ライフサイエンスコーパス: ALI

1 ALI culture provides an accessible model that will enabl

2 ALI cultures support parasite expansion > 100-fold and g

3 ALI cultures were evaluated by histology, immunohistoche

4 ALI developed in 4 patients in the placebo group and no

5 ALI is common in patients who test positive for SARS-CoV

6 ALI was a prespecified adjudicated end point using a for

7 ALI was categorized as mild if ALT was greater than the

8 ALI was quantified by weight loss, bronchoalveolar lavag

9 ALI-iAEC2 were used to study alveolar repair over a peri

10 ALI-induced HMGB1 leaks and is captured by arterial macr

11 A total of 150 ALI events occurred in 108 patients during follow-up (pl

12 Among 13 885 patients, 1.7% (n=232) had 293 ALI hospitalizations (0.8 per 100 patient-years).

13 Risk factors for and outcomes after ALI have not been fully evaluated.

14 hat changes in the ventilatory pattern after ALI result not only from sensory input due to pulmonary

15 in determining the ventilatory pattern after ALI.

16 tricularly during the week of survival after ALI.

17 sts as a therapeutic tool to protect against ALI caused by pneumococcal infection.

18 d-histone H3 levels, which protected against ALI and ameliorated pulmonary oedema and total protein i

19 NET-protein clearance and protected against ALI in mice; thus, DNase I may be a new potential adjuva

20 urines, adenosine and ATP, protected against ALI induced by purified LPS.

21 Phosphatiosomes significantly alleviated ALI in mice as revealed by examining their pulmonary app

22 was not significantly different between AMR-ALI and non-AMR-ALI.

23 cantly different between AMR-ALI and non-AMR-ALI.

24 d treatment to ticagrelor or clopidogrel and ALI.

25 e effect of TREM-1 on NLRP3 inflammasome and ALI is still unknown.

26 ischemic stroke causes lung inflammation and ALI in mice.

27 bution, activated neutrophil inhibition, and ALI treatment were performed to evaluate the feasibility

28 onfirmed in A549 cells, plus submersion, and ALI culture of HBE cells.

29 rapeutic window, as compared to NAC, in APAP-ALI.

30 ion in APAP-induced acute liver injury (APAP-ALI) and justifies development of anti-inflammatory ther

31 eatment improves survival in a model of APAP-ALI.

32 its mechanism of action in preclinical APAP-ALI.

33 is elevated in clinical and preclinical APAP-ALI.

34 n with h2G7 in vitro and in preclinical APAP-ALI.

35 B1-specific therapy as a means to treat APAP-ALI and other inflammatory conditions.

36 with more severe histological injury such as ALI or neutrophilic capillaritis.

37 submerged cultures without VIP, VIP-assisted ALI culture significantly boosted the number of EC cells

38 ctors for development of COVID-19-associated ALI in a large cohort in the United States.

39 important role in murine malaria-associated ALI.

40 nstream responses to cause sepsis-associated ALI.

41 portant pathophysiologic differences between ALI caused by different etiologies, we hypothesized that

42 onist, maraviroc, was protective against C5a-ALI.

43 alveolar-capillary barrier dysfunction (C5a-ALI; EC(50[C5a]) = 20 ng/g body weight).

44 role of C5aR1(+) hematopoietic cells in C5a-ALI.

45 The severity of C5a-ALI was aggravated in C5-deficient mice.

46 g how leukocytes interact with NiV and cause ALI in human lung xenografts is crucial for identifying

47 Stent thrombosis and thromboembolism caused ALI in 13% and 5%, respectively.

48 jury (ALI), we hypothesized that CIRP causes ALI via induction of ER stress.

49 ESIGN, SETTING, AND PARTICIPANTS: The CITRIS-ALI trial was a randomized, double-blind, placebo-contro

50 evated in C5a-induced and IgG immune complex ALI models, suggesting a common inflammatory mechanism.

51 ee-dimensional air-liquid interface culture (ALI) model was used to test whether TLR2 or TLR3 stimula

52 molecular mechanism underlying PLY-dependent ALI and suggests the possible use of CysLT1 antagonists

53 Although, COPD-derived ALI cultures preserved some features known from COPD pat

54 sed on blockade of TGF-beta1 activity during ALI differentiation.

