ライフサイエンスコーパス: alveoli

1 nchi, bronchioles) and gas-exchanging units (alveoli).

2 t the interface between lung capillaries and alveoli.

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

4 ungs are comprised of conducting airways and alveoli.

5 ion but promotes squamous hyperplasia in the alveoli.

6 airway tree and undergo gas exchange in the alveoli.

7 against physical forces tending to collapse alveoli.

8 al cells that are normally restricted to the alveoli.

9 atory cytokines and attract T cells into the alveoli.

10 Pneumonia results from bacteria in the alveoli.

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

12 ge tidal volumes and limitedly to subpleural alveoli.

13 ction was reduced and strongly restricted to alveoli.

14 protein for lowering surface tension in the alveoli.

15 olds with acellular vasculature, airways and alveoli.

16 leading to tissue destruction and a loss of alveoli.

17 tip cells only contribute descendents to the alveoli.

18 re generally considered as restricted to the alveoli.

19 protein for lowering surface tension in the alveoli.

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

21 thereby prevent damage to the gas-exchanging alveoli.

22 nt lipids that reduce surface tension in the alveoli.

23 air daily, allowing some pathogens access to alveoli.

24 h successfully lowers surface tension in the alveoli.

25 ell Ag recognition in the distal airways and alveoli.

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

27 mulates accumulation of lipid selectively in alveoli.

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

29 nd differentiates to produce the airways and alveoli.

30 physema with decreased septation in terminal alveoli.

31 causes marked destabilization of individual alveoli.

32 hilic inflammation of the distal airways and alveoli.

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

34 timately give rise to conducting airways and alveoli.

35 spholipids and proteins that lines pulmonary alveoli.

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

37 e expression and caused shrinkage of mammary alveoli.

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

39 e alveoli directly adjacent to normal stable alveoli.

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

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

42 ion of extracellular protein fibrils in lung alveoli.

43 ed surface tension when compared with normal alveoli.

44 nverting normal stable alveoli into unstable alveoli.

45 he epithelial cells of the lower airways and alveoli.

46 nt of neutrophils from the interstitium into alveoli.

47 lified AMPhi-induced PMN migration into lung alveoli.

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

49 e epithelial folds (secondary septa) to form alveoli.

50 stributed sporadically to branching ducts or alveoli.

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

52 n of the distal lung saccules into primitive alveoli.

53 nscription program leading to differentiated alveoli.

54 lting in a single AT1 cell spanning multiple alveoli.

55 ed by the accumulation of surfactants in the alveoli.

56 del the matrix and irreversibly simplify the alveoli.

57 , promoting a profound reduction in MECs and alveoli.

58 ys and thus impaired ventilation of attached alveoli.

59 r (29%; P < 0.01) and fewer (31%; P < 0.001) alveoli.

60 llows deposition of yeast spores in the lung alveoli.

61 lly stable cortical microtubules beneath the alveoli, a network of flattened membrane vesicles that s

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

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

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

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

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

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

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

69 oteins link the cortical microtubules to the alveoli and are required to maintain the shape and rigid

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

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

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

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

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

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

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

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

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

79 In two secondary analyses, the ALVEOLI and FACTT cohorts each, individually, served as

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

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

82 %) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by su

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

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

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

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

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

88 y stem/progenitors mobilize to cover denuded alveoli and restore normal barriers.

89 C2s) are the facultative progenitors of lung alveoli and serve as the surfactant-producing cells of a

90 PEEP stabilized alveoli and significantly reduced histologic evidence of

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

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

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

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

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

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

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

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

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

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

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

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

110 Alveoli are gas-exchange sacs lined by squamous alveolar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 e training data set (ARMA [High vs. Low Vt], ALVEOLI [Assessment of Low Vt and Elevated End-Expirator

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

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

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

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

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

132 Model accuracy was similar when ALVEOLI (AUC, 0.94; 95% CI, 0.92-0.96) and FACTT (AUC, 0

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

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

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

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

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

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

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

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

141 We previously demonstrated that unstable alveoli cause lung injury.

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

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

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

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

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

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

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

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

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

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

152 Instead, the alveoli contained eosinophils and neutrophils.

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

154 ber alveolar macrophages (AMs), which favors alveoli devoid of AMs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 d pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration an

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

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

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

175 ing, mesenchymal proliferation, and impaired alveoli formation.

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

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

178 s permeation which may bear significance for alveoli gas exchange imbalance in pneumonia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 Type III alveoli initially recruited with a relatively small area

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

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

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

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

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

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

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

207 ch includes the trachea, airways, and distal alveoli, is a complex multi-cellular organ that intimate

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

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

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

211 sweat glands in skin; type II cells in lung alveoli, macrophages, and dendritic cells in lymph nodes

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

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

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

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

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

217 The septation in terminal alveoli of lungs in mgR mice was reduced compared to wil

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

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

220 Individual alveoli of normal lungs clearly show heterogeneous infla

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

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

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

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

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

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

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

228 Interestingly, alveoli outnumber alveolar macrophages (AMs), which favo

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

230 classifier model-assigned phenotypes in both ALVEOLI (P = 0.0113) and FACTT (P = 0.0072) cohorts.Conc

231 Before reaching the alveoli, particles must transverse the bifurcating netwo

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

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

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

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

236 GAPM1a, an integral membrane protein of the alveoli, plays a role in maintaining microtubule stabili

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

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

239 -develop to maintain structural integrity of alveoli remains unclear.

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

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

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

243 In addition, insufficient generation of alveoli results in bronchopulmonary dysplasia, a disease

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

245 ping in vivo real-time intravital imaging of alveoli revealed AMs crawling in and between alveoli usi

246 independent of mutation (unlike newborn lung alveoli), selective proteome and possible lipidome chang

247 Unstable alveoli stent open pulmonary vessels, which may explain

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

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

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

251 canals extend into bulbous structures called alveoli that contain sensory cells capable of detecting

252 istal lung contains terminal bronchioles and alveoli that facilitate gas exchange.

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

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

255 ction of the facultative progenitors of lung alveoli, the alveolar epithelial type 2 cells (AT2s).

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

257 Damage to alveoli, the gas-exchanging region of the lungs, is a co

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

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

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

261 progenitors responsible for maintaining lung alveoli throughout life but are difficult to isolate fro

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

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

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

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

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

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

268 alveoli revealed AMs crawling in and between alveoli using the pores of Kohn.

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

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

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

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

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

274 ction of the right upper central incisor the alveoli were filled with SBC hydrated by two different m

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

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

277 Alveoli were recorded endoscopically and alveolar mechan

278 Alveoli were significantly larger at peak inspiration in

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

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

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

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

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

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

285 be immediately detrimental, such as in lung alveoli, where they affect respiration, or they can be h

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

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

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

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

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

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

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

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

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

295 racing shows that ALFs are retained in adult alveoli while AMFs are lost.

296 asing numbers of club cells are found in the alveoli with aging and after lung injury, but go undetec

297 asia in proximal alveolar ducts and adjacent alveoli with associated centriacinar fibrosis.

298 ngs confirmed that hyaluronan is obstructing alveoli with presence in exudate and plugs, as well as i

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