ライフサイエンスコーパス: alveoli

1 lified AMPhi-induced PMN migration into lung alveoli.

2 ways and type II and type I cells lining the alveoli.

3 Pneumonia results from bacteria in the alveoli.

4 s, and redirecting flow to better-ventilated alveoli.

5 ge tidal volumes and limitedly to subpleural alveoli.

6 ction was reduced and strongly restricted to alveoli.

7 protein for lowering surface tension in the alveoli.

8 olds with acellular vasculature, airways and alveoli.

9 leading to tissue destruction and a loss of alveoli.

10 tip cells only contribute descendents to the alveoli.

11 re generally considered as restricted to the alveoli.

12 protein for lowering surface tension in the alveoli.

13 s created at the air-liquid interface in the alveoli.

14 thereby prevent damage to the gas-exchanging alveoli.

15 nt lipids that reduce surface tension in the alveoli.

16 h successfully lowers surface tension in the alveoli.

17 ell Ag recognition in the distal airways and alveoli.

18 rmal AEC I population is damaged in the lung alveoli.

19 mulates accumulation of lipid selectively in alveoli.

20 receptors, the MR, and SP-A present in lung alveoli.

21 nd differentiates to produce the airways and alveoli.

22 physema with decreased septation in terminal alveoli.

23 causes marked destabilization of individual alveoli.

24 hilic inflammation of the distal airways and alveoli.

25 he gene is controlled by milk filling in the alveoli.

26 timately give rise to conducting airways and alveoli.

27 spholipids and proteins that lines pulmonary alveoli.

28 charide, but only IgG stained yeast cells in alveoli.

29 e expression and caused shrinkage of mammary alveoli.

30 n-mediated mechanisms as a means of entering alveoli.

31 e alveoli directly adjacent to normal stable alveoli.

32 n with increased PEEP (15cmH20) to stabilize alveoli.

33 with increased PEEP (15 cm H2O) to stabilize alveoli.

34 ed surface tension when compared with normal alveoli.

35 nverting normal stable alveoli into unstable alveoli.

36 he epithelial cells of the lower airways and alveoli.

37 stributed sporadically to branching ducts or alveoli.

38 nt of neutrophils from the interstitium into alveoli.

39 into the alveoli, and (2) engraftment in the alveoli.

40 growth and differentiation of mammary lobulo-alveoli.

41 ut also for postnatal modeling and repair of alveoli.

42 ion of lipoproteinaceous material within the alveoli.

43 te gas-exchanging airspaces called pulmonary alveoli.

44 in the conducting airways, bronchioles, and alveoli.

45 and reduced surface complexity of developing alveoli.

46 hange in VL is due to change in VA or R/D of alveoli.

47 lating development or maintenance of mammary alveoli.

48 n of the distal lung saccules into primitive alveoli.

49 nscription program leading to differentiated alveoli.

50 lting in a single AT1 cell spanning multiple alveoli.

51 ed by the accumulation of surfactants in the alveoli.

52 del the matrix and irreversibly simplify the alveoli.

53 , promoting a profound reduction in MECs and alveoli.

54 ys and thus impaired ventilation of attached alveoli.

55 llows deposition of yeast spores in the lung alveoli.

56 t the interface between lung capillaries and alveoli.

57 ll airways (bronchioles), or the most distal alveoli.

58 ungs are comprised of conducting airways and alveoli.

59 ion but promotes squamous hyperplasia in the alveoli.

60 airway tree and undergo gas exchange in the alveoli.

61 against physical forces tending to collapse alveoli.

62 al cells that are normally restricted to the alveoli.

63 atory cytokines and attract T cells into the alveoli.

64 gnificant change in the calculated number of alveoli (345.6+/-40.5 x 10(6)) compared with the normal

65 urfactant mixture actually reaches the adult alveoli/acinus in therapeutic amounts.

66 low to the airways and likely stabilizes the alveoli against collapse.

