ライフサイエンスコーパス: airspace

1 y excessive neutrophil infiltration into the airspace.

2 apoptotic cells, contributing to the loss in airspace.

3 ive neutrophils, CXCL2, and TNF-alpha in the airspace.

4 ect migration of virus-infected AMs from the airspace.

5 ed recruitment of mononuclear cells into the airspace.

6 leading to epithelial expansion and loss of airspace.

7 important immune effector cells of the lung airspace.

8 avage to recover human cancer cells from the airspace.

9 l in the lung parenchyma, but reduced in the airspace.

10 migration from the lung parenchyma into the airspace.

11 asation of protein-rich edema fluid into the airspace.

12 kocyte infiltration into the bronchoalveolar airspace.

13 epithelial migration of neutrophils into the airspace.

14 e airway-adjacent DCs to the contents of the airspace.

15 cruitment to, and cytokine induction in, the airspace.

16 signed to remove other drones from protected airspace.

17 nocyte chemoattractant concentrations in the airspaces.

18 h attenuated neutrophil recruitment into the airspaces.

19 eading to enhanced neutrophil recruitment to airspaces.

20 ts by instillation of acid (pH 1.5) into the airspaces.

21 dance at the basolateral membranes of distal airspaces.

22 ium, whereas sFasL is present throughout the airspaces.

23 of water-soluble antioxidants in the distal airspaces.

24 easing distances (up to 160 microm) from the airspaces.

25 hils and eosinophils, respectively, into the airspaces.

26 ng-positive cells in the alveolar septae and airspaces.

27 radiolabelled albumin was instilled into the airspaces.

28 with the mean linear intercept (Lm) of those airspaces.

29 and accumulating PGP and neutrophils in the airspaces.

30 arrier to the free diffusion of solutes into airspaces.

31 ulting in permanently scarred, nonfunctional airspaces.

32 noculum could be harvested from the alveolar airspace 3 h later.

33 ion of a protein solution instilled into the airspaces 5 h after the onset of haemorrhage.

34 /Delta) mice developed lung inflammation and airspace abnormalities associated with the accumulation

35 nificantly reduced levels of circulating and airspace acute-phase proteins, exhibited significantly e

36 increased fluid flux from the blood into the airspaces, additional experiments were carried out in wh

37 d proliferation within the alveolar wall and airspace after lung injury can lead to the development o

38 2 is shed from fibroblasts into the alveolar airspace after lung injury.

39 gas-phase (129)Xe emerging in the pulmonary airspaces after intravenous injection has the potential

40 y compared with control mice as evidenced by airspace albumin content, lung liquid accumulation, and

41 osmotic water permeability (Pf) between the airspace and capillary compartments.

42 molecule transport in a composite medium of airspace and cells.

43 ation drawdown capacity in the intercellular airspace and chloroplast stroma.

44 in ligands and alpha4 integrins to enter the airspace and interstitium during the response to SRBC.

45 brogenesis involves remodeling of the distal airspace and parenchyma of the lung, and is characterize

46 he relationship of cell size and patterning, airspace and photosynthesis by promoting and repressing

47 by impairing both chemokine induction in the airspace and PMN chemotaxis, thereby compromising pulmon

48 cilitating immune cell infiltration into the airspace and providing a more favorable replicative envi

49 and microvascular permeability, and altered airspace and serum cytokines after LPS.

50 re coupled with dramatic expansion of distal airspace and surface area.

51 on speeds clearance of excess fluid from the airspace and that CFTRs effect on active Na+ transport r

52 Water permeability measured between the airspace and vasculature in intact sheep and mouse lungs

53 Pf measured between the airspace and vasculature in the perfused fluid-filled ra

54 pidemia impacts responses to bacteria in the airspace and, if so, whether differently from its effect

55 n the levels of active collectins within the airspaces and distal airways may increase susceptibility

56 Enlargement of alveolar airspaces and fibrosis were detected as early as 1 week

57 CS exposure acidified the airspaces and induced localization of the LTA4H protein

58 n of excessive fluid (edema) in the alveolar airspaces and leads to hypoxemia and death if not correc

59 in-induced accumulation of leukocytes in the airspaces and neutrophil chemotaxis.