55 ellular histones appeared in the BALF during ALI and directly activated the NLRP3 inflammasome.

56 antly reduced IL-1beta levels in BALF during ALI.

57 ulate lung PMN (or macrophage) counts during ALI.

58 h eosinophils recruited into the lung during ALI appeared to be capable of phagocytizing bacteria, ne

59 eases pulmonary vascular permeability during ALI.

60 trol of pulmonary adenosine signaling during ALI.

61 Treatment during ALI hospitalization included endovascular revascularizat

62 epithelial 3-dimensional model system (EPC2-ALI) and murine models of EoE to define the relationship

63 id not translate into histologically evident ALI.

64 dized phospholipids as a factor exacerbating ALI in the aging lungs.

65 cell exposure to NPs, complementing existing ALI systems.

66 can limit lung inflammation in experimental ALI models, studies to date have not examined efficacy o

67 oid cells in multiple models of experimental ALI, leading to the conclusion that TF in myeloid cells

68 s is not a major contributor to experimental ALI.

69 Treatment of CS-exposed ALI cultures with interferon beta-1 abrogated the viral

70 tomatic PAD and without atrial fibrillation, ALI occurs at a rate of 1.3%/y, is most frequently cause

71 Vorapaxar reduced first ALI events by 41% (hazard ratio, 0.58; 95% confidence in

72 lar macrophages within the airways following ALI.

73 The heightened resistance observed following ALI correlated with enhanced early clearance of pneumoco

74 DNase I may be a new potential adjuvant for ALI therapy.

75 may be a potential therapeutic approach for ALI.

76 Aging is a risk factor for ALI.

77 tional estimate=51 914) hospitalizations for ALI, endovascular revascularization was performed in 500

78 tery disease patients at heightened risk for ALI, an event associated with subsequent cardiovascular

79 P<0.01) were associated with lower risk for ALI.

80 e the optimal revascularization strategy for ALI.

81 in the nucleus tractus solitarii (nTS) from ALI but not sham rats.

82 ve patterns of the in situ preparations from ALI pups retained these characteristics despite removing

83 in both LPS and TRALI models protected from ALI.

84 es not express NS3 and NS4 replicated in HAE-ALI as effectively as the wild-type virus; however, the

85 d NS4 underwent an abortive infection in HAE-ALI.

86 the NS2 protein in HBoV1 replication in HAE-ALI.

87 airway epithelium air-liquid interface (HAE-ALI) cultures, HBoV1 infection initiates a DNA damage re

88 ium cultured at an air-liquid interface (HAE-ALI).

89 AE) cultured at an air-liquid interface (HAE-ALI).

90 1.1-1.5, P<0.01) were associated with higher ALI risk.

91 ascular permeability, and induced histologic ALI in naive mice.

92 LPS-induced inflammatory injury and two-hit ALI caused by suboptimal mechanical ventilation and inje

93 a targeted small molecule screen in our iAT2 ALI system.

94 may be important interventions for improving ALI survivors' physical outcomes.

95 th combined inhibition of CXCR4 and PAI-1 in ALI and various disease stages of IPF.

96 e inhaled A2B adenosine receptor agonists in ALI treatment.

97 xes showed promising therapeutic efficacy in ALI and in early fibrinogenic stage of IPF.

98 rate that central pathophysiologic events in ALI (inflammation, IL-1beta levels, endothelial and alve

99 ed for potential therapeutic exploitation in ALI/ARDS.

100 show that TREM-1 aggravates inflammation in ALI by activating NLRP3 inflammasome, and blocking TREM-

101 s showed a significantly low TJ integrity in ALI cultures compared with HBECs from healthy subjects.

102 -4 and IL-13, decreased barrier integrity in ALI cultures of HBECs from control subjects but not in H

103 ain insight into aging-related mechanisms in ALI, we investigated the effects of SIRT7 depletion on l

104 induced effects were similarly pronounced in ALI cultures from patients compared to healthy controls.

