 95% of incident

137 treatment with a PPARgamma agonist prevented emphysema development and appeared to reduce emphysema-a

138 ent understanding of molecular mechanisms of emphysema development and may provide new therapeutic ta

139 lockade of RAGE ameliorates elastase-induced emphysema development and progression via RAGE-DAMP sign

140 could increase the susceptibility of mice to emphysema development by inhibiting beta-catenin signali

141 ed lung function and age-related spontaneous emphysema development in Hhip(+/-) mice may be caused by

142 of 5 mo improved lung function and prevented emphysema development in Hhip(+/-) mice, suggesting that

143 necting Hhip to age-related FEV1 decline and emphysema development is lacking.

144 ime, they exhibited pathologies that precede emphysema development, including increases in the follow

145 bstructive pulmonary disease and may precede emphysema development.

146 We identified five loci associated with emphysema distribution at genome-wide significance.

147 To identify the genetic influences of emphysema distribution in non-alpha-1 antitrypsin-defici

148 Two computed tomography scan emphysema distribution measures (difference between uppe

149 psin deficiency, the genetic determinants of emphysema distribution remain largely unknown.

150 otentially contribute to the pathogenesis of emphysema distribution.

151 tomography-measured percentage of lung with emphysema (% emphysema) and gas trapping (% gas trapping

152 while both CT and MR imaging measurements of emphysema explained symptoms.

153 uartile analysis, patients with the greatest emphysema extent (28 to 65%) showed the smallest FVC dec

154 In multivariate analyses, emphysema extent greater than or equal to 15% was associ

155 ients with idiopathic pulmonary fibrosis and emphysema extent greater than or equal to 15%.

156 low lung area percentage (LAA%) to quantify emphysema extent.

157 lmonary function at Week 48 were analyzed by emphysema extent.

158 orrelation was observed between fibrosis and emphysema extents (r = -0.232; P < 0.001).

159 struction is the prominent characteristic of emphysema, extracellular proteinases, particularly those

160 s could predict disease progression, such as emphysema, FEV1, and 6-minute-walk distance (6MWD), in f

161 is preliminary study of patients with severe emphysema followed up for 6 months, bronchoscopic treatm

162 ed susceptibility towards the development of emphysema following exposure to chronic cigarette smoke

163 ds, five sphingomyelins were associated with emphysema; four trihexosylceramides and three dihexosylc

164 he paradigm of the mechanism of AATD-induced emphysema from a pure elastase-antielastase imbalance to

165 American Society of Anesthesiologists class, emphysema grade, nodule size, and distance from pleura w

166 RATIONALE: Emphysema has considerable variability in the severity a

167 Upper lobe-predominant emphysema has emerged as an important predictor of respo

168 (heart disease, high blood pressure, stroke, emphysema, high cholesterol, diabetes, arthritis, and as

169 rasts could allow the diagnosis of pulmonary emphysema in a murine model.

170 The percentage of emphysema in each lung lobe and both lungs was correlate

171 ed increased lung compliance and spontaneous emphysema in Hhip(+/-) mice starting at 10 mo of age.

172 atment limits the progression of age-related emphysema in Hhip(+/-) mice.

173 Emphysema in mice was quantified by various methods incl

174 nine concentration and tobacco smoke-induced emphysema in mice.

175 ewise, nCB intranasal administration induced emphysema in mouse lungs.

176 ions at genome-wide significance for percent emphysema in or near SNRPF (rs7957346; P = 2.2 x 10(-8))

177 ation alternative to CT in the assessment of emphysema in patients with COPD.

178 greater with PRM gas trapping than with PRM emphysema in patients with mild (for gas trapping, SOC =

179 Progressive airway wall remodelling and emphysema in pIgR(-/-) mice are associated with an alter

180 nd to study the variations in the pattern of emphysema in relation to age, sex, FEV1, smoking index,

181 ithelial cell death, airway dysfunction, and emphysema in response to CS; however, the underlying mec

182 tween biomass exposure and the percentage of emphysema in RUL, RLL, and both lungs (P values of 0.024

183 nd reduced mortality, mucus obstruction, and emphysema in Scnn1b-Tg mice.

184 To evaluate the role of HRCT in quantifying emphysema in severe COPD patients and to study the varia

185 LAAI-950 may not be a reliable indicator of emphysema in subjects without spirometric impairment.

186 PS-ZM1 administration significantly reversed emphysema in the lung of mice.

187 ociation was found between the percentage of emphysema in the right lower lobe and BMI (P=0.015), bet

188 BMI decreases with increasing levels of emphysema in the right lower lobe.

189 ted airspace enlargement in elastase-induced emphysema in vivo.

190 this biomechanical stress likely influences emphysema initiation and progression.