60 epletion increases the dimensions of aerated airspaces and that lung recruitment reverses these chang

61 characterized by inflammation and dysmorphic airspaces and vasculature.

62 e density (decreasing the relative volume of airspace) and by altering the pattern of airspace distri

63 mortality, an increase in neutrophils in the airspace, and increases in tissue myeloperoxidase (MPO).

64 -2) and chemokine (KC) concentrations in the airspaces, and lung microvascular permeability compared

65 In acute lung injury, the distal airspace antioxidants ascorbate, urate, and glutathione

66 nt mice that have significantly reduced lung airspace APN but high serum APN levels had pulmonary inf

67 last or apoplast as a liquid, or through the airspace as vapor, but the dominant path remains in disp

68 omotes enhanced cellular infiltrate into the airspace, as well as increased concentration of the 12-l

69 may promote fracturing of the alveolar blood:airspace barrier.

70 nt TLR response phenotypes and dysregulating airspace/blood compartmental levels of PMNs and cytokine

71 fferently from its effects in other tissues, airspace, bloodstream, and i.p. responses to LPS and Kle

72 increased markers of oxidative stress in the airspaces, breath, blood, and urine of smokers and of pa

73 ma5(fl/-) lungs had dilated, enlarged distal airspaces, but basement membrane ultrastructure was pres

74 ion and soluble CX3CL1 was detectable in the airspaces, but cx3cr1(GFP/GFP) and cx3cr1(GFP/+) mice fa

75 enuates breast cancer cell invasion into the airspace by 33% when quantified by lavage recovery and u

76 lculate the volume of fluid cleared from the airspaces by mass balance.

77 This resulted in accumulation of PGP in the airspaces by suppressing the LTA4H aminopeptidase activi

78 ant treatment with N-acetylcysteine improved airspace caliber and attenuated oxidative stress and apo

79 ape-like clusters of delicate gas-exchanging airspaces called pulmonary alveoli.

80 Airspace-capillary osmotic water permeability (P(f)) was

81 Airspace-capillary osmotic water permeability (Pf) was m

82 lar endothelium is a significant barrier for airspace-capillary osmotic water transport.

83 Acid instillation into the distal airspaces caused an increase in the alveolar epithelial

84 AL) is a procedure for sampling the terminal airspace cell population to diagnose alveolitis, a condi

85 n in humans and experimental animals include airspace collapse, reduced lung compliance, and impaired

86 ice lacking CARM1 have substantially reduced airspace compared with their wild-type littermates.

87 d epithelial proliferation in the airway and airspace compartments during development.

88 Transport of water between the capillary and airspace compartments in lung encounters serial barriers

89 Clinically relevant airspace concentrations of beta2-adrenergic agonists a)

90 the selectin ligand-deficient cells into the airspace, confirming that its contribution is in part in

91 , pulmonary opacity (ground-glass opacity or airspace consolidation), interlobular septal thickening,

92 Lung parenchymal abnormalities that included airspace consolidation, ground-glass opacity (GGO), reti

93 ation, fibrosis, and enlargement of alveolar airspaces; conversely, CVT-6883-treated ADA-deficient mi

94 age of lung development, including undilated airspaces, cuboidal respiratory epithelium, thickened me

95 cologic LXR activation selectively modulates airspace cytokine expression induced by both LPS and K.

96 To determine the relationship between airspace cytokines and cellular inflammatory responses i

97 nd metaplasia, airway fibrosis, and alveolar airspace destruction.

98 umbers of lymphocytes and eosinophils in the airspaces did not change significantly.

