ライフサイエンスコーパス: alveolar

1 Alveolar adenomatous hyperplasia and adenocarcinoma were

2 ephrin-B2 is shed from fibroblasts into the alveolar airspace after lung injury.

3 cell giving rise to intermediate, restricted alveolar and hormone-sensing progenitors.

4 Alveolar and interstitial cells were isolated from lung

5 fferences in overall gene expression between alveolar and interstitial macrophages (IMs) at baseline

6 Alveolar and interstitial macrophages had subpopulations

7 odels of murine macrophages, such as primary alveolar and peritoneal macrophages and the macrophage c

8 Secondary endpoints included alveolar and plasma levels of cytokines and soluble form

9 replaced by altered extracellular matrix and alveolar architecture is destroyed, which leads to decre

10 kocyte infiltration in the small airways and alveolar area, induced oxidative stress, and triggered t

11 e locations and course of posterior superior alveolar artery (PSAA) using cone beam computed tomograp

12 urrent study paralleled human postextraction alveolar BL.

13 the periodontal diagnostic acumen regarding alveolar bone alterations influenced by orthodontic toot

14 on of antibiotics significantly improved the alveolar bone and PDL damage of the knockdown phenotype,

15 pact of genetic background on comorbidity of alveolar bone change and glucose tolerance after HFD con

16 Interleukin-6 significantly correlated with alveolar bone changes (P <0.05), whereas adipsin showed

17 Alveolar bone changes significantly varied among CC line

18 murine oral cavity and to prevent subsequent alveolar bone destruction and osteoclastogenesis.

19 he pathogenesis of periodontitis with severe alveolar bone destruction.

20 sease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory respo

21 (recently shown to play key roles in normal alveolar bone formation), significant loss in alveolar b

22 istically significant difference in residual alveolar bone height (P <0.001).

23 Both cKO models exhibited reduced alveolar bone height and 4-fold increased numbers of ost

24 matory reaction corresponded to reduction in alveolar bone height and density (r = 0.74; P <0.05; Spe

25 f the interface between the root surface and alveolar bone in the replantation/transplantation model,

26 miRNAs direct periodontal fibroblasts toward alveolar bone lineage differentiation and new bone forma

27 Higher linear alveolar bone loss (ABL) and lower interradicular bone d

28 depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histop

29 tigate effects of strontium ranelate (SR) on alveolar bone loss (ABL) in rats with experimental perio

30 se tolerance development are associated with alveolar bone loss (ABL) in susceptible individuals.

31 s HN019 promotes a protective effect against alveolar bone loss and CTALs attributable to EP in rats,

32 jection of anti-DC-STAMP-mAb also suppressed alveolar bone loss and reduced the total number of multi

33 classification of disease severity based on alveolar bone loss and tooth loss during follow-up.

34 severity of periodontitis for premolars with alveolar bone loss based on 3D's or 2D's measurement is

35 Mixed infection with capsulated Pg augmented alveolar bone loss compared with that of mixed infection

36 TLR9(-/-) mice exhibited significantly less alveolar bone loss than their wild-type (WT) counterpart

37 Postextraction alveolar bone loss, mostly affecting the buccal plate, o

38 hich is characterized by inflammation-driven alveolar bone loss.

39 STAMP-mAb downregulated the ligature-induced alveolar bone loss.

40 nt acid phosphatase-positive (TRAP+) OCs and alveolar bone loss.

41 lveolar bone formation), significant loss in alveolar bone mass ( P < 0.01), and a sharp reduction in

42 Alveolar bone mineral density and alveolar bone volume w

43 Concomitantly, alveolar bone mineral density was significantly lower in

44 nt acid phosphatase-positive cells along the alveolar bone surface was significantly decreased after

45 g the positive or deleterious changes on the alveolar bone surrounding natural teeth undergoing ortho

46 Changes in the alveolar bone thickness and height around natural teeth

47 nt between the responses of human and rodent alveolar bone to osteotomy site preparation.

48 1(phox) KO mice revealed significant loss of alveolar bone volume and enhanced inflammatory cell infi

49 mellitus (t2DM) development and significant alveolar bone volume change (P <0.05), whereas others sh

50 there was no significant correlation between alveolar bone volume changes and increased BW or glucose

51 es were quantified by multiplex immunoassay, alveolar bone volume was quantified by microcomputed tom

52 Alveolar bone mineral density and alveolar bone volume were quantified by three-dimensiona

53 points after osteotomy, the fate of the dead alveolar bone was followed.