191 Smoking-related emphysema is a chronic inflammatory disease driven by th

192 Advanced emphysema is a lung disease in which alveolar capillary

193 Emphysema is classified as centrilobular (subclassified

194 In addition, there is growing evidence that emphysema is not solely a destructive process because it

195 tive pulmonary disease (COPD), in particular emphysema, is characterized by loss of parenchymal alveo

196 ssociated with a decrease (-1.3%) in percent emphysema (LAAI-950), a 3.3-Hounsfield unit increase in

197 decline over 48 weeks versus no emphysema or emphysema less than 15%.

198 PM10) and nitrogen oxides (NOx) with percent emphysema-like lung on computed tomography (CT).

199 Greater emphysema-like lung was independently associated with in

200 ween ambient air pollution and percentage of emphysema-like lung were inconclusive in this cross-sect

201 measurement of airway remodeling instead of emphysema may correlate with PH in COPD.

202 ients with idiopathic pulmonary fibrosis and emphysema may have artificially preserved lung volumes.

203 the other indices of COPD severity, such as emphysema measured by CT density, COPD assessment test s

204 MR imaging emphysema measurements also made the greatest relative c

205 ients with mild-to-moderate COPD, MR imaging emphysema measurements played a dominant role in the exp

206 coefficient (ADC), and PRM gas trapping and emphysema measurements.

207 aneous emphysema and cigarette smoke-induced emphysema models.

208 d in human lungs with emphysema and in mouse emphysema models; however, the mechanisms by which IL-6

209 Genetic blockade of IL-6 trans-signaling in emphysema mouse models and therapy with the IL-6 trans-s

210 complex 1 hyperactivation, and treatment of emphysema mouse models with the mechanistic target of ra

211 from spontaneous and cigarette smoke-induced emphysema mouse models, were characterized by excessive

212 Enrollment of patients with emphysema occurred from March to October 2013, with 12-m

213 correlation with quantitative CT percentage emphysema on a lobar basis and with PFT results on a who

214 Emphysema on computed tomography (CT) was defined by the

215 tion is related to the greater percentage of emphysema on computed tomography.

216 f the independent prognostic significance of emphysema on CT among patients without COPD on spirometr

217 nominally (P < 0.05) associated with either emphysema or airway phenotypes.

218 PD and spirometric loci were associated with emphysema or airway phenotypes.

219 reduced FVC decline over 48 weeks versus no emphysema or emphysema less than 15%.

220 f this pathway in tissues from patients with emphysema or IPF.

221 Although CS-exposed NHPs did not develop emphysema over the study time, they exhibited pathologie

222 female sex (P = .001), older age (P = .003), emphysema (P = .004), coaxial technique (P = .025), nons

223 of 3.32% at Week 48 versus patients with no emphysema (P = 0.047).

224 oderate, confluent, and advanced destructive emphysema), panlobular, and paraseptal (subclassified as

225 tage emphysema-950HU and radiologist-defined emphysema, particularly panlobular and centrilobular emp

226 Because of the established association of emphysema pathogenesis to macrophage influx, we evaluate

227 In 10 emphysema patients receiving A1AT therapy (Prolastin), p

228 These risk factors of emphysema patterns are helpful in deciding on the manage

229 ndex, chronic obstructive pulmonary disease, emphysema, personal history of cancer, personal history

230 (2), pack-years history greater than 60, and emphysema presence were independently associated with LC

231 spiratory and expiratory CT images to define emphysema (PRM(emph)) and functional small airways disea

232 onal small airway abnormality (PRM(FSA)) and emphysema (PRM(EMPH)) in the SPIROMICS (Subpopulations a

233 ghts into the microscopic origins underlying emphysema progression before and after lung volume reduc

234 ed alpha1 proteinase inhibitor (A1PI) slowed emphysema progression in patients with severe alpha1 ant

235 The rate of emphysema progression quantified by CT scans among ever-

236 In multivariable analyses, the rate of emphysema progression was greater in subjects who had lo

237 destruction of elastic networks representing emphysema progression, which we use to track the respons

238 positive association with the annual rate of emphysema progression.

239 ns (34 to 65 mo apart) were used to quantify emphysema progression.

240 s (GOLD stage III or more) was done using an emphysema protocol.

241 ciations with distinct patterns of pulmonary emphysema quantified by computed tomography scan.

242 s trapping (r = 0.58, P < .001) and with PRM emphysema (r = 0.68, P < .001).

243 th COPD (gas trapping: r = 0.47 and P = .03; emphysema: r = 0.62 and P < .001) but not in healthy ex-

244 fference between upper-third and lower-third emphysema; ratio of upper-third to lower-third emphysema

245 Smoking resulted in homogenously distributed emphysema regardless of the severity of smoking.

246 We identified five loci associated with emphysema-related phenotypes, one with airway-related ph

247 wever, the mechanisms by which IL-6 promotes emphysema remain obscure.