99 notype comprising rapidly progressive distal airspace dilation, impaired gas exchange, and perinatal

100 Airspace dimensions were estimated by measuring the appa

101 mined two independent measures of peripheral airspace dimensions: apparent diffusion coefficient (ADC

102 on may predispose to inflammatory airway and airspace diseases.

103 hysema is commonly defined as enlargement of airspaces distal to terminal bronchioles accompanied by

104 essure and surfactant administration reduces airspace distension.

105 of airspace) and by altering the pattern of airspace distribution within the leaf.

106 t increased TGF-beta1 activity in the distal airspaces during ALI promotes alveolar edema by reducing

107 urfactant protein D (SP-D) accumulate in the airspaces during P. carinii pneumonia and are particular

108 ning alveolar fluid balance and in resolving airspace edema.

109 the proinflammatory effects of CS leading to airspace enlargement and alveolar damage.

110 and was accompanied by development of distal airspace enlargement and alveolar destruction.

111 -deficient adeno-associated virus attenuated airspace enlargement and emphysema caused by inhibition

112 -/- lung leukocytes to wild-type mice led to airspace enlargement and impaired lung function, indicat

113 g mice, neutrophilia, mucus obstruction, and airspace enlargement are IL-4Ralpha- and TNF-alpha-indep

114 exposure and elastase administration caused airspace enlargement as well as impaired lung function a

115 results in changes in pulmonary function and airspace enlargement characteristic of pulmonary emphyse

116 still led to pronounced permanent postnatal airspace enlargement due to impaired paracrine function

117 g-specific WNT-5A overexpression exacerbated airspace enlargement in elastase-induced emphysema in vi

118 Airspace enlargement was also significantly increased at

119 and a semiautomated quantitative analysis of airspace enlargement was applied to whole histology slic

120 nperturbed during the first 2 weeks of life, airspace enlargement was observed by 3 weeks and progres

121 Differences in distal airspace enlargement were obvious at day 6 after birth.

122 ctivity of matrix metalloproteinases (MMPs), airspace enlargement, and decreased lung elastance compa

123 protected against mitochondrial dysfunction, airspace enlargement, and mucociliary clearance (MCC) di

124 t to cause increases in total lung capacity, airspace enlargement, and pulmonary inflammation.

125 pression, goblet cell metaplasia, and distal airspace enlargement, but had no effect on airway mucus

126 Airspace enlargement, goblet cell hyperplasia, increased

127 individuals with Marfan syndrome have distal airspace enlargement, historically described as emphysem

128 helium, but not in myeloid cells, aggravated airspace enlargement, impaired lung function, and reduce

129 displayed pronounced pulmonary inflammation, airspace enlargement, increased MMP-2 and MMP-9 levels,

130 Severe airspace enlargement, loss of alveolar septae, and sloug

131 ent destruction of alveolar walls leading to airspace enlargement, loss of elastic recoil, decrease i

132 These changes included airspace enlargement, loss of small airspaces, increased

133 Airspace enlargement, lung inflammation, lung mechanical

134 sure, and displayed resistance to CS-induced airspace enlargement, relative to WT littermate mice.

135 ual loss of lung elasticity and irreversible airspace enlargement, usually in the later decades of li

136 ent of cigarette smoke-induced emphysema and airspace enlargement, with concurrent reductions in infl

137 e stress and apoptosis culminate in profound airspace enlargement.

138 that may contribute to genetic and acquired airspace enlargement.

139 irflow obstruction and lung destruction with airspace enlargement.

140 ads to the loss of alveolar septal cells and airspace enlargement.

141 ascular and endothelial function, leading to airspace enlargement.

142 lmonary inflammation, fibrosis, and alveolar airspace enlargement.

143 on, proinflammatory cytokine expression, and airspace enlargement.

144 l abrogated both macrophage accumulation and airspace enlargement.

145 way pathologies, pulmonary inflammation, and airspace enlargement.

146 to increased lung inflammation and increased airspace enlargement.

147 ed from elastase and cigarette smoke induced airspace enlargement.

