ライフサイエンスコーパス: lung parenchyma

1 (T2 signal into both the mediastinum and the lung parenchyma).

2 ype mast cells (MC(TC)s) can be found in the lung parenchyma.

3 axation properties when compared with normal lung parenchyma.

4 progressive, bilateral tumor invasion of the lung parenchyma.

5 activity impeded bacterial invasion into the lung parenchyma.

6 t stress in bronchoalveolar lavage fluid and lung parenchyma.

7 reting fibroblasts and myofibroblasts in the lung parenchyma.

8 mation of the airways and destruction of the lung parenchyma.

9 alveolar epithelial and endothelial cells in lung parenchyma.

10 ity at the molecular level in the ECM of the lung parenchyma.

11 zation, subsequent to extravasation into the lung parenchyma.

12 livered to tumor tissue instead of to normal lung parenchyma.

13 an increase in the rate of apoptosis in the lung parenchyma.

14 onocytes and dendritic cells from blood into lung parenchyma.

15 pressed in human airway epithelia as well as lung parenchyma.

16 CL10 correlated with high viral loads in the lung parenchyma.

17 rtionate to the growth of the air-exchanging lung parenchyma.

18 nd morphologic maturation of the hypoplastic lung parenchyma.

19 ppress the inflammation in small airways and lung parenchyma.

20 dicating myofibroblast transformation in the lung parenchyma.

21 lobulation, and formation of the peripheral lung parenchyma.

22 cturer variability of RFs extracted from the lung parenchyma.

23 merous inflammatory cells accumulated in the lung parenchyma.

24 mary cell type expressing alpha8beta1 in the lung parenchyma.

25 on the dynamic behavior of both ASM and the lung parenchyma.

26 without a change in compliance of the distal lung parenchyma.

27 ynamic response is of airways to that of the lung parenchyma.

28 decreased inflammation of the airway and the lung parenchyma.

29 s typical of nonciliated cells of the distal lung parenchyma.

30 of this toxic granule protein throughout the lung parenchyma.

31 igh lung volumes does not suggest changes in lung parenchyma.

32 host macrophages increased in number in the lung parenchyma.

33 l in membranes prepared from all bronchi and lung parenchyma.

34 ancies, EBV-immortalised B-cells, and normal lung parenchyma.

35 cans to evaluate enhancement of consolidated lung parenchyma.

36 proliferation cell nuclear antigen (PCNA) in lung parenchyma.

37 nse to injury contributes to GBS invasion of lung parenchyma.

38 disrupted gene were born dead and lacked the lung parenchyma.

39 an increase in the levels of collagen in the lung parenchyma.

40 lper 1 (T(H)1) cytokines and trafficked into lung parenchyma.

41 e development of diseases of the airways and lung parenchyma.

42 nd aberrant re-epithelialization of fibrotic lung parenchyma.

43 human disease with persistent destruction of lung parenchyma.

44 erentially in the transition zone to healthy lung parenchyma.

45 d as CD103+) that localize to the airways or lung parenchyma.

46 tructural deterioration of the emphysematous lung parenchyma.

47 PCSK6 protein was highly expressed in IPF lung parenchyma.

48 is (IPF) causes irreversible fibrosis of the lung parenchyma.

49 ic CD4 T cells migrate from the blood to the lung parenchyma.

50 th the mucus-lined respiratory airway and in lung parenchyma.

51 n the chest, focusing on lesions outside the lung parenchyma.

52 d remodeling of both the lung epithelium and lung parenchyma.

53 t of M1 proinflammatory macrophages into the lung parenchyma.

54 ween metabolic and structural changes in the lung parenchyma.

55 beds from which inhaled pathogens enter the lung parenchyma.

56 ated within the airway lumen rather than the lung parenchyma.

57 is characterized by abnormal scarring of the lung parenchyma.

58 ality for visualization of small vessels and lung parenchyma.

59 lymphatic flow from the thoracic duct toward lung parenchyma.

60 obe, with a tendency to occur in the central lung parenchyma.

61 une response affecting the small airways and lung parenchyma.

62 model of solitary metastatic latency in the lung parenchyma.

