ライフサイエンスコーパス: airspace

1 e airway-adjacent DCs to the contents of 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 colonised despite sharing of environment and airspace.

12 y excessive neutrophil infiltration into the airspace.

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

14 signed to remove other drones from protected airspace.

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

16 kocyte infiltration into the bronchoalveolar airspace.

17 epithelial migration of neutrophils into the airspace.

18 ulting in permanently scarred, nonfunctional airspaces.

19 nocyte chemoattractant concentrations in the airspaces.

20 h attenuated neutrophil recruitment into the airspaces.

21 eading to enhanced neutrophil recruitment to airspaces.

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

23 dance at the basolateral membranes of distal airspaces.

24 ium, whereas sFasL is present throughout the airspaces.

25 of water-soluble antioxidants in the distal airspaces.

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

27 hils and eosinophils, respectively, into the airspaces.

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

29 radiolabelled albumin was instilled into the airspaces.

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

31 and accumulating PGP and neutrophils in the airspaces.

32 arrier to the free diffusion of solutes into airspaces.

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

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

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

36 These airspace abnormalities included reduced isolectin B4(+)

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

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

39 2 is shed from fibroblasts into the alveolar airspace after lung injury.

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

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

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

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

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

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

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

47 te forcing for flight track data in Japanese airspace and propagates uncertainties arising from meteo

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 Of the AMs, 95% were contained in diffusing airspaces and 5% in airways.

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

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 Changes in distal and interstitial airspaces and the activation of Th2 inflammatory and pro

62 characterized by inflammation and dysmorphic airspaces and vasculature.

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

64 hange, and the humidity of the leaf internal airspace) and found evidence for both.

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

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

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

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

69 longed presence of PEGylated rhDNase in lung airspaces appears ideal for its mucolytic action in pati

70 ar counts, increased surface area, increased airspace area and increased mean linear intercept.

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

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

73 MPs are present in the alveolar airspace at steady state, however little is known about

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 this relates to the regulation of mesophyll airspace configuration is poorly understood.

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

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

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

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

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

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

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

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

103 Airspace dimensions were estimated by measuring the appa

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

105 on may predispose to inflammatory airway and airspace diseases.

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

107 essure and surfactant administration reduces airspace distension.

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

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

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

111 ning alveolar fluid balance and in resolving airspace edema.

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

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

114 ts, the lung lesion had progressed to severe airspace enlargement and alveolar simplification, with c

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

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

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

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

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

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

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

122 Airspace enlargement was also significantly increased at

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

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

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

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

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

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

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

130 Airspace enlargement, goblet cell hyperplasia, increased

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

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

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

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

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

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

137 Airspace enlargement, lung inflammation, lung mechanical

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

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

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

141 ed from elastase and cigarette smoke induced airspace enlargement.

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

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

144 e stress and apoptosis culminate in profound airspace enlargement.

145 that may contribute to genetic and acquired airspace enlargement.

146 irflow obstruction and lung destruction with airspace enlargement.

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

148 ascular and endothelial function, leading to airspace enlargement.

149 lmonary inflammation, fibrosis, and alveolar airspace enlargement.

150 l abrogated both macrophage accumulation and airspace enlargement.

151 on, proinflammatory cytokine expression, and airspace enlargement.

152 way pathologies, pulmonary inflammation, and airspace enlargement.

153 to increased lung inflammation and increased airspace enlargement.

154 ed inflammation, airway hyperresponsiveness, airspace enlargements, and loss of lung function.

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

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

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

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

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

160 pithelium and accelerate clearance of excess airspace fluid.

161 lial tight junctions are crucial to regulate airspace fluid.

162 In a highly dynamic airspace, flying animals are predicted to adjust foragin

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

164 lonies is higher on crowded ledges with more airspace for manoeuvring.

165 ed the presence of PEGylated rhDNase in lung airspaces for at least 7 days.

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

167 wheat and Arabidopsis to show that mesophyll airspace formation is linked to stomatal function in bot

168 e degree and spatial patterning of mesophyll airspace formation, and indicate that this relationship

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

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

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

172 ng the influence of anthropogenic factors on airspace habitat.

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

174 transmigration of human neutrophils into the airspace in response to A. fumigatus Together, these dat

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

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

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

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

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

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

181 ation of stomatal pores in the epidermis and airspaces in the underlying mesophyll tissue is vital fo

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

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

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

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

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

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

188 8-independent neutrophil emigration into the airspaces induced by either Streptococcus pneumoniae, a

189 Following alveolar airspace infiltration, the bronchoalveolar lavage (BAL)

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

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

192 to diffuse alveolar damage, interstitial and airspace inflammation, or acute respiratory failure.

193 ruitment maneuvers did not reduce markers of airspace inflammation.

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

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

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

197 Airspace instillation of dibutyryl cAMP, a stable analog

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

199 Whereas the airspace instillation of PA103 caused acute lung injury

200 The airspace instillation of the cytotoxic P. aeruginosa str

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

202 3, and pulmonary inflammation, fibrosis, and airspace integrity were assessed.

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

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

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

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

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

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

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

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

211 ationale: Interstitial macrophages (IMs) and airspace macrophages (AMs) play critical roles in lung h

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

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

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

215 The formation of stomata and leaf mesophyll airspace must be coordinated to establish an efficient a

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

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

218 coinfected mice exhibited significantly more airspace neutrophil infiltration at 6 hours following P.

219 is cytokine is effective in driving alveolar airspace neutrophilia.

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

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

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

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

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

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

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

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

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

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

230 The airspaces of Col6a1(-/-) lungs appeared simplified, with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 The airspaces of the lungs were filled with liquid containin

253 The airspaces of the lungs were filled with liquid containin

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

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

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

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

258 s before presentation, and who had bilateral airspace opacification on chest imaging (CT or x-ray).

259 t common radiologic findings in COVID-19 are airspace opacities (consolidations and/or ground-glass o

260 d were found to be hypoxaemic with bilateral airspace opacities on chest imaging.

261 stic curve for pneumothorax, nodule or mass, airspace opacity, and fracture were, respectively, 0.95

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

263 , releasing 3,078.6 tons of biomass into the airspace over several hours, but in recent years, produc

264 at the coordination of stomata and mesophyll airspace pattern underpins water use efficiency in crops

265 Unlike static airspace pressures, which, in theory, apply universally

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

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

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

269 ited monocytes and DCs rapidly adopt typical airspace-resident MP gene expression profiles.

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

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

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

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

274 lcCer levels were negatively correlated with airspace size.

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

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

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

278 raction, and presence of large intercellular airspaces, the spatial distribution of chlorophyll in la

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

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

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

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

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

284 aratively across BM, blood, and the alveolar airspaces to deploy an influenza lethality-associated re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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