67 Gas exchange in the lung occurs within alveoli, air-filled sacs composed of type 2 and type 1 e

68 Examples include surfactant proteins in lung alveoli, albumin in liver parenchyma, and lipase in the

69 Understanding the function of these cells in alveoli and airways may provide clues to the pathogenesi

70 e, a surface tension gradient exists between alveoli and airways that should lead to surfactant flow

71 are the absence of draining lymph nodes and alveoli and alveolar macrophages (MPhs).

72 tilation is essential for oxygenation of the alveoli and arterial blood.

73 ophages and neutrophils were observed in the alveoli and bronchioles, and lymphocytes were observed i

74 imarily localized in epithelial cells of the alveoli and bronchioles, as well as in adjoining capilla

75 ruginosa enters the terminal bronchioles and alveoli and comes into contact with alveolar lining flui

76 sed cellular turnover in structurally normal alveoli and ducts compared with single transgenic female

77 ases proliferation in morphologically normal alveoli and ducts, as well as in lesions.

78 dominantly in the luminal areas of secretory alveoli and ductular tissue, indicating that much of the

79 at should lead to surfactant flow out of the alveoli and elimination of the surface tension gradient.

80 on, genetically tagged AMs persisted in lung alveoli and expressed transferred genes for the lifetime

81 by abundant neutrophil infiltration into the alveoli and fibrin deposition.

82 n is necessary for the normal development of alveoli and for the activation of endocrine signalling p

83 %) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by su

84 sh (microvillous) cell in normal airways and alveoli and in respiratory diseases involving the alveol

85 eal mucosal-submucosal separation, pulmonary alveoli and intestinal villi.

86 preads from affected alveoli into contiguous alveoli and leads to death by asphyxiation.

87 followed by inadequate PEEP permits unstable alveoli and may result in ventilator-induced lung injury

88 re (PEEP) may cause overdistension of normal alveoli and redistribution of blood flow to diseased lun

89 PEEP stabilized alveoli and significantly reduced histologic evidence of

90 d emphysema-associated structural changes in alveoli and small airways and improved lung function.

91 alpha1-antitrypsin can also form within the alveoli and small airways of the lung where they may dri

92 sease with inflammation of small airways and alveoli and systemic spread of the virus to livers and s

93 LK-/- lungs exhibited smaller and compressed alveoli and the mesenchyme remained thick and hyperplast

94 to the physical structures of lipids in the alveoli and to the regulation of surfactant function and

95 ibuted on epithelial surfaces of airways and alveoli and was very rapidly ( approximately 1 min) loca

96 develop in serum-free spaces (eg, pulmonary alveoli) and open options for new therapeutic approaches

97 lar hemorrhage (76 +/- 11% vs. 26 +/- 18% of alveoli), and underwent larger fractional declines in st

98 hage precursors: (1) transmigration into the alveoli, and (2) engraftment in the alveoli.

99 cytokines, recruited neutrophils to the lung alveoli, and cleared the infection without progression t

100 lia that line the distal nephron, airway and alveoli, and distal colon.

101 nt, the film of lipid and protein lining the alveoli, and is the subject of great interest for its ro

102 airways, reduction of surface tension in the alveoli, and maintenance of near sterility have been acc

103 pithelium developed ducts but failed to form alveoli, and no milk protein gene expression was observe

104 uman lung stem cells form human bronchioles, alveoli, and pulmonary vessels integrated structurally a

105 reduced inflammatory cell recruitment to the alveoli, and reduced histological evidence of PcP-relate

106 tous inflammation of the peripheral airways, alveoli, and surrounding interstitial tissue which devel

107 helial cell of kidney collecting ducts, lung alveoli, and the Purkinje cells of the cerebellum.

108 tissues including arterial walls, skin, lung alveoli, and the uterus.

109 the AMs remained sessile and attached to the alveoli, and they established intercommunication through

110 of the conducting airways and gas-exchanging alveoli are briefly reviewed, and controversial, newly p

111 Mammary alveoli are composed of luminal (secretory) and basal (m

112 Alveoli are gas-exchange sacs lined by squamous alveolar

113 entilator-induced lung injury whereas stable alveoli are not.