63 and elsewhere in the bronchial epithelium or lung parenchyma.

64 les (5-mm diameter) embedded randomly in the lung parenchyma.

65 production and leukocyte recruitment to the lung parenchyma.

66 h was measured in comparison to disease-free lung parenchyma.

67 ayers of the airway mucosa as well as in the lung parenchyma.

68 to defective T cell localization within the lung parenchyma.

69 achea and alpha2,6-linked SA residues in the lung parenchyma.

70 s to discriminate between aeration levels in lung parenchyma.

71 ethering forces imposed by tidally expanding lung parenchyma.

72 of HRCT is a very detailed depiction of the lung parenchyma.

73 ne CXCL1 in bronchoalveolar lavage fluid and lung parenchyma.

74 compared lung adenomas, lung ACs, and normal lung parenchyma, 24 developmentally regulated genes were

75 s (3.5 +/- 0.7 vs 2.9 +/- 0.5, P = .002) and lung parenchyma (3.8 +/- 0.5 vs 2.2 +/- 0.2, P < .001).

76 reas of lung scarring (56%), and hyperlucent lung parenchyma (50%).

77 ited eosinophilia of the airway (by 93%) and lung parenchyma (91%), but also significantly inhibited

78 polycythemia and hemorrhagic patches in the lung parenchyma, a pathological observation consistent w

79 r data suggest that mechanical stretching of lung parenchyma activates NF-kappaB and AP-1, at least i

80 Migration of Tg lymphocytes to the lung parenchyma after adoptive transfer was significantl

81 creased beta-catenin expression was noted in lung parenchyma after bleomycin.

82 Furthermore, examination of the lung parenchyma (an endothelial-rich tissue) shows hyper

83 ofiles of chemokines produced locally in the lung (parenchyma and bronchoalveolar lavage fluid) and s

84 osure and those of tobacco smoke exposure on lung parenchyma and airway remodeling.

85 act leukocytes from the circulation into the lung parenchyma and airway, and may also modify nonchemo

86 13 is necessary for eosinophils to reach the lung parenchyma and airways of vvG-immunized mice underg

87 Lung parenchyma and airways were evaluated for pattern (

88 D(b)NP(366-74)CD8(+) T cell response in the lung parenchyma and airways.

89 r HLMC-HLF or HLMC-HASMC interactions in the lung parenchyma and airways.

90 ung lumina within 24 h and was only found in lung parenchyma and alveolar macrophages thereafter.

91 induced accumulation of neutrophils into the lung parenchyma and alveolar space.

92 with both rejection and/or infection in both lung parenchyma and aortic endothelial cells.

93 ion of abnormal smooth muscle (ASM) cells in lung parenchyma and axial lymphatics.

94 Recruitment of eosinophils to lung parenchyma and bronchoalveolar lavage (BAL) fluid w

95 wed increased cellular infiltration into the lung parenchyma and bronchoalveolar space compared with

96 scle-alpha-actin-positive cells that destroy lung parenchyma and by the formation of benign renal neo

97 sent in high numbers in both the airways and lung parenchyma and can be distinguished from memory cel

98 cy (AATD) is characterized by destruction of lung parenchyma and development of emphysema, caused by

99 t destructive effects of the organism on the lung parenchyma and exuberant host immune responses.

100 ulating memory Th2 cells trafficked into the lung parenchyma and ignited perivascular inflammation to

101 ltration of leukemic blast cells (LBCs) into lung parenchyma and interstitium.

102 n decreases the total leukocyte count in the lung parenchyma and lavage fluid, through specific inhib

103 Lung parenchyma and lesion signal intensities and vascul

104 ltrashort echo time can be used to image the lung parenchyma and lung motion.

105 s out of total CD4 T cells is similar in the lung parenchyma and lymph nodes.

106 latory B cells, myeloid regulatory cells) in lung parenchyma and markedly decreased proliferation rat

107 cause scoliosis, pressure on the neighboring lung parenchyma and mediastinal displacement.