105 rolled inflammation plays a critical role in ALI.

106 myeloid cells, DRP1 or MMP12 suppression in ALI-inflicted mice repress arterial stress and brake MMP

107 A-4, as a mechanistically relevant target in ALI, and the accuracy of VLA-4-targeted PET in quantific

108 rats, but mitigated changes in fR and VPV in ALI rats.

109 ced ALI, bleomycin-induced ALI) and indirect ALI (systemic LPS, cecal ligation and puncture).

110 acheally injected either bleomycin to induce ALI or saline as a sham control.

111 Taken together, acid-induced ALI results in epithelial MV shuttling of miR-17/221 tha

112 ar dynamics and gas exchange in acid-induced ALI, yet not in Tween-induced surfactant depletion.

113 in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls.

114 a, ventilator-induced ALI, bleomycin-induced ALI) and indirect ALI (systemic LPS, cecal ligation and

115 osine or ATPgammaS mitigates E. coli-induced ALI in mice and may be useful as an adjuvant therapy in

116 hat during LPS-/IgG immune complexes-induced ALI, the DNA binding activities of C/EBPgamma are obviou

117 exosomes in the development of T/HS-induced ALI and the role of TLR4 in the ML exosome-mediated infl

118 to ML as a critical mediator of T/HS-induced ALI through macrophage TLR4 activation.

119 treatment approach for inflammation-induced ALI and pulmonary edema.

120 ovided mechanistic insights into IVI-induced ALI and repair process.

121 ing mechanisms that give rise to IVI-induced ALI are poorly understood.

122 a mouse model of lipopolysaccharide-induced ALI.

123 e effect of TREM-1 modulation on LPS-induced ALI and activation of the NLRP3 inflammasome.

124 d a prophylactic and therapeutic LPS-induced ALI model in C57BL/6 male mice.

125 n conclusion, NETs formed during LPS-induced ALI, caused organ damage and initiated the inflammatory

126 In settings of LPS-induced ALI, we show that Src tethered to the endosome tyrosine

127 urce of TF during intra-tracheal LPS-induced ALI.

128 ation by 40% in a mouse model of LPS-induced ALI.

129 ice at baseline and subjected to LPS-induced ALI.

130 -3, CD44, CD137, and PDI) in malaria-induced ALI.

131 ect (bacterial pneumonia, ventilator-induced ALI, bleomycin-induced ALI) and indirect ALI (systemic L

132 in (OVA)-induced allergic lung inflammation (ALI) was induced in mice followed by intranasal infectio

133 ratio (INR) characterise acute liver injury (ALI) and failure (ALF), yet a wide heterogeneity in clot

134 s unclear if the risk of acute liver injury (ALI) is increased for statin initiators compared to nonu

135 has been associated with acute liver injury (ALI) manifested by increased liver enzymes in reports wo

136 ive patients with ALF or acute liver injury (ALI; INR >= 2.0 with no encephalopathy), over two decade

137 pathological features of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

138 saccharide (LPS)-mediated acute lung injury (ALI) and assessed the use of DNase I, for the treatment

139 Acute lung injury (ALI) and idiopathic pulmonary fibrosis (IPF) are severe

140 Acute lung injury (ALI) and its more severe form, acute respiratory distres

141 oding plasmid ameliorated acute lung injury (ALI) and reduced cytokine/chemokine levels in BALF.

142 ia, which may progress to acute lung injury (ALI) and respiratory failure with a potentially fatal ou

143 to the lungs for treating acute lung injury (ALI) by intravenous administration.

144 Although acute lung injury (ALI) contributes significantly to critical illness, reso

145 he impact of feeding from acute lung injury (ALI) diagnosis to hospital discharge, an interval that,

146 le in the pathogenesis of acute lung injury (ALI) during both the acute pneumonitis stage and progres

147 m rats, rats a week after acute lung injury (ALI) express more pro-inflammatory cytokines in their br

148 tion of PLY caused lethal acute lung injury (ALI) in BLT2-deficient mice, with evident vascular leaka

149 the onset of LPS-induced acute lung injury (ALI) in mice led to improved survival (48 h), and blocki

150 Acute lung injury (ALI) increases respiratory rate (fR) and ventilatory pat

151 Acute lung injury (ALI) is a common cause of morbidity in patients after se

152 Malaria-associated acute lung injury (ALI) is a frequent complication of severe malaria that i

153 Acute lung injury (ALI) is a major component of multiple organ dysfunction

154 Acute lung injury (ALI) is an acute inflammatory lung disease that causes m

155 Acute lung injury (ALI) is associated with high mortality and uncontrolled

156 mmune response and NiV to acute lung injury (ALI) is still unknown.