148 used to model smoke-related cell stress and airspace enlargement.

149 to CS-induced lung inflammatory response and airspace enlargement.

150 on of maximal airway hyperresponsiveness and airspace eosinophilia required administration of ovalbum

151 nary disease examined, with the exception of airspace eosinophilia.

152 e oxidative inactivation of antiproteinases, airspace epithelial injury, increased sequestration of n

153 ome, a frequently lethal condition caused by airspace flooding.

154 agonists a) stimulate maximal cAMP-dependent airspace fluid clearance in normal lungs and b) reduce p

155 ntial to regulate alveolar ion transport and airspace fluid content.

156 situ perfused lungs using 125I-albumin as an airspace fluid volume marker.

157 pithelium and accelerate clearance of excess airspace fluid.

158 lial tight junctions are crucial to regulate airspace fluid.

159 regulation of the volume and composition of airspace fluid.

160 TNF-alpha and neutrophil accumulation in the airspaces following intratracheal administration of LPS.

161 hing of airways, but show significant distal airspace formation and pneumocyte differentiation.

162 xpanding cell, at the sites of intercellular airspace formation, and at the bases of leaves, cotyledo

163 ion during fetal development disrupts distal airspace formation, mesenchymal and vascular remodeling,

164 ion in modifying cell walls to allow growth, airspace formation, the development of vasculature, and

165 ing with protoplast size and increasing with airspace fraction and cell wall thickness.

166 es across the thin tissue barrier separating airspace from the capillary red blood cells (RBCs).

167 esis that mechanical recruitment of terminal airspaces from a previously unventilated compartment wil

168 and medical science applications beyond lung airspace imaging requires methods of efficient delivery

169 lopment determines the pattern and volume of airspace in a leaf.

170 y enhanced recruitment of neutrophils to the airspace in response to both inhaled lipopolysaccharide

171 reduced neutrophil (PMN) recruitment to the airspace in response to LPS and K. pneumoniae by impairi

172 he time of birth and removes liquid from the airspaces in adults.

173 s of the alveolar septa surrounding enlarged airspaces in human emphysema with the mean linear interc

174 n influencing neutrophil recruitment to lung airspaces in response to both an invasive and noninvasiv

175 r buds and decreased bronchioles and dilated airspaces in SPC-PDGFA transgenic mice.

176 ation of neutrophils and macrophages in lung airspaces in vivo following intranasal instillation into

177 LR4 expression, whereas macrophages from the airspace, in which cholesterol was maintained constant d

178 gnation of growth, followed by distension of airspaces, increased cell proliferation, and accelerated

179 included airspace enlargement, loss of small airspaces, increased collagen, and thickened pleural sep

180 in increased neutrophil recruitment into the airspaces, increased levels of protein and proinflammato

181 cantly reduced leukocyte accumulation to the airspaces, independent of pulmonary cytokine or chemokin

182 of LPS-induced neutrophil recruitment to the airspaces, independent of suppression of other inflammat

183 8-independent neutrophil emigration into the airspaces induced by either Streptococcus pneumoniae, a

184 oid cells may have distinct contributions to airspace inflammation and permeability between direct an

185 global TF deficiency resulting in increased airspace inflammation, alveolar-capillary permeability,

186 ruitment maneuvers did not reduce markers of airspace inflammation.

187 y edema and hemorrhage, and interstitial and airspace inflammation.

188 ted lung pathology characterized by enlarged airspaces, inflammation, and fibrosis.

189 v. administration of anti-PcrV IgG after the airspace instillation of a lethal dose of P. aeruginosa

190 Airspace instillation of dibutyryl cAMP, a stable analog

191 g injury and death of the infected mice, the airspace instillation of isogenic mutants secreting cata

192 Whereas the airspace instillation of PA103 caused acute lung injury

193 The airspace instillation of the cytotoxic P. aeruginosa str

194 Despite the importance of airspace integrity in vertebrate gas exchange, the molec

195 3, and pulmonary inflammation, fibrosis, and airspace integrity were assessed.