108 ritic cells, T cells, and eosinophils in the lung parenchyma and more eosinophils in the airway than

109 s study, we use two-photon microscopy of the lung parenchyma and note accumulation of CD11b(+) dendri

110 CDN vaccines elicit CD4 T cells that home to lung parenchyma and penetrate into macrophage lesions in

111 nic inflammation affecting predominantly the lung parenchyma and peripheral airways that results in l

112 ulted in peptide distribution throughout the lung parenchyma and pulmonary endothelium and decreased

113 ed in mice that CXCR3(+) Th1 cells enter the lung parenchyma and suppress M. tuberculosis growth, whi

114 nd type III (ecNOS) nitric oxide synthase in lung parenchyma and systemic endothelial cells with reje

115 y-venous ECs (COL15A1(neg)) localized to the lung parenchyma and systemic-venous ECs (COL15A1(pos)) l

116 ng that abnormal interdependence between the lung parenchyma and the airways is unlikely to play a ma

117 sis of CD45-expressing immune cells in whole lung parenchyma and the bronchoalveolar space of mice, e

118 d RSV-specific CD8+ T cells infiltrating the lung parenchyma and the development of pulmonary CD8+ T-

119 tial distribution of tuberculosis within the lung parenchyma and the nature of lesions with uptake (i

120 ited an increased severity of lesions in the lung parenchyma and the spleen, increased apoptosis in t

121 the alveolar and bronchiolar regions of the lung parenchyma and was associated with increased apopto

122 8 was primarily located in the AECs of human lung parenchyma and was markedly induced in IPF AECs.

123 oelastin expression were seen throughout the lung parenchyma and within the cortex of the spleen in t

124 veolar hypoxia causes vascular remodeling in lung parenchyma, and are consistent with capillary wall

125 ivity, damage to the airways and surrounding lung parenchyma, and extrapulmonary factors.

126 ere identified in both the airway lumens and lung parenchyma, and in some instances in close proximit

127 d CS-induced inflammatory cell infiltrate in lung parenchyma, and inhibited adhesion of CS-stimulated

128 inophilic crystal deposition, destruction of lung parenchyma, and pulmonary hemorrhage).

129 ells expressing the same TCR in the airways, lung parenchyma, and spleen following influenza virus in

130 sue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did n

131 ergy required to cause visible damage to the lung parenchyma are lacking.

132 Since the peripheral airways and lung parenchyma are supplied by the pulmonary circulatio

133 marrow-derived cells engrafted in recipient lung parenchyma as cells with the morphological and mole

134 5.68; p < 0.001), and the extent of affected lung parenchyma assessed visually (stage 1vs4 OR 10.36;

135 the structural abnormalities of the neonatal lung parenchyma associated with premature birth.

136 rized by inflammation and/or fibrosis of the lung parenchyma associated with progressive dyspnea that

137 en deposition, and the restrictive nature of lung parenchyma associated with pulmonary fibrosis.

138 quired for the presence of CD103+ DCs in the lung parenchyma at baseline and for their sufficient act

139 e both morphologic and functional changes of lung parenchyma at low-field-strength MRI in children an

140 ity), increased hyaluronan deposition in the lung parenchyma (attributed to asthma progression), and

141 localization of T cell responses within the lung parenchyma between pathogens that can replicate loc

142 Time-activity curves for tumor and normal lung parenchyma binding were generated using the region-

143 of mRNA for ecNOS decreased significantly in lung parenchyma but not in aortic endothelial cells from

144 tes dysanaptic lung growth by increasing the lung parenchyma but not the airways.

145 buted to the increasing number of DCs in the lung parenchyma, but not in the airway mucosa.

146 d that neutrophil numbers were normal in the lung parenchyma, but reduced in the airspace.

147 Given that COVID-19 primarily affects the lung parenchyma by causing pneumonia, our directive is t

148 olon and lung, and infiltration of colon and lung parenchyma by eosinophils and mast cells.

149 This led to infiltration of the colon and lung parenchyma by eosinophils and mast cells.

150 the average rate of Th1 cell entry into the lung parenchyma by half, while CX3CR1 deficiency doubles

151 acterized by infiltration of the airways and lung parenchyma by inflammatory cells.

