ライフサイエンスコーパス: emphysema

1 n of RAGE prevents development of CS-induced emphysema.

2 derstanding the genetics and pathogenesis of emphysema.

3 X, which activates DSBs repair signaling, in emphysema.

4 entrations is associated with progression of emphysema.

5 D and can be used to predict the severity of emphysema.

6 tive immune cells to the lungs and developed emphysema.

7 and inspiratory chest CT to quantify percent emphysema.

8 use and is causative for bronchiectasis and emphysema.

9 ia and features of lung injury that resemble emphysema.

10 associated with greater increases in percent emphysema.

11 cted in the peripheral blood of smokers with emphysema.

12 he only well established cause of hereditary emphysema.

13 failed to develop pulmonary inflammation or emphysema.

14 ed NHEJ may contribute to ATII cell death in emphysema.

15 e reduction involving 2794 participants with emphysema.

16 demonstrated benefit in severe heterogeneous emphysema.

17 was inversely correlated with the extent of emphysema.

18 aimed at reducing hyperinflation in advanced emphysema.

19 ases such as asthma, chronic bronchitis, and emphysema.

20 s AAT replacement therapy is therapeutic for emphysema.

21 pulations including smokers and persons with emphysema.

22 cs, smoking history, and computed tomography emphysema.

23 exposure produces predominantly right-sided emphysema.

24 lid nodules, and more nodule spiculation and emphysema.

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

26 levels in sera is responsible for pulmonary emphysema.

27 linical improvement for patients with severe emphysema.

28 n and gene coexpression in bronchiolitis and emphysema.

29 ing progressive small airway remodelling and emphysema.

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

31 that EBVs are also effective in homogeneous emphysema.

32 5416, a VEGFR2 inhibitor, was used to induce emphysema.

33 the lungs leading to AAT deficiency-related emphysema.

34 ubjects had minimal radiographic evidence of emphysema.

35 t 5 years compared with those without visual emphysema.

36 art failure, cancer, chronic bronchitis, and emphysema.

37 g/L +/- 1.3 (P < .001) for those with trace emphysema.

38 g/L +/- 1.0 (P < .001) for those with trace emphysema.

39 h a study population for treatment trials of emphysema.

40 l outcomes for those with and without visual emphysema.

41 tivity, airway obstruction, inflammation and emphysema.

42 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

43 d cysts (76%), ground-glass opacities (73%), emphysema (49%), and reticulations (39%).

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

45 itectures was trained to classify pattern of emphysema according to Fleischner criteria.

46 ep learning algorithm as having any grade of emphysema (adjusted hazard ratios were 1.5, 1.7, 2.9, 5.

47 mice.Methods: Mouse lungs were examined for emphysema after either the loss or the overexpression of

48 Patients with orbital emphysema after vitreoretinal surgery who were diagnosed

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

50 aortic diameter, quantitative evaluation of emphysema, airway wall thickness, and expiratory gas tra

51 7 [95% confidence interval {CI}: 1.4, 4.9]), emphysema along the needle path (P = .02, OR = 2.1 [95%

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

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

54 olume in 1 second (FEV(1)) and CT-quantified emphysema and air trapping in smokers.

55 Conclusion CT measures of emphysema and air trapping increased over 5 years in smo

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

57 ification of novel quantitative measures for emphysema and airway disease, evaluation of dose reducti

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

59 Emphysema and chronic obstructive lung disease were prev

60 ciency (AATD) is associated with early-onset emphysema and chronic obstructive pulmonary disease.

61 usly reported a negative correlation between emphysema and circulating glycosphingolipids (GSLs).

62 ship between computed tomography measures of emphysema and distal pulmonary arterial morphology with

63 etylcystein significantly improved pulmonary emphysema and dysfunction.

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

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

66 The manifestation of emphysema and fibrosis within a 10-mm radius of the CP-N

67 ciated with increased symptoms, radiographic emphysema and gas trapping, exacerbations, and progressi

68 emphysema visual subtypes and progression of emphysema and gas trapping.

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

70 ditional insight into the pathophysiology of emphysema and inflammatory lung diseases.

71 tracellular protein inclusions, causing lung emphysema and liver cirrhosis.

72 TD) is an inherited disease characterized by emphysema and liver disease.

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

74 e (adjusted for lung volume) as a measure of emphysema and percentage of lung volume with attenuation

75 y was found with the qualitative scoring for emphysema and presence and inhomogeneous attenuation.