114 ventilator-induced lung injury while stable alveoli are not.

115 age markers, revealed that mammary ducts and alveoli are polyclonal, and putative early preneoplastic

116 pores that are similar in size to mammalian alveoli are presented.

117 dynamic physical forces as airway tubes and alveoli are stretched and compressed during ventilation.

118 irst study to directly confirm that unstable alveoli are subjected to ventilator-induced lung injury

119 irst study to directly confirm that unstable alveoli are subjected to ventilator-induced lung injury

120 Nonetheless, normal alveoli are very stable and change size very little with

121 lt lung epithelial compartments (airways and alveoli) are separately maintained by distinct lineage-r

122 o thin surfactant layers that stabilize lung alveoli, are integral to living systems.

123 nary compliance, lower shunt fraction, lower alveoli-arterial gradient and lower oxygenation index co

124 7) and III (15,418 +/- 1995 microm2, n = 12) alveoli as compared with type I (8214 +/- 655 microm2, n

125 taneous presence of secretory and involuting alveoli as well as resting ductules.

126 simple isotropic (balloon-like) expansion of alveoli, as evidenced by the horizontal (no change in al

127 d alveolar development with fewer but larger alveoli, as well as a reduced Vc.

128 ly deposited in the terminal bronchioles and alveoli, as well as following release from lysed macroph

129 NeuroD-deficient mice had enlarged alveoli associated with reduced epithelial proliferation

130 he epithelial surfaces in the airway and the alveoli at 2 and 4 h postinoculation.

131 for both) with a greater percentage of large alveoli at expiration.

132 vious studies have been therefore limited to alveoli at lung apices or subpleural alveoli under open

133 duced lung damage, and assemble into nascent alveoli at sites of interstitial lung inflammation.

134 of the lung morphometry, with an increase in alveoli beyond what has been previously viewed as the ma

135 Bronchiolization of the alveoli (BOA), a potential precursor of lung cancer, is

136 substantially enhanced gene transfer to the alveoli but was much less effective in the airways.

137 n life by expansion of an existing number of alveoli, but rather from increased alveolarization early

138 mber rather than the enlargement of existing alveoli, but the alveoli in the growing lung were shallo

139 stromal cells (MSCs) in the terminal airways-alveoli by bronchoalveolar lavage (BAL) of human adult l

140 ovectors could efficiently transduce injured alveoli by exposing adult, male Sprague-Dawley rats to 1

141 end expiration (E) on individual subpleural alveoli by image analysis.

142 an important role in the bronchiolization of alveoli by promoting proliferation, migration, and atten

143 We previously demonstrated that unstable alveoli cause lung injury.

144 sary for reduction of surface tension in the alveoli, cause lethal respiratory distress at birth or i

145 l stable alveoli and in a lung with unstable alveoli caused by surfactant deactivation (Tween lavage)

146 eins accumulate excessively within pulmonary alveoli, causing severe respiratory distress.

147 In contrast, deletion of Cdc42 in alveoli cells prevents Kras (G12D) -induced cell prolife

148 In the ALVEOLI cohort, the effects of ventilation strategy (hig

149 sitive end-expiratory pressure (PEEP) in the ALVEOLI cohort.

150 ients: 473 in the ARMA cohort and 549 in the ALVEOLI cohort.

151 ith ventilation, regardless of whether these alveoli collapse totally (type III) at end expiration.

152 e number of alveolar type II cells in mutant alveoli compared to controls.

153 pread of viral infection from the airways to alveoli compared with challenge with IAV alone, based on

154 Instead, the alveoli contained eosinophils and neutrophils.

155 preads from affected alveoli into contiguous alveoli, creating a reticular network that leads to deat

156 Once recruited, alveoli did not demonstrate any further volume change, w

157 tivation in the lung, with areas of unstable alveoli directly adjacent to normal stable alveoli.

158 imize the flow of lung surfactant out of the alveoli due to surface tension gradients.

159 ng injury may be caused by overdistension of alveoli during high-pressure ventilation.

160 ited a greater influx of phagocytes into the alveoli during infection.