152 sinophils were visualized and quantitated in lung parenchyma by means of immunostaining.

153 which the immune response is focused on the lung parenchyma by transfer of Th2 cells from a novel TC

154 memory CD4 and CD8 T cells isolated from the lung parenchyma can be rescued by stimulation with exoge

155 scans of the chest, bronchial disorders and lung parenchyma cavities were the most frequent abnormal

156 t only in the pleural cavity but also in the lung parenchyma, conferring significantly prolonged surv

157 ents with cardiogenic edema, and five normal lung parenchyma controls were enrolled from 2004 to 2006

158 --including blood vessels, mesentery tissue, lung parenchyma, cornea and blood clots--stiffen as they

159 cidation of the biology of stem cells of the lung parenchyma could revolutionise treatment of patient

160 g between the bronchovascular bundle and the lung parenchyma, decreasing lung compliance without impa

161 The mean lung parenchyma density values on inspiration and expira

162 mbrane disruptions between small airways and lung parenchyma depends on the type of injurious mechani

163 y visible changes in the proximal airway and lung parenchyma despite provoking AHR, the OVA challenge

164 a2(-/-)) bone marrow-derived macrophages and lung parenchyma displayed significantly larger capsules

165 nhibiting interleukin (IL)-6 generation from lung parenchyma during an alloimmune response.

166 ut a rate four times slower than that of the lung parenchyma during rapid lung inflation and deflatio

167 e or mechanical coupling between airways and lung parenchyma during the inflammatory processes that o

168 et of PD-1(+) cells is maintained within the lung parenchyma during tuberculosis (TB).

169 technique due to the high-resolution for the lung parenchyma evaluation, the study of the vascular sy

170 d for extent of decreased attenuation of the lung parenchyma; expiration CT scans were scored for ext

171 jority of the CD8 T cells in the airways and lung parenchyma expressed CD49a, the alpha-chain of the

172 After manual segmentation of the lung parenchyma, flow-volume loops of each voxel were co

173 of 1280 patients to localize parietal pleura/lung parenchyma followed by classification of COVID-19 p

174 In contrast, apoptosis in the liver and lung parenchyma following IL-2 therapy was blocked compl

175 owever, to date extensive examination of the lung parenchyma for the expression of destructive enzyme

176 -kappaB-regulated enzyme, was also higher in lung parenchyma from asthmatic mice than in normal mice.

177 smoke-induced experimental COPD and in human lung parenchyma from COPD donors.

178 alveolar stem cell source for restoring the lung parenchyma from genetic or environmentally induced

179 y in its late stages when a great portion of lung parenchyma has been already destroyed by the diseas

180 f the tumor (A2) was marked; it included all lung parenchyma having any tumor cells.

181 average, radiologists searched 26.7% of the lung parenchyma in 3 minutes and 16 seconds and encompas

182 allowing them to invade and bronchiolize the lung parenchyma in a process reminiscent of submucosal g

183 n reduced in lung fibroblasts from human and lung parenchyma in experimental COPD.

184 lar landscape of upper and lower airways and lung parenchyma in healthy lungs, and lower airways in a

185 higher perfusion between the tumor edge and lung parenchyma in hypoxic tumors.

186 ration of augmentation treatment to preserve lung parenchyma in individuals with emphysema secondary

187 Small, low-signal regions were seen in the lung parenchyma in preterm but not in term infants, whic

188 al growth and differentiation of airways and lung parenchyma in response to ICS pose risks for develo

189 acity to rapidly migrate within the infected lung parenchyma in response to influenza infection.

190 ary edema and neutrophil infiltration in the lung parenchyma in response to subacute alveolar hypoxia

191 gate how AHR manifests in the airway and the lung parenchyma in vivo following exposure to different

192 d continue cell-cycle progression within the lung parenchyma in vivo.

193 d repair between proximal airways and distal lung/parenchyma in asthma and other respiratory diseases

194 Cryptococcus, Treg cells accumulated in the lung parenchyma independently of priming in the draining

195 nt mediator of neutrophil migration from the lung parenchyma into the airspace.