54 edic treatment on periodontal tissues (i.e., alveolar bone) were included.

55 ament (PDL), which connects the teeth to the alveolar bone, is essential for periodontal tissue homeo

56 olved, and there was progressive loss of the alveolar bone, likely as a result of increased colonizat

57 llular cementum, and osteoid accumulation in alveolar bone.

58 o solution for the long-term preservation of alveolar bone.

59 dvanced emphysema is a lung disease in which alveolar capillary units are destroyed and supporting ti

60 s to both infection and structural damage of alveolar-capillary barrier cells that hinders regenerati

61 The alveolar-capillary barrier is composed of epithelial and

62 y interstitium, impaired lung expansion, and alveolar-capillary membrane thickening.

63 associated with increased RUNX3 expression, alveolar cell apoptosis, and the antiangiogenic factor G

64 vo counterparts and generate both airway and alveolar cell types in vitro.

65 se gaps in knowledge in a model of pulmonary alveolar cell-cell communication.

66 l cell polarity and functional maturation of alveolar cells.

67 denote significance; associations with mean alveolar chord length (MACL), a quantitative measure of

68 ctive mechanical ventilation aims to prevent alveolar collapse and overdistension, but reliable bedsi

69 te more homogenous ventilation by preventing alveolar collapse at end expiration.

70 Evidence was found that alveolar collapse might already be present in an early s

71 rial oxygenation and on prevention of cyclic alveolar collapse with the harmful potential of overdist

72 cency of alveolar walls was seen, suggesting alveolar collapse.

73 y oscillations can be modelled from a single alveolar compartment and a constant oxygen uptake, witho

74 s increased in central airway tissue and the alveolar compartment in uncontrolled as compared to cont

75 t, without recruitment of macrophages to the alveolar compartment or changes in the number of residen

76 recovery of weight, fewer neutrophils in the alveolar compartment, and greater macrophage M2 polariza

77 Distinct Lgr5(+) cells are located in alveolar compartments and are sufficient to promote alve

78 Exhaled NO was measured, and alveolar concentration and bronchial flux were calculate

79 th sevoflurane delivered at a median minimum alveolar concentration of 0.45% (interquartile range, 0.

80 d Richmond Agitation Sedation Scale, minimum alveolar concentration, inspired and expired sevoflurane

81 Scale from -3 to -5 by adaptation of minimum alveolar concentration.

82 es/mL; above this cutoff was associated with alveolar consolidation at chest radiography, very severe

83 blood pneumococcal load was associated with alveolar consolidation on chest radiograph in nonconfirm

84 ted by measuring cemento-enamel junction and alveolar crest distance.

85 Pathologic findings included diffuse alveolar damage with pulmonary edema and hyaline membran

86 of lung volume, increased shunt, and diffuse alveolar damage-are also present in several critical neo

87 e to intrapulmonary shunt, whereas increased alveolar dead space explains the alteration of CO2 clear

88 critically mediates polarity establishment, alveolar development, and secretory function in the lact

89 r compartments and are sufficient to promote alveolar differentiation of epithelial progenitors throu

90 on as the morphological transition occurs at alveolar dimensions.

91 voflurane improves gas exchange, and reduces alveolar edema and inflammation in preclinical studies o

92 virus titers, enhanced vascular leakage, and alveolar edema.

93 to FVC ratio (FEV1/FVC), hyperinflation, and alveolar enlargement, but little is known about how age

94 plied pressure to the basolateral surface of alveolar epithelia.

95 died NPs were investigated in vitro in human alveolar epithelial A549 and macrophage-like THP1 cells.

96 Alveolar epithelial cell (AEC) apoptosis, proliferation,

97 Alveolar epithelial cell (AEC) mitochondrial dysfunction

98 e, expresses Pdgfralpha, and is critical for alveolar epithelial cell growth and self-renewal.