161 ts during puberty and terminate in secretory alveoli during lactation.

162 cient newborns, but neutrophil emigration to alveoli during LPS-induced pneumonia was severely reduce

163 LPS-induced endotoxin shock, and in the lung alveoli during papain-induced allergic airway inflammati

164 o clears the exudate that normally fills the alveoli during Pcp and decreases lung inflammation.

165 GFR-3 and FGFR-4 to promote the formation of alveoli during postnatal lung development.

166 Establishment and differentiation of mammary alveoli during pregnancy are controlled by prolactin thr

167 bility to form structurally normal ducts and alveoli during pregnancy resulted in lactation failure.

168 tors were greatly reduced and unable to form alveoli during pregnancy.

169 ion, maintenance and cellular composition of alveoli during pregnancy.

170 proliferation and differentiation of mammary alveoli during pregnancy.

171 In-vivo, real-time visualization of the alveoli during respiration has been hampered by active l

172 hase and confers mechanical stability to the alveoli during the breathing process.

173 y, we visualized the inflation of individual alveoli during the generation of a pressure/volume curve

174 haracterized by neutrophilic infiltration of alveoli, edema, and hemorrhage.

175 rmidable hurdles to gene transfer, including alveoli filled with fluid, inflammatory cells, and cytok

176 delta2(+) T cells in the blood and pulmonary alveoli following BCG infection and reinfection.

177 lial cells of nasal mucosa, bronchioles, and alveoli for up to 4 days postinfection.

178 consistent with the emerging theory that as alveoli form through secondary septation, alveolar flow

179 ing, mesenchymal proliferation, and impaired alveoli formation.

180 tely 0.1 microm) liquid layer that lines the alveoli, forming a film that reduces surface tension and

181 ificant increase in the calculated number of alveoli from before transplantation (172.5+/-35.9x 106)

182 (AEC2s), the facultative progenitors of lung alveoli, from human PSCs.

183 emporally linked, as early antigen uptake in alveoli gives rise to DC and antigen retention in the ai

184 greater accumulation of glycoproteins in the alveoli (glycoproteins, including harmful hydrolytic enz

185 However, alveoli have never been directly observed during the gen

186 an even greater size change than did type II alveoli (I - EDelta = 15,418 +/- 1995 microm2), and were

187 ntiate whether the PM may be retained in the alveoli (i.e., galena) or if it may be dissolved and pas

188 changes in alveolar mechanics of individual alveoli in a porcine ARDS model by direct visualization

189 sels decreased with increasing distance from alveoli in control samples but not in CFA or FASSc sampl

190 Type I alveoli in either the control or Tween group demonstrate

191 virgin females, for the de novo induction of alveoli in males, and for the formation of tumors.

192 down to tissue volumes less than that of ten alveoli in septic lungs compared with controls (p < or =

193 inherently beta-catenin-responsive and form alveoli in the absence of PR.

194 tumours are fast-growing tumours filling the alveoli in the absence of vascular remodelling.

195 Normal alveoli in the control group are all type I and do not c

196 the enlargement of existing alveoli, but the alveoli in the growing lung were shallower than in norma

197 The pulmonary microvasculature and alveoli in the intact animal were imaged with comparable

198 t in adult females, and fewer milk-producing alveoli in the lactating glands.

199 t film of lipids and proteins that coats the alveoli in the lung is compressed to high surface pressu

200 ntrol differentiation of skeletal muscle and alveoli in the lungs.

201 omy model that promotes the formation of new alveoli in the remaining lobes.

202 In the Tween group, type II alveoli increased significantly in area, with lung infla

203 In normal alveoli, increasing tidal volume did not change alveolar

204 iency, Foxa1 null glands form milk-producing alveoli, indicating that the defect is restricted to exp

205 Type III alveoli initially recruited with a relatively small area

206 to VILI than WT mice, as evidenced by poorer alveoli integrity and quantified by lung chemokine and c

207 The fibrosis spreads from affected alveoli into contiguous alveoli and leads to death by as

208 The fibrosis spreads from affected alveoli into contiguous alveoli, creating a reticular ne

209 uring ventilation), converting normal stable alveoli into unstable alveoli.