196 roposes that spread of organisms outside the lung parenchyma is essential to induce adaptive immunity

197 showed that expression of TOLLIP gene in the lung parenchyma is globally lower in IPF compared to con

198 Diagnosis of fungal infection in lung parenchyma is relatively difficult.

199 essive inflammation in the small airways and lung parenchyma, is mediated by the increased expression

200 Mechanical stretching of lung parenchyma led to increased activation of NF-kappaB

201 ients with comorbidities, moderate extent of lung parenchyma lesions but significant hypoxemia, infla

202 hest CT performed at admission the extent of lung parenchyma lesions was established by artificial in

203 y (92% vs. 70%) than CT for the detection of lung parenchyma lesions; however, the sensitivity was be

204 rion standard imaging modality to assess the lung parenchyma, may not accurately and reliably disting

205 The following study examines the lung parenchyma of 23 patients with emphysema and 8 norm

206 ere identified within airways and alveoli in lung parenchyma of 40% of severe acute respiratory syndr

207 Eosinophils (Eos) accumulate in airways and lung parenchyma of active asthmatics.

208 ing virus in the upper and lower airways and lung parenchyma of nonhuman primates following high-dose

209 NA, protein, and activity are present in the lung parenchyma of patients with emphysema and not in th

210 is used to quantify abnormal changes in the lung parenchyma of smokers that might overlap chronic ob

211 Subtle interstitial changes in the lung parenchyma of smokers, known as Interstitial Lung A

212 upregulated small noncoding RNA in blood and lung parenchyma of TB patients and during murine TB.

213 In the large subgroup of men with normal lung parenchyma on chest radiograph at baseline, there w

214 The extent of affected lung parenchyma on CT images demonstrates prognostic val

215 echanical stretch and induced stimulation of lung parenchyma on the activation of proinflammatory tra

216 ns that are either CXCR3(hi) and localize to lung parenchyma or are CX3CR1(hi)KLRG1(hi) and are retai

217 e of lymphadenopathy or abnormalities in the lung parenchyma or interstitium.

218 of 29 positive lesions involved the pleura, lung parenchyma, or chest wall and were all (18)F-FDG av

219 sponsiveness, eosinophil infiltration of the lung parenchyma, or IL-5 production in the local lymph n

220 hest CT is useful to evaluate changes in the lung parenchyma over time.

221 Absorbed dose to tumors and lung parenchyma per unit activity in lung tumors was cal

222 c multifunctional CD4 and CD8 T cells to the lung parenchyma prior to challenge and indicated the rou

223 on, which better reflects the dose to normal lung parenchyma, ranged from 4.9 to 55 Gy.

224 lity of CD4 T cells to efficiently enter the lung parenchyma rather than produce high levels of IFN-g

225 mulation in the lung-draining lymph node and lung parenchyma relative to a primary infection.

226 activation/apoptosis, and ultimately loss of lung parenchyma resembling emphysema.

227 s characterized by excessive scarring of the lung parenchyma, resulting in a steady decline of lung f

228 Analysis of lung parenchyma revealed that the inflammation in allerg

229 h 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals.

230 act caveolar membrane system, the Cav-2-null lung parenchyma shows hypercellularity, with thickened a

231 Jacobian maps demonstrated lung parenchyma shrinkage of the posterior lung bases in

232 In tracheal rings and lung parenchyma strips, OVA caused a concentration-depen

233 ies performed on small-airway epithelium and lung parenchyma, suggesting that transcriptomic alterati

234 The change in HU seen in the non-vessel lung parenchyma suggests this metric is a potential biom

235 stently developed more severe disease in the lung parenchyma than did female mice.

236 ial lymph nodes, bronchoalveolar lavage, and lung parenchyma than in mice bearing lung tumors alone.

237 hat hyperpnea has significant effects on the lung parenchyma that contribute to airflow limitation in

238 x of inflammatory cells into the airways and lung parenchyma that occurs in COPD, including adhesion

239 x of inflammatory cells into the airways and lung parenchyma that occurs in COPD; these include agent

240 muscle had slower dynamic responses than the lung parenchyma, the timing of the deep inspiratory mane

241 e persistence of CD8 effector T cells in the lung parenchyma, thereby allowing the transition to Trm.