99 ratory distress syndrome is characterized by alveolar epithelial cell injury, edema formation, and in

100 sion of beta-catenin-driven target genes and alveolar epithelial cell markers in the elastase, as wel

101 iciency promotes lung fibrosis by augmenting alveolar epithelial cell mitochondrial DNA damage and ap

102 odifications regulate Aqp5 expression during alveolar epithelial cell transdifferentiation, suggestin

103 o determine the effects of FZD4 signaling on alveolar epithelial cell wound healing and repair, as we

104 ature WNT-5A attenuated canonical WNT-driven alveolar epithelial cell wound healing and transdifferen

105 Exposure of the human-type II cell alveolar epithelial cells (A549) to DPM derived from FBC

106 ties of TH are associated with protection of alveolar epithelial cells and restoration of mitochondri

107 d club cells' capacity to differentiate into alveolar epithelial cells at the single-cell level.

108 tenuated mitochondria-regulated apoptosis in alveolar epithelial cells both in vivo and in vitro.

109 Extensive infection of alveolar epithelial cells caused apoptosis and leakage o

110 ommunication between macrophages and type II alveolar epithelial cells during influenza infection whe

111 phage-derived MVs were fully internalized by alveolar epithelial cells in a time-, dose-, and tempera

112 at miR-34a expression is increased in type 2 alveolar epithelial cells in neonates with respiratory d

113 sitive correlation between CDC42 and type II alveolar epithelial cells marker SP-A, indicating the po

114 In addition, type I alveolar epithelial differentiation appeared to be dimin

115 ion factors and genes, which are involved in alveolar epithelial differentiation, was demonstrated.

116 ecent understanding of CO2 modulation of the alveolar epithelial function (lung oedema clearance), ep

117 evels of circulating Krebs Von Den Lungen 6 (alveolar epithelial injury marker), local caspase-3/7, a

118 ed persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasm

119 lating in the lung during the peak of type 2 alveolar epithelial stem cell (AEC2) proliferation.

120 level, arsenic-exposed mice had evidence for alveolar epithelial type 1 cell injury.

121 Here we report the generation of alveolar epithelial type 2 cells (AEC2s), the facultativ

122 l 358-bp promoter/enhancer (p358P/E) of lung alveolar epithelial type I (AT1) cell-specific gene aqua

123 ression was analyzed in lung homogenates and alveolar epithelial type II (ATII) cells of never-smoker

124 er-specific histone modifications in primary alveolar epithelium and A549 lung adenocarcinoma cells.

125 We showed that AKAP13 is expressed in the alveolar epithelium and lymphoid follicles from patients

126 Repair of the alveolar epithelium is critical for clinical recovery; h

127 ral infection from conducting airways to the alveolar epithelium is therefore a pivotal event in infl

128 ving effects on injured lung endothelium and alveolar epithelium, including enhancing the resolution

129 ells (AT1s) during the repair of the damaged alveolar epithelium.

130 hat causes endocytosis of Na,K-ATPase by the alveolar epithelium.

131 ms of injury to the lung endothelium and the alveolar epithelium.

132 evels of activated Stat5, another inducer of alveolar expansion and a known mediator of the Elf5 effe

133 -14 days after infection, and differences in alveolar extracellular matrix integrity and respiratory

134 nary edema by up-regulating sodium-dependent alveolar fluid clearance.

135 by reducing lung inflammation and enhancing alveolar fluid clearance.

136 fluid and showed that PRELP can be found in alveolar fluid, resident macrophages/monocytes, myofibro

137 that play a key role in airway branching and alveolar formation.

138 red alteration in elastic fiber composition, alveolar geometry and surfactant composition.

139 reduced vascular permeability and suppressed alveolar hemorrhage in an orthotopic transplant model fo

140 the right upper pulmonary lobe suggestive of alveolar hemorrhage.

141 ory and immune cells enabling restoration of alveolar homeostasis.

142 Alveolar hypoxia occurs in disorders ranging from altitu

143 ity, thereby preventing vascular leak during alveolar hypoxia.

144 the lung parenchyma in response to subacute alveolar hypoxia.

145 o maintain vascular integrity in the face of alveolar hypoxia.

146 tein film covering the interface of the lung alveolar in mammals is vital for proper lung function an

147 ccus pneumoniae is characterized by a robust alveolar infiltration of neutrophils (polymorphonuclear

148 ciferol treatment 6 hours postinjury reduced alveolar inflammation, cellular damage, and hypoxia.

149 ated nor were a host of circulating or intra-alveolar inflammatory cytokines.

150 may act as persistent stimuli for repetitive alveolar injury in IPF.