157 Acute lung injury (ALI) occurs in up to 30% of patients with subarachnoid h

158 mechanisms of NiV-induced acute lung injury (ALI) remain unclear.

159 Acute lung injury (ALI) remains a serious health issue with little improvem

160 , we find that inflicting acute lung injury (ALI) to mice doubles their incidence of AAA and accelera

161 ributes to sepsis induced acute lung injury (ALI) via integrin beta6.

162 itical mediator of direct acute lung injury (ALI) with global TF deficiency resulting in increased ai

163 Acute lung injury (ALI), a common condition in critically ill patients, has

164 piratory diseases such as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), chroni

165 Acute lung injury (ALI), endotheliitis, capillary inflammation, and C4d pos

166 flammation, a hallmark of acute lung injury (ALI), in mice, which was not recapitulated in Nrf2 knock

167 ls suggest that increased acute lung injury (ALI), potentially due to enhanced viral spread and decre

168 a have been implicated in acute lung injury (ALI), resulting in inflammation and fibrosis.

169 stress is associated with acute lung injury (ALI), we hypothesized that CIRP causes ALI via induction

170 ysaccharide (LPS)-induced acute lung injury (ALI), we observed augmented temporal generation of cytok

171 o induce NET formation in acute lung injury (ALI), which is associated with a high mortality rate in

172 hit cell culture model of acute lung injury (ALI).

173 eptibility to LPS-induced acute lung injury (ALI).

174 scular leak thus inducing acute lung injury (ALI).

175 es in the pathogenesis of acute lung injury (ALI).

176 pression in the lungs and acute lung injury (ALI).

177 ysaccharide (LPS)-induced acute lung injury (ALI).

178 barrier dysfunction, and acute lung injury (ALI).

179 disease states including acute lung injury (ALI).

180 y, and the development of acute lung injury (ALI).

181 S- and bleomycin-mediated acute lung injury (ALI).

182 inhalation mouse model of acute lung injury (ALI).

183 , a major risk factor for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).

184 in two distinct models of acute lung injury (ALI): LPS-induced inflammatory injury and two-hit ALI ca

185 cells were grown at an air-liquid interface (ALI) and subjected to light mechanical stimulation from

186 We directly exposed air-liquid interface (ALI) cultures derived from primary human nonsmoker airwa

187 TJs were determined in air-liquid interface (ALI) cultures of control and asthmatic primary human bro

188 elivering particles on air-liquid interface (ALI) cultures reproducing normal and susceptible health

189 A new prototype air-liquid interface (ALI) exposure system, a flatbed aerosol exposure chamber

190 an epithelium layer in air-liquid interface (ALI) interacting with BSM.

191 em cell (iPSC)-derived air-liquid interface (ALI) model of alveolar epithelial type II (ATII)-like ce

192 tiated and cultured at air-liquid interface (ALI) on the underside of 3 microm pore-sized transwells,

193 0 cells cultured at an air-liquid interface (ALI) responded to apically or basolaterally applied PAR-

194 ) at the physiological air-liquid interface (ALI) resulted in type 2 AEC-like cells (iAEC2) with alve

195 uman lung cells at the air-liquid interface (ALI) to ambient aerosol could help identify acute biolog

196 n differentiated in an air-liquid interface (ALI) usually provide a pseudostratified airway epitheliu

197 th the culture method [air-liquid interface (ALI) vs submerged] and the presence of vasoactive intest

198 ted with SARS-CoV-2 at air-liquid interface (ALI).

199 l (HBE) cells grown at air-liquid interface (ALI).