196 r channels facilitate fluid movement between airspace, interstitial, and capillary compartments, we m

197 o differentially image its transfer from the airspaces into the tissue barrier spaces and RBCs in the

198 Neutrophil homing to airspaces involve multiple factors produced by several d

199 We propose that the airspace is a "privileged" site, thereby uniquely sensit

200 ascular space into the lung interstitium and airspace is an early step in the host innate immune resp

201 e resulting balance of cellular material and airspace is expected to significantly influence the prim

202 thelial-epithelial barrier into the alveolar airspace is highly regulated by the adhesion molecules o

203 terized by diffuse alveolar damage, elevated airspace levels of pro-inflammatory cytokines, and flood

204 ntiation is blocked, as indicated by smaller airspaces, many fewer attenuated type I cells, and reduc

205 ion abrogated the lung tissue PMN uptake and airspace migration of PMN and prevented lung vascular in

206 btain a more complete protein profile of the airspace milieu in acute respiratory distress syndrome (

207 egree to which cell division patterns affect airspace networks and photosynthesis remains largely une

208 saccharide, leptin also appeared to decrease airspace neutrophil apoptosis.

209 is cytokine is effective in driving alveolar airspace neutrophilia.

210 While neither recruited airspace neutrophils nor lung injury was altered in endo

211 LPS- and KC-induced airspace neutrophils were reduced by lovastatin, an effe

212 terial clearance, the altered recruitment of airspace neutrophils, and the defective alveolar macroph

213 o Duffy wild-type endotoxemic mice increased airspace neutrophils, inflammatory cytokine concentratio

214 geldanamycin, would attenuate the release of airspace nitric oxide (NO) responsible for the shock-med

215 Abundant secreted surfactant in the narrowed airspaces, normal levels of surfactant protein mRNAs, an

216 nhibited neutrophil influx into the alveolar airspace of injured lungs.

217 pattern on neutrophils in both the blood and airspace of LPS-injured mice and that Ab-mediated SDF-1

218 eded to clear excess fluid from the alveolar airspace of normal and injured lungs.

219 e found to co-exist in calprotectin-enriched airspaces of a cystic fibrosis lung explant.

220 /+) lung fibrocytes also migrated to injured airspaces of CCR2(-/-) recipients in vivo.

221 olated in significantly greater numbers from airspaces of fluorescein isothiocyanate-injured CCR2(+/+

222 TGF-beta applied to the alveolar airspaces of live rabbits or isolated rabbit lungs block

223 I-labelled albumin was instilled into distal airspaces of lungs, and the resulting (125)I-labelled al

224 data indicate that sFasL is released in the airspaces of patients with acute lung injury and suggest

225 biologically active cytokines in the distal airspaces of patients with ALI.

226 t STAT3-activating cytokine expressed in the airspaces of pneumonic lungs, but its physiological sign

227 transfer conductance from the intercellular airspaces of the leaf into the chloroplast, defined as m

228 ffect of administering MSC directly into the airspaces of the lung 4 h after the intrapulmonary admin

229 Airspaces of the lung are lined by an epithelium whose c

230 n vivo evidence that NO, released within the airspaces of the lung probably secondary to the NF-kappa

231 hypothesis that the release of NO within the airspaces of the lung was responsible for the shock-medi

232 In the distal airspaces of the lung, alveolar epithelial tight junctio

233 and develop pelvic organ prolapse, enlarged airspaces of the lung, loose skin and vascular abnormali

234 of surfactant phospholipid membranes in the airspaces of the lung.

235 shock is mediated by NO released within the airspaces of the lung.

236 orrhage by decreasing NO released within the airspaces of the lung.

237 st accumulation and activation in the distal airspaces of the lung.

238 eactive nitrogen species released within the airspaces of the lung.

