ライフサイエンスコーパス: ALI

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

2 ALI was a prespecified adjudicated end point using a for

3 ALI was quantified by weight loss, bronchoalveolar lavag

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

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

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

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

8 thesized that NADPH oxidase protects against ALI by limiting neutrophilic inflammation and activating

9 l in which proinflammatory T cells aggravate ALI in different phases of the disease.

10 Nase1(-/-)/Trap1(m/m) mice had an aggravated ALI, suggesting that NETs directly influence the severit

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

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

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

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

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

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

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

18 its mechanism of action in preclinical APAP-ALI.

19 is elevated in clinical and preclinical APAP-ALI.

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

21 important role in murine malaria-associated ALI.

22 The pathophysiology of SAP-associated ALI is poorly understood, but elevated serum levels of I

23 nhibition of IL-6 may prevent SAP-associated ALI.

24 nstream responses to cause sepsis-associated ALI.

25 cute pancreatitis-associated (AP-associated) ALI to determine the role of IL-6 in ALI lethality.

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

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

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

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

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

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

32 similar to those of surgery patients caused ALI.

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

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

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

36 neutrophil accumulation, but Nrf2 decreased ALI without affecting neutrophil recovery.

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

38 Nineteen patients developed ALI at least 6 hours after the sample draw.

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

40 he endogenous production of adenosine during ALI resolution.

41 ury revealed induction of the ADORA2B during ALI in vivo that was abolished following HIF inhibition

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

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

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

45 onary edema and improved gas exchange during ALI in conjunction with elevated adenosine levels in the

46 pulmonary edema and lung inflammation during ALI in vivo.

47 tant attenuation of lung inflammation during ALI were specific for alveolar-epithelial expressed HIF1

48 tes alveolar-capillary barrier injury during ALI in mice.

49 nd ENT2 transcript and protein levels during ALI.

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

51 atory cell trafficking into the lungs during ALI resolution revealed that regulatory T cells (Tregs)

52 eases pulmonary vascular permeability during ALI.

53 r full extracellular histone presence during ALI, suggesting a positive feedback mechanism.

54 epithelial Adora2b in lung protection during ALI opens possibilities for combined therapies targeted

55 ing role for HIF1A in lung protection during ALI, where normoxic HIF1A stabilization and HIF-dependen

56 trol of pulmonary adenosine signaling during ALI.

57 y adenosine receptor (ADOR) signaling during ALI.

58 cell exposure to NPs, complementing existing ALI systems.

59 The majority of patients experiencing ALI require mechanical ventilation.

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

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

62 s is not a major contributor to experimental ALI.

63 acute liver injury and acute liver failure (ALI/ALF).

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

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

66 lar macrophages within the airways following ALI.

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

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

69 0 patients taken on the day of admission for ALI/ALF.

70 may be a potential therapeutic approach for ALI.

71 cores and identify patients at high risk for ALI.

72 elastase-deficient mice protected mice from ALI, whereas DNase1(-/-)/Trap1(m/m) mice had an aggravat

73 in both LPS and TRALI models protected from ALI.

74 Patients who had ALI at baseline or in the subsequent 6 hours were exclud

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

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

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

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

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

80 luded were a control group that did not have ALI (n = 6) and 2 additional groups (n = 6 each) that ha

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

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

83 mCI is a potent inhibitor of experimental IC-ALI, equally dependent on both C5 inhibition and LTB4 bi

84 data highlight the importance of LTB4 in IC-ALI and activation of C5 by the complement pathway C5 co

85 immune complex-induced acute lung injury (IC-ALI).

86 llular adenosine breakdown revealed impaired ALI resolution.

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

88 In ALI (vs. submerged) cultures, pIgR expression was strong

89 ciated) ALI to determine the role of IL-6 in ALI lethality.

90 e inhaled A2B adenosine receptor agonists in ALI treatment.

91 t in nearly 19-fold higher concentrations in ALI/ALF patients, compared to healthy controls (P < 0.00

92 ole in the development of pulmonary edema in ALI through activation of p55-mediated death signaling,

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

94 ed for potential therapeutic exploitation in ALI/ARDS.

95 TNF has been implicated in ALI pathogenesis, but the precise mechanisms remain unde

96 was associated with significant increases in ALI survival time (277 vs. 395 min; P<0.05).

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

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

99 -4 and IL-13, decreased barrier integrity in ALI cultures of HBECs from control subjects but not in H

100 nes and the NLRP3 inflammasome, resulting in ALI.

101 rolled inflammation plays a critical role in ALI.

102 Acid aspiration caused increased ALI (as assessed by bronchoalveolar lavage fluid albumin

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

104 gh-pressure mechanical ventilation to induce ALI.

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

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

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

108 -28-oyl]imidazole limited aspiration-induced ALI in wild-type mice and reduced endothelial cell injur

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

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

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

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

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

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

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

116 t SOCS3 has a protective role in LPS-induced ALI by suppressing C/EBPdelta activity in the lung.

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

118 olecular mechanism(s) leading to LPS-induced ALI remain elusive.

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

120 In the setting of LPS-induced ALI, enhanced efferocytosis and decreased numbers of neu

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

122 al downstream target of SOCS3 in LPS-induced ALI.

123 that CREMalpha is upregulated in LPS-induced ALI.

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

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

126 -3, CD44, CD137, and PDI) in malaria-induced ALI.

127 itions in vitro or during ventilator-induced ALI in vivo occurs under normoxic conditions.