200 arvum in vitro using "air-liquid interface" (ALI) cultures derived from intestinal epithelial stem ce

201 pithelium (cultured in air-liquid interface, ALI) obtained from a large series of patients (n = 116)

202 Using the optimized inverted ALI/postincubation procedure, pro-inflammatory immune re

203 Acute limb ischemia (ALI) is an important clinical event and an emerging card

204 larization strategy for acute limb ischemia (ALI) remains unclear, and contemporary comparative effec

205 e at heightened risk of acute limb ischemia (ALI), a morbid event that may result in limb loss.

206 levels increase 10-fold during LPS-mediated ALI in wild-type mice (due to increases in leukocyte-der

207 ecrotic alveolar macrophages in LPS-mediated ALI, as a critical initiator of increased vascular perme

208 are critical in transducing sepsis mediated ALI, we now demonstrate that intrapulmonary alphavbeta3

209 Methods: ALI was induced by a single intratracheal administration

210 Independent of injury mode, ALI resulted in asynchronous alveolar ventilation charac

211 NETs formation was detected in murine ALI tissue in vivo and was associated with increased NET

212 lly-relevant E.coli (non-sterile LPS) murine ALI model.

213 more resistant to lethal infection than non-ALI mice.

214 n rates were obtained compared to the normal ALI setup.

215 , it appears that lung inflammation, but not ALI, occurs after experimental ischemic stroke in mice.

216 for the previously described attenuation of ALI.

217 on, leading to the subsequent attenuation of ALI.

218 ction in lung endothelium and attenuation of ALI.

219 In a mouse model of sepsis, a major cause of ALI, 3-O-beta-d-glycosyl aesculin significantly enhanced

220 bility between direct and indirect causes of ALI.

221 s important to understand the development of ALI following the initial ischemic injury to the brain.

222 ruitment and migration during development of ALI.

223 er of the pathogenesis of the development of ALI.

224 hospitalizations with a primary diagnosis of ALI.

225 i-inflammatory drug, mitigates the effect of ALI on fR and ventilatory pattern variability.

226 ubarachnoid haemorrhage but the incidence of ALI after ischemic stroke is unclear.

227 ol 4 linker, at day 2 after the induction of ALI.

228 The majority of ALI events occurred as a result of surgical graft thromb

229 prevent RhoA nitration in the management of ALI.

230 To better understand the mechanism of ALI in malaria infection, here we investigated the roles

231 preserved lung function in a mouse model of ALI.

232 al oximetry in experimental murine models of ALI induced by hydrochloric acid, Tween instillation, or

233 ng three well-characterized murine models of ALI known to require NLRP3 inflammasome activation.

234 le in determining the ventilatory pattern of ALI rats.

235 the ankle-brachial index were predictive of ALI.

236 ated the causes, sequelae, and predictors of ALI in a contemporary population with symptomatic PAD an

237 ges in coagulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulabil

238 conducted a cohort study to compare rates of ALI in statin initiators vs nonusers among 7686 HIV/HCV-

239 tatus, statin initiators had a lower risk of ALI and death within 18 months compared with statin nonu

240 endothelial barrier function in settings of ALI in vitro and in vivo, through enhanced recycling of

241 endothelial barrier function, in settings of ALI.

242 to provide a robust platform for studies of ALI and ARDS to evaluate vaccine and antiviral drug perf

243 hysical Function score) for 203 survivors of ALI enrolled from 12 hospitals participating in the ARDS

244 ion is a promising strategy for treatment of ALI and IPF.

245 dings suggest novel targets for treatment of ALI, for which there is currently no known efficacious d

246 sed the use of DNase I, for the treatment of ALI.

247 uld be a valuable candidate for treatment of ALI.

248 promising new direction for the treatment of ALI.

249 of vorapaxar was consistent across types of ALI.

250 same family as C/EBPbeta and C/EBPdelta, on ALI has not been elucidated.

251 f 3,155 patients (2.2%) who developed ALF or ALI during pregnancy were reviewed to determine how many

252 maCult-Ex Plus (expansion medium)/PneumaCult-ALI (differentiation medium).