248 5 (95% CI: 0.1, 0.9%) higher average percent emphysema, respectively.

249 r smokers, current smokers, and persons with emphysema, respectively.

250 0 (95% confidence interval: -1.8, 0.5) or of emphysema score, with a change in C index of 0.0 [95% co

251 preserve lung parenchyma in individuals with emphysema secondary to severe alpha1 antitrypsin deficie

252 (CXCL13, CCL19, and POU2AF1) correlated with emphysema severity; (4) there were lymphoid follicles (C

253 In families, emphysema showed an autosomal dominant inheritance patte

254 elationship for ventilation defects with PRM emphysema (SOC = 64% +/- 30) was significantly greater t

255 ild (for gas trapping, SOC = 36% +/- 28; for emphysema, SOC = 1% +/- 2; P = .001) and moderate (for g

256 ate (for gas trapping, SOC = 34% +/- 28; for emphysema, SOC = 7% +/- 15; P = .006) COPD.

257 smoking model and twenty genes with previous emphysema studies.

258 tially useful biomarker specifically for the emphysema subpopulation is the soluble receptor for adva

259 ield units on full-lung computed tomography; emphysema subtypes were scored by radiologists.

260 usly unreported rare variant contributing to emphysema susceptibility.

261 progression in alpha1 antitrypsin deficiency emphysema than spirometry is, so we aimed to assess the

262 t option in selected patients with COPD with emphysema that improves breathing mechanics and lung fun

263 ell-related genes in patients with COPD with emphysema that is absent in bronchiolitis.

264 Combining NLST criteria and emphysema to select screening candidates results in high

265 dictive Surrogate Endpoints), NETT (National Emphysema Treatment Trial), and GenKOLS (Genetics of COP

266 ependymomas, one had severe and progressive emphysema, two had Huntington's disease and one had a gr

267 examine RV changes in contemporary COPD and emphysema using cardiac magnetic resonance (CMR) imaging

268 esized that MMP-28 has contributory roles in emphysema via alteration of macrophage numbers and activ

269 Fibrosis and emphysema visual scores were independently determined by

270 e mean (SD) annual rate of change in percent emphysema was +0.46 (0.92), ranging from -1.8 to +4.1.

271 Although emphysema was also significantly associated with lower F

272 The extent of emphysema was assessed using the density mask method wit

273 Percent emphysema was defined as lung regions < -910 Hounsfield

274 The percentage of emphysema was defined as the percentage of lung regions

275 The extent of emphysema was disproportionately low compared to the amo

276 Emphysema was estimated by using the MR imaging apparent

277 Emphysema was identified in 38% of patients.

278 PRM emphysema was predicted by the diffusing capacity for ca

279 Airway remodeling and emphysema were determined morphometrically in male, fema

280 h incipient emphysema and when patients with emphysema were matched for the severity of airflow limit

281 iques to dissect (small) airways disease and emphysema were not available.

282 Telomerase mutation carriers with emphysema were predominantly female and had an increased

283 1 decline, continued smoking and presence of emphysema were the strongest predictors of progression;

284 physema; ratio of upper-third to lower-third emphysema) were tested for genetic associations in all s

285 smoke is the most common cause of pulmonary emphysema, which results in an irreversible loss of lung

286 g systemic AAT deficiency leads to pulmonary emphysema, while intracellular polymers are toxic and ca

287 aseline CT scans of 146 subjects with severe emphysema who underwent endobronchial valve LVR were ana

288 (bronchiolitis) and parenchymal destruction (emphysema), whose relative proportion varies from patien

289 75 years with severe, upper lobe-predominant emphysema with a forced expiratory volume in 1 s (FEV1)

290 with a relatively homogenous distribution of emphysema with no regional predilection.

291 ate CT measurements of airway remodeling and emphysema with PH.

292 esistant (n = 65) or susceptible (n = 64) to emphysema with severe airflow obstruction in the Pittsbu

293 PTPRO is a novel candidate gene in emphysema with severe airflow obstruction, and rs6175441

294 ntified several suggestive associations with emphysema with severe airflow obstruction, including a s

295 ns of rare genetic variation contributing to emphysema with severe airflow obstruction.

296 ave a role in the treatment of patients with emphysema with severe hyperinflation and less parenchyma

297 d, open-label Sequential Staged Treatment of Emphysema with Upper Lobe Predominance (STEP-UP) trial,

298 in hyperinflated patients with heterogeneous emphysema without collateral ventilation resulted in cli

299 EBV in patients with homogeneous emphysema without collateral ventilation results in clin

300 nal alveolar tissue without adequate repair (emphysema), yet the underlying mechanisms are poorly def