76 Pulmonary functional abnormalities, such as emphysema and restrictive lung diseases, are frequently

77 hich large airway wall abnormalities precede emphysema and small airway dysfunction.

78 normal structure-function results related to emphysema and small airways disease, both of which were

79 d lung parenchymal diseases, such as asthma, emphysema, and chronic bronchitis, or to alleviate recur

80 e been detected in the serum of smokers with emphysema, and elastin-specific T cells have also been d

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

82 s associated with increased gas trapping and emphysema, and higher rates of progression to COPD at 5

83 ne studies have linked TGF-beta signaling to emphysema, and human genome-wide association studies (GW

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

85 obstruction associated with inflammation and emphysema, and it is currently one of the leading causes

86 nous factor that prevents the development of emphysema, and its upregulation has the potential to fos

87 d-glass-opacity, bronchiectasis, cicatricial emphysema, and lobar atelectasis were similar in the two

88 ress-influenced diseases, such as pneumonia, emphysema, and lung cancer following exposure to environ

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

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

91 ller than 5 mm(2) in cross section (BV5), CT emphysema, and pectoralis muscle area were retrospective

92 ls of lung volume reduction in patients with emphysema, and we did an updated search on Embase and Pu

93 were used to explore the association between emphysema, arterial BV5, and RV(EV) with exercise capaci

94 Neither emphysema score nor emphysema as a dichotomous variable was an independent p

95 The identification of emphysema as a shared risk factor suggests that addition

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

97 Emphysema as such had no effect on pneumothorax rate, bu

98 lculated by using Cox regression models with emphysema as the main predictor.

99 was significantly associated with increasing emphysema assessed quantitatively using CT imaging and l

100 al presence of mild, moderate, and confluent emphysema at baseline CT showed a mean decline in lung d

101 se with visual presence of mild and moderate emphysema at baseline CT showed a mean decline in lung d

102 Conclusion The pattern of parenchymal emphysema at baseline CT was an independent predictor of

103 arning automation of the Fleischner grade of emphysema at chest CT is associated with clinical measur

104 BackgroundPattern of emphysema at chest CT, scored visually by using the Flei

105 dard deviation]) had trace or greater visual emphysema at CT and 51.7% (2116 participants; 1068 men a

106 At 5 years, participants with visual emphysema at CT demonstrated progressive airflow obstruc

107 Conclusion The presence of visual emphysema at CT in current and former Global Initiative

108 Greater percent emphysema at CT was associated with greater regurgitant

109 Percent emphysema at CT was associated with statistically signif

110 e whether participants with visually evident emphysema at CT were more likely to have progressive dis

111 1048 women; mean age, 56 years +/- 8) had no emphysema at CT.

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

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

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

115 Rationale: Endothelial injury may provoke emphysema, but molecular pathways of disease development

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

117 ution can be used to determine the extent of emphysema by using both qualitative visual scoring and f

118 higher (320 x 320 pixels) resolution inputs, emphysema, cardiomegaly, hernia, and pulmonary nodule de

119 ixels for binary decision networks targeting emphysema, cardiomegaly, hernias, edema, effusions, atel

120 ciation with COPD-related phenotypes such as emphysema, chronic bronchitis, and hypoxemia.

121 In the COPDGene test cohort, deep learning emphysema classification improved the fit of linear mixe

122 Deep learning emphysema classifications were associated with impaired

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

124 rypsin had greater computed tomography-based emphysema compared with those without rare variants.

125 Although orbital emphysema constitutes a very unusual complication of vit

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

127 Percent emphysema, defined as the percent of lung pixels less th

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

129 s a novel role for FSTL-1 protecting against emphysema development independent of smoke exposure.

130 damage in alveolar type II (ATII) cells and emphysema development.

131 bstructive pulmonary disease and may precede emphysema development.

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

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

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

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

136 otentially contribute to the pathogenesis of emphysema distribution.

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

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

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

140 Qualitative scoring of emphysema extent was performed by two readers.

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

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

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

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

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

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

147 ater grades of emphysema severity within the emphysema group.

148 RATIONALE: Emphysema has considerable variability in the severity a

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

150 uction procedures in the treatment of severe emphysema have shown excellent results in selected patie

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

152 well-controlled HIV and minimal radiographic emphysema, HIV infection contributes to pulmonary perfus

153 This FSTL-1-deficient emphysema implicates regulation of immune tolerance in l

154 o identify the genetic ecause of early-onset emphysema in a five-generation French-Canadian family fr

155 , could attenuate aortic root remodeling and emphysema in a mouse model of MFS.