253 In the overall population, ALI hospitalization was associated with subsequent MACE

254 or grams of protein per kilogram early post-ALI diagnosis at recommended levels was associated with

255 ng to the primary outcome, postrandomization ALI hospitalization.

256 terol was well tolerated but did not prevent ALI.

257 processes are a potential therapy to prevent ALI.

258 Pseudomonas aeruginosa infection of primary ALI barriers through a hepoxilin A3-directed mechanism.

259 o WT, but not Ripk3(-/-) mice, recapitulates ALI-induced proteolytic collapse of arterial architectur

260 bese (ob/ob) mice (OBKO) resulted in reduced ALI and impaired viral spread, like their lean counterpa

261 receptor 1 antagonism with vorapaxar reduced ALI overall and by type.

262 Vorapaxar reduces ALI in patients with symptomatic PAD with consistency ac

263 jury) and 10 patients with nonimmune-related ALI.

264 potential of kallistatin for sepsis-related ALI/ARDS.

265 or in antibody-mediated transfusion-related ALI.

266 liver aminotransferases >200 U/L, (2) severe ALI (coagulopathy with hyperbilirubinemia), and (3) deat

267 creases (HR, 0.52 [95% CI, .40-.66]), severe ALI (HR, 0.26 [95% CI, .13-.55]), and death (HR, 0.19 [9

268 vations (HR, 0.57 [95% CI, .45-.72]), severe ALI (HR, 0.15 [95% CI, .06-.37]), and death (HR, 0.42 [9

269 200 U/L (HR, 0.66 [95% CI, .53-.83]), severe ALI (HR, 0.23 [95% CI, .12-.46]), and death (HR, 0.36 [9

270 In multivariable analysis, severe ALI was significantly associated with elevated inflammat

271 or role for elevated Tr-OxPLs in more severe ALI and delayed resolution in aging lungs.

272 WT mice had significantly more severe ALI than CIRP KO mice.

273 injury/acute respiratory distress syndrome (ALI/ARDS) in C57BL/6J mice.

274 olar repair using hiPSC-AEC2 cultured at the ALI and indicated that this model can be used in the fut

275 A549 cells were exposed to DEA at the ALI and under submerged conditions in different electros

276 induced biological responses of cells at the ALI using electrode-assisted deposition and may be usefu

277 gas flow combined with cells exposed at the ALI.

278 mbrane impairment increased for cells at the ALI; submerged cells were unaffected.

279 TLR3 stimulation did not change TEER in the ALI model.

280 with tissue-specific deletion of Adora2b to ALI, utilizing a two-hit model where intratracheal LPS t

281 PA) and that NPA significantly contribute to ALI.

282 limits NiV dissemination and contributes to ALI and inform efforts to identify therapeutic targets.I

283 a member of NLRs family that contributes to ALI.

284 of immunoregulatory pathways contributing to ALI pathogenesis.

285 within short time, i.e. One hour exposure to ALI-deposited CuO-NPs and 2.5 h postincubation.

286 ence interval, 0.39-0.86; P=0.006) and total ALI events by 41% (94 versus 56 events; risk ratio, 0.59

287 nors and three COPD patients, cultured under ALI (air-liquid interface) conditions.

288 differentiating epithelial cells grown under ALI conditions undergo profound changes in metabolism an

289 However, there are many instances where ALI resolves spontaneously through endogenous pathways t

290 In the present study, we determine whether ALI induced by LPS and IgG immune complexes is affected

291 ore than 6 months prior were associated with ALI (adjusted HR 2.63, 95% CI 1.75-3.96).

292 Baseline factors associated with ALI were identified using Cox proportional hazards model

293 r of endothelial dysfunction associated with ALI.

294 Surprisingly, mice with ALI were significantly more resistant to lethal infectio

295 clearance or resistance to IPD in mice with ALI.

296 Models with ALI hospitalization as a time-dependent covariate were d

297 In patients with ALI, endovascular revascularization was associated with

298 Amputation occurred in 17.6% presenting with ALI.

299 the ventilatory pattern similar to rats with ALI.

300 Patients with versus without ALI were younger and more often had previous peripheral