242 the control cells that were scattered in the lung parenchyma, throughout the alveolar region.

243 Lung parenchyma TNF-alpha, DNA damage-inducible transcri

244 ts isolated from proximal airways and distal lung parenchyma to determine phenotypic differences.

245 e than 50%) and for air trapping (failure of lung parenchyma to increase in attenuation during expira

246 at different time points tissue biopsies of lung parenchyma to isolate RNA and DNA to identify each

247 plastic compensatory growth of the remaining lung parenchyma to restore normal lung mass, structure,

248 cells migrate from the pleural space to the lung parenchyma to secrete polyreactive emergency immuno

249 asound, which can also be used to assess the lung parenchyma, to identify pleural fluid; CT scanning

250 features were extracted from the subpleural lung parenchyma traversed by needle.

251 howed a wide area without ventilation in the lung parenchyma treated with SPACE.

252 characterized by extensive remodeling of the lung parenchyma, ultimately resulting in respiratory fai

253 In IPF, the lung parenchyma undergoes extensive remodeling.

254 al CD4 T cells migrate rapidly back into the lung parenchyma upon adoptive transfer, whereas the intr

255 ed from the ratio between maximal uptake and lung parenchyma uptake.

256 red fluorescence fiberoptic bronchoscopy, in lung parenchyma using intravital microscopy, and in the

257 Both ventilated and perfused lung parenchyma (ventilation-perfusion [V/Q] match) was

258 f mRNA encoding some, but not all ECM in the lung parenchyma was attenuated in RELM-beta-/- mice.

259 Lung parenchyma was most often irradiated.

260 s marked; it included only solid tumor where lung parenchyma was no longer preserved.

261 dependent migration of CF monocytes into the lung parenchyma was normal, whereas, in contrast, integr

262 No difference in lung parenchyma was observed by light microscopy.

263 Lung parenchyma was prepared for histology or isolation

264 Image quality of pulmonary arteries and lung parenchyma was scored on a four-point-scale (1 = po

265 For image and statistical analysis, the lung parenchyma was segmented as a region of interest by

266 Lung parenchyma was segmented using a Gaussian mixture m

267 nal-to-noise ratio in pulmonary arteries and lung parenchyma was significantly higher for UTE than fo

268 Receptor density in distal arteries and lung parenchyma was twofold greater (p < 0.05) in pulmon

269 determined by leakage of [125I]albumin into lung parenchyma) was significantly diminished.

270 The densities of lung parenchyma were evaluated by quantitative computed

271 The dynamic changes of the airway and lung parenchyma were evaluated with ultra-high-resolutio

272 Images of lung parenchyma were examined and relative proton densit

273 produced by nonciliated epithelial cells in lung parenchyma were lacking.

274 nd volumes of high- and low-signal intensity lung parenchyma were quantified by segmentation and thre

275 In the lung parenchyma, where epithelial-mesenchymal interactio

276 n of leukemic or maturing myeloid cells into lung parenchyma, which is sometimes associated with pleu

277 rolled proliferation of LAM cells within the lung parenchyma, which results from loss-of-function mut

278 e and recurrent extensive BAC limited to the lung parenchyma who underwent lung transplantation with

279 develop multifocal tumors embedded in normal lung parenchyma with a longer latency.

280 and submillimeter imaging of the bronchi and lung parenchyma with high CNR and SNR and may be an alte

281 Incubation of lung parenchyma with methacholine increased the activati

282 produced by H226 cells were confined to the lung parenchyma with no PE.

283 isorders characterized by replacement of the lung parenchyma with scar tissue.

284 ear to actively search less than half of the lung parenchyma, with substantial interreader variation

285 (18)F-alpha(v)beta(6)-BP was noted in normal lung parenchyma, with uptake being elevated in areas cor

286 volume s) were defined as the portion of the lung parenchyma within 50 pixels (approximately 3 cm) of

287 recurrent or unresectable BAC limited to the lung parenchyma without nodal involvement and (2) suitab