151 The levels of both bronchial and alveolar iNOS are increased in uncontrolled as compared

152 eas there was no difference in the number of alveolar lesions between WT and Tlr2/4(-/-) mice.

153 Consistent with barrier disruption at the alveolar level, arsenic-exposed mice had evidence for al

154 e into both AT2- and AT1-like cells and form alveolar-like structures.

155 ngs differentiated into all major airway and alveolar lineages in vivo in a region-appropriate fashio

156 oles and alveoli and comes into contact with alveolar lining fluid (ALF), which contains homeostatic

157 Ivacaftor significantly improved alveolar liquid clearance in isolated pig lung lobes ex

158 ited with 100% penetrance: arrest of mammary alveolar/lobular development and mammary tumorigenesis.

159 rmation, prolactin receptor trafficking, and alveolar lumen development.

160 ls into paratracheal lymph nodes from distal alveolar lung was diminished in leukotriene C4 synthase-

161 sted the role of Stat5 in dendritic cell and alveolar macrophage (AM) homeostasis in the lung using C

162 The effect of COPD on alveolar macrophage (AM) microbicidal responses was inve

163 CD163, C2+ and WSL, were compared to porcine alveolar macrophage (PAM) in terms of surface marker phe

164 Small alveolar macrophage CD206 expression was lower in COPD p

165 led DK128 was correlated with an increase in alveolar macrophage cells in the lungs and airways, earl

166 single-cell metabolomic profiling using rat alveolar macrophage cells incubated with different conce

167 nfection was exacerbated under conditions of alveolar macrophage depletion and in mice with a macroph

168 ated with global monocyte or tissue-resident alveolar macrophage depletion.

169 Rgamma is known to promote M2-macrophage and alveolar macrophage development.

170 flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously

171 findings suggest that selectively targeting alveolar macrophage differentiation within the lung may

172 Moreover, aging decreases alveolar macrophage phagocytosis of apoptotic neutrophil

173 Alveolar macrophage TNFalpha production was unaltered.

174 lease, and evaluated for in vivo absorption, alveolar macrophage uptake, and safety.

175 Alveolar macrophage-derived MVs were fully internalized

176 Toll-like receptors in alveolar macrophages (AMPhi) recognize the molecular con

177 Murine alveolar macrophages (AMs) were cultured ex vivo with/wi

178 Immunophenotyping of porcine alveolar macrophages (PAMs) showed that pigs with the KO

179 pecific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung

180 ureus and B. anthracis compared with E. coli Alveolar macrophages and CD14(+) cells were overall more

181 n of innate immunity mediators, initiated by alveolar macrophages and dependent on transcription driv

182 hus, aging induces defective phagocytosis by alveolar macrophages and increases lung damage.

183 Legionella pneumophila infects human alveolar macrophages and is responsible for Legionnaire'

184 sis (PAP), we evaluated lipid composition in alveolar macrophages and lung surfactant, macrophage-med

185 infected, most prominently CD45(neg) cells, alveolar macrophages and neutrophils.

186 sion studies demonstrated robust recovery of alveolar macrophages and recruitment of CD4+ lymphocytes

187 Alveolar macrophages at both day 4 and 14 and IMs at day

188 rated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis.

189 During the fibrotic phase, monocyte-derived alveolar macrophages differ significantly from tissue-re

190 ic genes expressed by mouse monocyte-derived alveolar macrophages during fibrosis were up-regulated i

191 Alveolar macrophages from female mice exhibited greater

192 that IL-4-stimulated bone marrow-derived and alveolar macrophages from female mice exhibited greater

193 s during fibrosis were up-regulated in human alveolar macrophages from fibrotic compared with normal

194 ure increased mitochondrial Ca(2+) influx in alveolar macrophages from wild-type, but not MCU(+/-), m

195 Alveolar macrophages had similar numbers of small and la

196 Small alveolar macrophages had the highest phagocytic ability.

197 ammatory gene expression levels, while large alveolar macrophages had the lowest.

198 Alveolar macrophages have emerged as major mediators of

199 WTI induced a pronounced reduction of alveolar macrophages in both strains that recovered with

200 abolism and accumulation of CD103(+) DCs and alveolar macrophages in lung.

