ライフサイエンスコーパス: lung parenchyma

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

2 ality for visualization of small vessels and lung parenchyma.

3 zation, subsequent to extravasation into the lung parenchyma.

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

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

6 onocytes and dendritic cells from blood into lung parenchyma.

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

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

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

10 nd morphologic maturation of the hypoplastic lung parenchyma.

11 ppress the inflammation in small airways and lung parenchyma.

12 dicating myofibroblast transformation in the lung parenchyma.

13 lobulation, and formation of the peripheral lung parenchyma.

14 lymphatic flow from the thoracic duct toward lung parenchyma.

15 merous inflammatory cells accumulated in the lung parenchyma.

16 mary cell type expressing alpha8beta1 in the lung parenchyma.

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

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

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

20 decreased inflammation of the airway and the lung parenchyma.

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

22 of this toxic granule protein throughout the lung parenchyma.

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

24 host macrophages increased in number in the lung parenchyma.

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

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

27 cans to evaluate enhancement of consolidated lung parenchyma.

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

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

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

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

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

33 model of solitary metastatic latency in the lung parenchyma.

34 and elsewhere in the bronchial epithelium or lung parenchyma.

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

36 production and leukocyte recruitment to the lung parenchyma.

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

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

39 to defective T cell localization within the lung parenchyma.

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

41 is characterized by abnormal scarring of the lung parenchyma.

42 ethering forces imposed by tidally expanding lung parenchyma.

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

44 ne CXCL1 in bronchoalveolar lavage fluid and lung parenchyma.

45 axation properties when compared with normal lung parenchyma.

46 progressive, bilateral tumor invasion of the lung parenchyma.

47 activity impeded bacterial invasion into the lung parenchyma.

48 t stress in bronchoalveolar lavage fluid and lung parenchyma.

49 reting fibroblasts and myofibroblasts in the lung parenchyma.

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

51 alveolar epithelial and endothelial cells in lung parenchyma.

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

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

54 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).

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

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

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

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

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

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

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

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

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

64 13 is necessary for eosinophils to reach the lung parenchyma and airways of vvG-immunized mice underg

65 Lung parenchyma and airways were evaluated for pattern (

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

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

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

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

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

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

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

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

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

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

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

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

78 Lung parenchyma and lesion signal intensities and vascul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 The mean lung parenchyma density values on inspiration and expira

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Analysis of lung parenchyma revealed that the inflammation in allerg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 In IPF, the lung parenchyma undergoes extensive remodeling.

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

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

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

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

184 Lung parenchyma was most often irradiated.

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

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

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

188 Lung parenchyma was prepared for histology or isolation

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

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

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

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

193 Images of lung parenchyma were examined and relative proton densit

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

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

196 In the lung parenchyma, where epithelial-mesenchymal interactio

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

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

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

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

201 Incubation of lung parenchyma with methacholine increased the activati

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

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

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

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

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