156 Results: EC Hif-2alpha deletion resulted in emphysema in association with fewer ECs and pericytes.

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

158 variation affecting the TGF-beta pathway to emphysema in humans.

159 r Notch3 signaling plays a role in pulmonary emphysema in MFS.

160 at Notch3 signaling contributes to pulmonary emphysema in mgR mice.

161 -cell (EC) HIF-2alpha in the pathogenesis of emphysema in mice.Methods: Mouse lungs were examined for

162 ndent predictor of subsequent progression of emphysema in participants who are current or former ciga

163 oducibly quantified the volumetric extent of emphysema in participants with chronic obstructive pulmo

164 rt echo time (UTE) MRI for the assessment of emphysema in patients with chronic obstructive pulmonary

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

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

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

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

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

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

171 he gene PTPN6 is responsible for early-onset emphysema in this family.

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

173 alveolar ductitis with B-cell follicles and emphysema, in lung tissue samples from control subjects,

174 ults: FSTL-1 Hypo mice developed spontaneous emphysema, independent of smoke exposure.

175 0.20 (%LSV(0.20)) at MRI were the respective emphysema indexes.

176 this biomechanical stress likely influences emphysema initiation and progression.

177 Severe emphysema is a debilitating condition with few treatment

178 Advanced emphysema is a lung disease in which alveolar capillary

179 : The loss of pulmonary endothelial cells in emphysema is associated with increased lung ceramide.

180 Emphysema is characterized by alveolar wall destruction

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

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

183 expression of this endogenous factor causes emphysema; its pivotal protective function is suggested

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

185 was delayed by SIL treatment, and the severe emphysema-like alveolar destruction was prevented.

186 t agents exhibited a significant decrease in emphysema-like pathology compared to vehicle-treated mic

187 tivation in MVPC was sufficient to elicit an emphysema-like phenotype characterized by increased MLI,

188 Human emphysema lung samples exhibited reduced EC HIF-2alpha e

189 the destruction of alveolar walls leading to emphysema, making it potentially a valid target for phar

190 t heart in individuals with chronic COPD and emphysema.Materials and MethodsThe Multi-Ethnic Study of

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

192 0.7) and greater progression in quantitative emphysema measured by 15th percentile lung density (-3.3

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

194 OPD-related phenotypes, such as quantitative emphysema measures, have been found.

195 udy, we report an animal model of autoimmune emphysema mediated by the loss of tolerance to elastin.

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

197 Compared with participants without emphysema, mortality was greater in participants classif

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

199 disease (normal CT, not ventilated) and mild emphysema (normal CT, abnormal ADC) were negatively corr

200 , and III/IV disease, respectively) and mild emphysema (normal CT, abnormal apparent diffusion coeffi

201 xpression is important in the development of emphysema.Objectives: The objective of this study was to

202 rgical approaches are needed to treat severe emphysema.Objectives: To evaluate the effectiveness and

203 nambiguous expression of the typical form of emphysema observed in this family).

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

205 he clinical significance of visually evident emphysema on CT images in individuals without spirometri

206 ung volume reduction in patients with severe emphysema on maximal medical treatment has clinically me

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

208 Emphysema or reduced diffusion capacity was observed in

209 ted in smokers, but were not associated with emphysema or severity of airflow limitation.

210 ot having asthma, rhinitis, eczema, allergy, emphysema, or chronic bronchitis as diagnosed by a docto

211 HU (0.17 vs -0.20) than participants without emphysema (P < .001 for each).

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

213 .003), and greater computed tomography-based emphysema (P = 0.02) compared with 1,411 white individua

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

215 Gender of the patient (p = 0.7761), emphysema (p = 0.2724), site of the lesion (p = 0.9320),

216 oderate, confluent, and advanced destructive emphysema; P < .05).ConclusionDeep learning automation o

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

218 duction in response to CS may be involved in emphysema pathogenesis, associated with autophagy with i

219 urposeTo determine whether participant-level emphysema pattern could predict impairment and mortality