201 es differ significantly from tissue-resident alveolar macrophages in their expression of profibrotic

202 Transplantation of infected Cftr-deficient alveolar macrophages into the lungs of noninfected CF mi

203 , although mitochondrial oxidative stress in alveolar macrophages is critical for fibrosis developmen

204 MARC-145 cells and primary porcine pulmonary alveolar macrophages led to significant reduction of STA

205 that therapies that enhance the function of alveolar macrophages may improve outcomes in older peopl

206 lso reveal the potential mechanisms by which alveolar macrophages mediate protection in vivo, namely

207 A population of monocyte-derived alveolar macrophages persisted in the lung for one year

208 We demonstrate that alveolar macrophages play a dominant role in conferring

209 Human alveolar macrophages produced CCL2 in a PGL-dependent fa

210 Large alveolar macrophages showed lower marker expression in C

211 stimulates pathogen killing and clearance by alveolar macrophages through extracellular signal-regula

212 Aging impairs the ability of alveolar macrophages to limit lung damage during influen

213 phagocytic function respectively, and large alveolar macrophages with low pro-inflammatory and phago

214 subpopulations; Small interstitial and small alveolar macrophages with more pro-inflammatory and phag

215 eaction in mammalian macrophages (NR8383 rat alveolar macrophages) exposed to a centrifuge regime of

216 o isoforms 5a and 5b) is highly expressed in alveolar macrophages, but its function there is unclear

217 With aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostas

218 Here, we examine the roles of alveolar macrophages, natural killer cells, and neutroph

219 Aside from alveolar macrophages, subsets of Langerin(+), BDCA1(-)CD

220 Aerosolized H5N1 exposure decimated alveolar macrophages, which were widely infected and cau

221 artment or changes in the number of resident alveolar macrophages.

222 e the bacteria first encounter lung-resident alveolar macrophages.

223 rculosis in humans and predominantly infects alveolar macrophages.

224 aused proinflammatory cytokine production in alveolar macrophages.

225 uorescent particles showed reduced uptake by alveolar macrophages.

226 tiologic agent of TB, usually resides in the alveolar macrophages.

227 cally downregulates cell cycling pathways in alveolar macrophages.

228 sive genes in murine bone marrow-derived and alveolar macrophages.

229 ion of markers for alternative activation on alveolar macrophages.

230 came increasingly similar to tissue-resident alveolar macrophages.

231 However, intra-alveolar matrix metalloproteinase activity and levels of

232 xpression and subsequent activation of intra-alveolar matrix metalloproteinases.

233 ics the micro/nano-scale architecture of the alveolar microenvironment and have used this system to i

234 Alveolar morphology, milk yield, and pup weights were si

235 g lactation, with no effect on milk yield or alveolar morphology.

236 The mesenchymal alveolar niche cell is Wnt responsive, expresses Pdgfral

237 alysis of the secretome and receptome of the alveolar niche reveals functional pathways that mediate

238 nd compare it with the exhaled bronchial and alveolar NO levels in patients with asthma vs a control

239 entral and alveolar tissue did not relate to alveolar NO, nor to bronchial flux of NO.

240 NOS in BAL macrophages were not reflected by alveolar NO.

241 te to ventilator-induced lung injury through alveolar overdistention.

242 the floor of the mouth) to 60% (OSCC in the alveolar part of the mandible).

243 viruses during childhood community-acquired alveolar pneumonia (CAAP).

244 osphatase (TRAP)-positive osteoclasts in the alveolar process surface and number of IL-6, MMP-1, and

245 rter lines, we track and purify human SFTPC+ alveolar progenitors as they emerge from endodermal prec

246 cells enhanced animal survival and decreased alveolar protein and proinflammatory cytokine concentrat

247 asis and how its disruption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid compositi

248 ce of Stat5 signaling in AMs, mice developed alveolar proteinosis with altered lipid homeostasis.

249 ed, whereas the added protection afforded by alveolar recruiting strategies remains controversial.

250 To determine whether an intensive alveolar recruitment strategy could reduce postoperative

251 rgery, the use of an intensive vs a moderate alveolar recruitment strategy resulted in less severe pu

252 o episodic inhaled nicotine via a novel lung alveolar region-targeted aerosol method produced nicotin

253 4 expression in COPD contributes to impaired alveolar repair capacity.