210 We hypothesize that the disappearance of alveoli involves apoptosis of septal endothelial cells a

211 Neutrophil migration to lung alveoli is a characteristic of lung diseases and is thou

212 The number of alveoli is estimated to increase 1.94-fold (95% CI, 1.64

213 escribes chaotic mixing in small airways and alveoli is highly complex; it not readily accessible by

214 The integrity of lung alveoli is maintained by proper circulating levels of al

215 zed by injury, inflammation, and scarring of alveoli, leading to impaired function.

216 with tight junction, were maintained in the alveoli-like structures of PrlR- and Stat5-null epitheli

217 nonpolar fashion, the cells formed globular, alveoli-like structures with a large central lumen inste

218 In contrast, PrlR-null epithelium formed alveoli-like structures with small open lumina.

219 In the normal lung, all alveoli measured exhibited type I mechanics.

220 tion and reveal that direct viral effects in alveoli mediate H5N1 disease.

221 lly collapse at end expiration; and type III alveoli (n = 12) demonstrated an even greater size chang

222 8 microm2) during tidal ventilation; type II alveoli (n = 37) changed size dramatically (I - EDelta =

223 atterns were observed and classified: type I alveoli (n = 37) changed size minimally (I - EDelta = 36

224 o monitor the morphological changes that the alveoli network undergoes in the progression of these di

225 t adenovectors can efficiently transduce the alveoli of acutely injured, edematous lungs.

226 signaling mechanisms, we microinfused single alveoli of blood-perfused rat lung with TNF-alpha, and d

227 trypsin co-localizes with neutrophils in the alveoli of individuals with Z alpha(1)-antitrypsin-relat

228 report direct and real-time visualization of alveoli of live intact mice during respiration using tra

229 NETs are found in alveoli of mice experiencing antibody-mediated TRALI.

230 e interstitia, they were not detected in the alveoli of neonatal lungs.

231 Individual alveoli of normal lungs clearly show heterogeneous infla

232 ular composition with that of the airways or alveoli of the adult lung.

233 Alveolar macrophages are found in the alveoli of the lung and represent the first line of defe

234 by leukocyte migration to small airways and alveoli of the lung grafts, and accelerated oxidative st

235 s that varies between conducting airways and alveoli of the lung.

236 cells or spores are inhaled and lodge in the alveoli of the lungs.

237 Neutrophils infiltrated the alveoli of tumor-bearing lungs and within the periphery

238 We tested the hypothesis that collapsed alveoli opened by a recruitment maneuver would be unstab

239 ources include leakage of plasma PAF-AH into alveoli or release of PAF-AH from injured cells; however

240 itment/derecruitment occurred in neighboring alveoli over short-time scales in all tested positive en

241 area, as well as estimation of the number of alveoli per acinus using stereologic methods.

242 owing parameters measured: (1) the number of alveoli per field and (2) alveolar stability (i.e., the

243 airway radii, alveolar depth, and number of alveoli per unit lung volume.

244 The number of alveoli per volume decreased proportionately to the incr

245 The number of alveoli per volume remained constant (P=0.21) despite th

246 l that the endothelial lining of the hypoxic alveoli plays a key role in sensing hypoxia and transmit

247 eterogeneous lung microanatomy, whereby some alveoli remain collapsed throughout the breath cycle whi

248 had collapsed whereas in control glands the alveoli remained intact and distended.

249 lveolar inflation pattern of type II and III alveoli "repetitive alveolar collapse and expansion" (RA

250 arly pregnancy, but failed to develop lobulo-alveoli, resulting in a defect in lactation.

251 asts and their deposition of collagen within alveoli, resulting in permanently scarred, nonfunctional

252 t formation of the tracheobronchial tree and alveoli results from heterogeneity of the epithelial-mes

253 second premolar and lower canine and incisor alveoli, reveal a number of derived morphological simila

254 Unstable alveoli stent open pulmonary vessels, which may explain

255 the polyclonal architecture of ducts and/or alveoli, suggesting that hyperplasia formation can be th

256 related to the balance between the number of alveoli that are recruited to participate in ventilation

257 s in the same microscopic field and included alveoli that changed area greatly with tidal ventilation

258 o birth in association with formation of the alveoli that mediate efficient gas exchange.