239 a fluid and inflammatory cells in the distal airspaces of the lung.

240 rculation and patrolled the interstitium and airspaces of the lung.

241 (125)I-labeled IL-8 was injected into the airspaces of the lungs and the dermis of the skin and th

242 The airspaces of the lungs were filled with liquid containin

243 The airspaces of the lungs were filled with liquid containin

244 e water fraction of the edema fluid from the airspaces of the lungs.

245 ndicated that elevated levels of SP-B in the airspaces of transgenic mice did not confer resistance t

246 Increased concentration of lysozyme in the airspaces of transgenic mice enhanced bacterial killing

247 of the central-peripheral axis of olfactory airspace onto the dorsal-ventral axis of the MOB, encomp

248 ntify airborne volcanic ash in order to keep airspace open and avoid aircraft groundings.

249 as early as 1 week of age, and the increased airspace progressed with advancing age.

250 ation of protein thiols, and accumulation of airspace protein-associated carbonyl moieties, blocked t

251 , resulting in markedly enlarged parenchymal airspace, pulmonary fibrosis, and physiological abnormal

252 of atelectasis (and recruitment) on aerated airspaces remain elusive.

253 gulation of pulmonary macrophage activation, airspace remodeling, and surfactant lipid homeostasis.

254 al instillation of endotoxin into the distal airspaces resulted in pulmonary edema with the loss of a

255 ell PPARgamma-targeted mice display enlarged airspaces resulting from insufficient postnatal lung mat

256 The increase in airspace size is accompanied by alterations in lung phys

257 The lung inflammatory response and airspace size were assessed in Fam13a(-/-) and Fam13a(+/

258 roinflammatory pathways (except LTB4) in the airspaces supports the hypothesis that the mechanism for

259 less on neutrophils that emigrated into the airspaces than on circulating neutrophils.

260 ) is a collectin produced in the distal lung airspaces that is believed to play an important role in

261 ced a strong gas-phase (129)Xe signal in the airspaces that resulted from (129)Xe transport through t

262 ng dehydration (i.e. in whole leaf, cell and airspace thickness, and leaf area) is associated with re

263 stage of lung development, including dilated airspaces, thin respiratory epithelium and mesenchyme, a

264 O-1 would attenuate the release of NO in the airspaces, thus preventing the inhibition of the c-AMP s

265 cell counts, bacterial load, and intraacinar airspace/tissue volume were measured.

266 Propagation of inflammatory signals from the airspace to the vascular space is pivotal in lung inflam

267 y increased mean linear intercept, increased airspace-to-septal ratio, decreased nodal density, and d

268 PMN migration into the airspace was delayed; the value peaked at 6 h and remain

269 e of chemotactic cytokines into the alveolar airspace was determined by ELISA.

270 ular endothelial barrier in intact lung, the airspace was filled with a water-immiscible fluorocarbon

271 ral surface fluorescence method in which the airspace was filled with inert perfluorocarbon, was redu

272 Recovery of MIP-2 and KC from the airspaces was not affected by inhibition of p38 MAPK, an

273 eutrophils, but not other leukocytes, to the airspaces was significantly reduced.

274 orescence method to measure net capillary-to-airspace water transport.

275 precursors, are released into the airway and airspace where they bind high-affinity cognate receptors

276 cells in both the proximal airway and distal airspace, whereas aberrant repair of the lung may result

277 of mice induced monocyte accumulation in the airspace, whereas combined bronchoalveolar instillation

278 posure reversibly suppresses IL-33 levels in airspaces which, in turn, results in reduced neutrophil

279 mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leu

280 show recruitment of CX3CR1(+) cells into the airspaces with cigarette smoke.

281 haracterized by the flooding of the alveolar airspaces with protein-rich edema fluid and diffuse alve

282 actant protein B (SP-B) is secreted into the airspaces with surfactant phospholipids where it reduces

283 gnificantly elevated lysozyme protein in the airspaces without any increase in muramidase activity.