254 Alveolar rhabdomyosarcoma (ARMS) is a devastating pediat

255 ormal conditions, while in a patient-derived alveolar rhabdomyosarcoma cell line, harbouring the diag

256 The chromosomal translocation that leads to alveolar rhabdomyosarcoma development generates a novel

257 view, we specifically focus on embryonal and alveolar rhabdomyosarcoma, synovial sarcoma, and adult s

258 ional organisation of the fused landscape in alveolar rhabdomyosarcoma.

259 contralateral, both buccal-lingually in the alveolar ridge (P = 0.007) and in buccal wall thickness

260 Likewise, buccal-lingual width of alveolar ridge as well as thickness of buccal wall was c

261 of this study is to radiographically compare alveolar ridge changes with and without RP with cone-bea

262 riance, t test) at days 0, 7, 14, and 28 for alveolar ridge height and width and for markers of infla

263 Significantly greater loss in alveolar ridge height was found in molar sites allowed t

264 e allografts (FDBA) are available for use in alveolar ridge preservation after tooth extraction.

265 The alveolar ridge was measured pre- and postoperatively to

266 Loss of alveolar ridge width and height after tooth extraction i

267 Stage 1 involved adjustment of the alveolar segments (mean age 15.6 days), while Stage 2 ad

268 ing (NAM) is commonly employed to reduce the alveolar segments into proper alignment and to improve n

269 ormation of the elastin ECM, thereby driving alveolar septa formation to increase the gas-exchange su

270 haracterized by the formation of millions of alveolar septa that constitute the vast gas-exchange sur

271 mmary ductal elongation and induces aberrant alveolar side-branching.

272 in Fgfr3;Fgfr4 (Fgfr3;4) global mutant mice, alveolar simplification is first observed at the onset o

273 rization, marked airway hyperresponsiveness, alveolar simplification, decreased lung compliance, and

274 (+) mice had pronounced epithelial necrosis, alveolar space consolidation, and lymphoid hyperplasia;

275 Ns) after transepithelial migration into the alveolar space.

276 istics of small and large macrophages in the alveolar spaces and lung interstitium of COPD patients a

277 myofibroblasts in the focus core and normal alveolar structures, defining this region as an active f

278 ema, is characterized by loss of parenchymal alveolar tissue and impaired tissue repair.

279 ls of iNOS or iNOS expression in central and alveolar tissue did not relate to alveolar NO, nor to br

280 eling and destruction of the bronchiolar and alveolar tissue is associated with macrophage, CD4, CD8,

281 al feature of COPD is the loss of functional alveolar tissue without adequate repair (emphysema), yet

282 stress syndrome, epithelial cells, primarily alveolar type (AT) I cells, die and slough off, resultin

283 ive rise to alveolar type 2 cells (AT2s) and alveolar type 1 cells (AT1s) during the repair of the da

284 n recently that club cells also give rise to alveolar type 2 cells (AT2s) and alveolar type 1 cells (

285 ted CysLT2R-dependent production of IL-33 by alveolar type 2 cells, which engaged in a bilateral feed

286 ways that mediate growth and self-renewal of alveolar type 2 progenitor cells, including IL-6/Stat3,

287 signatures characteristic of differentiated alveolar type I (AT1) cells.

288 outstanding in vitro cytocompatibility with alveolar Type I cells, and dose-dependent caveolae-media

289 rcentages of proliferating and IAV-infected, alveolar type II (AECII) cells in dispersed lung cell po

290 Alveolar type II (AT2) cell dysfunction contributes to a

291 VEGF-A isoform deletion specifically in the alveolar type II (ATII) cells of adult mice.

292 Idiopathic pulmonary fibrosis lung alveolar type II cells have increased MnSOD(K68) acetyla

293 f active C' 3a (C3a) in normal primary human alveolar type II epithelial cells (AECs).

294 Alveolar type II epithelial cells (ATII) are instrumenta

295 ng tissue can robustly regenerate functional alveolar units after injury, but the mechanisms are unkn

296 derstand when improvement in oxygenation and alveolar ventilation is related to a lower degree or ris

297 It guarantees sufficient alveolar ventilation, high FiO2 concentration, and high

298 istinctive membranous structure of flattened alveolar vesicles supported by a proteinaceous network,

299 rivascular fluid cuff formation around extra-alveolar vessels with decreased respiratory compliance.

300 nning of Limusaurus specimens, reveal dental alveolar vestiges and indicate that ontogenetic tooth lo

301 fibroblastic foci, an abnormal adjacency of alveolar walls was seen, suggesting alveolar collapse.