259 RACE describes all alveoli that visibly change volume with ventilation, reg

260 has not been fully understood how pulmonary alveoli, the elementary gas exchange units in mammalian

261 H3K27me3 marks and the formation of mammary alveoli, the presence of EZH2 is required to control pro

262 G to pneumolysin blocks these effects in the alveoli, thereby protecting the host against bacteremic

263 to represent radial diffusion of oxygen from alveoli through the alveolar-capillary membrane into pul

264 grity and consequently in the failure of the alveoli to correctly respond to injury and to face the s

265 nt causes the surface tension, gamma, in the alveoli to drop to nearly zero on exhalation; in the upp

266 randomised controlled trials (ARMA trial and ALVEOLI trial), sponsored by the National Heart, Lung, a

267 syndrome (ALI/ARDS) who were enrolled in the ALVEOLI trial.

268 iency inhibits the Kras (G12D) -induced lung alveoli tumor formation, while conversely promotes bronc

269 ited to alveoli at lung apices or subpleural alveoli under open thorax conditions.

270 cruitment demonstrated improved oxygenation, alveoli ventilated with 10 PEEP were stable, whereas alv

271 ventilated with 10 PEEP were stable, whereas alveoli ventilated with 5 PEEP showed significant instab

272 ly collapse at end expiration; and type III, alveoli visibly change size during tidal ventilation and

273 n alveolar size during ventilation; type II, alveoli visibly change size during ventilation but do no

274 ts, a positive chemokine gradient toward the alveoli was induced by intratracheal instillation of end

275 y incision, in vivo microscopy of subpleural alveoli was performed as the degassed lung was inflated

276 The percentage fractional area of collapsed alveoli was significantly higher for 0 PEEP compared wit

277 us secretory morphology, albeit with smaller alveoli, was maintained in thrice-daily milked glands.

278 d in proliferating tissue but both ducts and alveoli were grossly and histologically normal.

279 pression levels achieved in both airways and alveoli were higher with AAV2/5 than with AAV2/1 and wer

280 In triple null glands, alveoli were poorly organized and differentiated, and mi

281 Alveoli were recorded endoscopically and alveolar mechan

282 Alveoli were significantly larger at peak inspiration in

283 peripheral airways (bronchioles, acini, and alveoli), were established well before formation of the

284 rate the lower respiratory tract and blanket alveoli where target cells reside.

285 e on the luminal surfaces of the airways and alveoli where they maintain host defense and promote alv

286 ighly branched tubes that bring air into the alveoli, where gas exchange takes place.

287 or cells were not correctly localized to the alveoli, where GM-CSF is produced.

288 e host in aerosol droplets deposited in lung alveoli, where the bacteria first encounter lung-residen

289 to penetrate deep into the lungs, e.g., the alveoli, where they may cause damage to cells and tissue

290 ological unit of the lung ( approximately 25 alveoli), which we refer to as a respiratory unit (RU).

291 resence of H5N1 virus receptors in the human alveoli, which are the site of inflammation during pneum

292 Lung alveoli, which are unique to air-breathing organisms, ha

293 of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaire

294 l lung development characterized by enlarged alveoli, which is associated with decreased tissue elast

295 d alveolar development with larger and fewer alveoli, which is consistent with our previous physiolog

296 rong tendency of the seal H3 to bind to lung alveoli, which was in direct contrast to the human-adapt

297 ment maneuver opened a significant number of alveoli, which were stable during the recruitment maneuv

298 All responses were blocked by pretreating alveoli with a mAb against TNF receptor 1 (TNFR1).

299 in the expression of GFP in bronchioles and alveoli within 5 days.

300 topathology only in lung areas with unstable alveoli without an increase in neutrophil-derived protea