220 Centrilobular was the predominant emphysema pattern occurring alone (36.5%) or in combinat

221 Background The correlation between visual emphysema patterns and subsequent progression of disease

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

223 We performed the largest GWAS of emphysema patterns to date, identifying 10 GWAS loci inc

224 associated with greater increases in percent emphysema per 10 years (O3: 0.13 per 3 parts per billion

225 In fully adjusted models, higher emphysema percentage (beta = -4.2; 95% confidence interv

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

227 rare SERPINA1 variants on lung function and emphysema phenotypes in subjects with significant tobacc

228 0.4%), in which small airway dysfunction and emphysema precede large airway wall abnormalities, and a

229 Among COPD phenotypes, emphysema predominant was the commonest (44.3%), followe

230 eliably categorise COPD into phenotypes like emphysema predominant, airway predominant, or mixed, whi

231 COPD was categorised into the following: emphysema predominant; airway predominant; or mixed phen

232 cantly higher (1.94 +/- 0.28 mm) than in the emphysema-predominant subgroup (1.79 +/- 0.23 mm) with a

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

234 in one second accounted for less than 10% of emphysema progression and less than 50% of air trapping

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

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

237 The rate of quantitative emphysema progression increased with greater grades of e

238 d 50% of normal; however, outside of slowing emphysema progression, its effects in other clinical out

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

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

241 This new autoimmune model of emphysema provides a useful tool to examine the immunolo

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

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

244 For a given amount of emphysema, relative preservation of the arterial BV5 was

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

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

247 Emphysema, reticulation, and honeycombing were separatel

248 Neither emphysema score nor emphysema as a dichotomous variable

249 were used to evaluate relationships between emphysema scores and survival.

250 2011 included those with baseline CT, visual emphysema scores, and survival data through 2018.

251 progression increased with greater grades of emphysema severity within the emphysema group.

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

253 ledge, this is the second form of hereditary emphysema since the discovery of A1AT deficiency in the

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

255 smoking model and twenty genes with previous emphysema studies.

256 usly unreported rare variant contributing to emphysema susceptibility.

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

258 ic bronchitis, small airway obstruction, and emphysema that represents a leading cause of death world

259 bnormalities, visual presence and pattern of emphysema, the ratio of pulmonary artery to ascending ao

260 se inhibitors and predisposes to early-onset emphysema through a loss-of-function mechanism.

261 1 antitrypsin deficiency, lung function, and emphysema, thus significantly increasing the frequency o

262 ntrol smokers, nonsmokers, and patients with emphysema to determine DNA damage and repair.

263 his complication and patients suffering with emphysema, typically receiving donor lungs smaller than

264 were used to explore the association between emphysema, venous BV5, pectoralis muscle area, and LV(EV

265 lore the relationships between CT metrics of emphysema, venous vascular volume, and sarcopenia with t

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

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

268 evaluate the potential relationship between emphysema visual subtypes and progression of emphysema a

269 ogy and function, the effects of SIL against emphysema warrant further investigation in the settings

270 Median percent emphysema was 3% at baseline and increased a mean of 0.5

271 me between vitreoretinal surgery and orbital emphysema was 8 days (interquartile range [IQR] 5-15 day

272 Although emphysema was also significantly associated with lower F

273 Emphysema was assessed by CT and perfusion by (13)N ((13

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

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

276 Quantitative evaluation of emphysema was done using inbuilt software, and volume of

277 Emphysema was identified in 38% of patients.

278 Emphysema was quantified by using adjusted lung density

279 Using a murine model of elastase-induced emphysema we demonstrated that the most potent agents ex

280 in cross-section), and objective measures of emphysema were extracted from 3,506 COPDGene computed to

281 y members with computed tomography-confirmed emphysema were heterozygotes for the Ala455Thr mutation.

282 Lungs from patients with emphysema were measured for endothelial HIF-2alpha expre

283 ance of the mutation and variable degrees of emphysema were observed in never smokers.

284 Fibrosis and emphysema were present in 66 (17.7%) and 95 (25.5%) pati

285 40 years or older with severe, heterogeneous emphysema were randomized 2:1 to SVS with medical manage

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

287 f-2alpha-knockout mice developed more severe emphysema, whereas EC Hif-2alpha-overexpressing mice wer

288 ed DJ-1 and XLF interaction in ATII cells in emphysema, which suggests the impairment of their functi

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

290 nrelated individuals (n=80) with and without emphysema who underwent surgery for lung cancer at our i

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

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

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

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

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

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

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

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