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

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

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

131 th acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currentl

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

133 Fifty patients with acute liver injury (ALI), 78% of whom also had hepatic encephalopathy (HE; A

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

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

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

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

138 While acute lung injury (ALI) contributes significantly to critical illness, it r

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

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

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

142 Using a standard model of acute lung injury (ALI) in mice featuring airway instillation of LPS, ALI w

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

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

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

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

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

148 Acute lung injury (ALI) is an inflammatory disease with a high mortality ra

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

150 Acute lung injury (ALI) is characterized by alveolar injury and uncontrolle

151 Acute lung injury (ALI) is characterized by increased endothelial hyperperm

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

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

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

155 During sepsis, acute lung injury (ALI) results from activation of innate immune cells and

156 with normal lungs develop acute lung injury (ALI) secondary to mechanical ventilation, with 60% to 80

157 Acute lung injury (ALI) secondary to sepsis is a complex syndrome associate

158 r physical impairments in acute lung injury (ALI) survivors were potentially limited by single-center

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

160 lity in a murine model of acute lung injury (ALI) was associated with increased vascular permeability

161 Patients with acute lung injury (ALI) who retain maximal alveolar fluid clearance (AFC) h

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

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

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

165 For development of acute lung injury (ALI), the invasion and regulation of immune cells are hi

166 le in the pathogenesis of acute lung injury (ALI), the precise molecular mechanisms underlying the de

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

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

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

170 disease states including acute lung injury (ALI).

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

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

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

174 and proteases, a cause of acute lung injury (ALI).

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

176 ses in conditions such as acute lung injury (ALI).

177 implicated in attenuating acute lung injury (ALI).

178 orbidity and mortality in acute lung injury (ALI).

179 ant of oxygenation during acute lung injury (ALI).

180 ogenic components driving acute lung injury (ALI).

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

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

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

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

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

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

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

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

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

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

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

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

193 with IL-6 were more likely to develop lethal ALI.

194 int to Nrf2 as a therapeutic target to limit ALI by attenuating neutrophil-induced cellular injury.

195 n mice featuring airway instillation of LPS, ALI was dependent on availability of NLRP3 as well as ca

196 lastin during LPS- and/or bleomycin-mediated ALI.

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

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

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

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

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

202 of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of ov

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

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

205 f wild-type Tregs was associated with normal ALI resolution.

206 On day 3 of ALI, CREMalpha transgenic mice present a stronger inflam

207 rial injury, limiting the true assessment of ALI incidence.

208 for the previously described attenuation of ALI.

209 Since most cases of ALI resolve spontaneously, understanding the endogenous

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

211 gastric aspiration injury, a major cause of ALI.

212 bility between direct and indirect causes of ALI.

213 tly associated with increased development of ALI (P = 0.0008, 0.004, respectively).

214 plays a critical role in the development of ALI during severe sepsis and is a suggested risk factor

215 between Ang-2 and subsequent development of ALI was robust to adjustment for sepsis and vasopressor

216 The primary outcome was development of ALI within 72 hours of surgery.

217 er of the pathogenesis of the development of ALI.

218 ruitment and migration during development of ALI.

219 ng patients were followed for development of ALI.

220 za+TSA after lipopolysaccharide induction of ALI through epigenetic modification of lung endothelial

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

222 prevent RhoA nitration in the management of ALI.

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

224 and histone deacetylase in the mechanism of ALI.

225 trans-signaling is an essential mediator of ALI in SAP across species and suggest that therapeutic i

226 t-stimulated AFC in an experimental model of ALI in rats.

227 tion in a clinically relevant mouse model of ALI induced by acid aspiration and investigated the effe

228 preserved lung function in a mouse model of ALI.

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

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

231 of CREM in T cells determine the outcome of ALI, and CREMalpha transgenic animals represent a model

232 stemic complications, and adverse outcome of ALI/ALF.

233 othelial injury in the early pathogenesis of ALI.

234 and determining the early pathophysiology of ALI.

235 the ankle-brachial index were predictive of ALI.

236 le IL-6 receptor was a reliable predictor of ALI in SAP.

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

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

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

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

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

242 endothelial barrier function, in settings of ALI.

243 that NETs directly influence the severity of ALI.

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

245 al decision-making, both in the treatment of ALI and the design/execution of patient-individualized t

246 get for clinical prevention and treatment of ALI in severe sepsis.

247 The goal for treatment of ALI is to target pathways that lead to profound dysregul

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

249 promising new direction for the treatment of ALI.

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

251 uld be a valuable candidate for treatment of ALI.

252 of vorapaxar was consistent across types of ALI.

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

254 terol was well tolerated but did not prevent ALI.

255 processes are a potential therapy to prevent ALI.

256 combinatorial Aza+TSA therapy in preventing ALI in lipopolysaccharide-induced endotoxemia and raise

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

258 nding the endogenous mechanisms that promote ALI resolution is important to developing effective ther

259 t adenosine generation in Tregs in promoting ALI resolution.

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

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

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

263 or in antibody-mediated transfusion-related ALI.

264 73(-/-) mice; P<0.05) and failure to resolve ALI adequately.

265 h typically seen in individuals with sepsis, ALI is also a major complication in severe acute pancrea

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

271 MGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital

272 ncentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients p

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

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

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

276 gas flow combined with cells exposed at the ALI.

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

278 also significantly reduced mortality in the ALI model.

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

280 PA) and that NPA significantly contribute to ALI.

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

282 a member of NLRs family that contributes to ALI.

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

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

285 or a new generation of drugs needed to treat ALI.

286 Secondary outcomes were ALI within 28 days, organ failure, adverse events, survi

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

288 Pigs were randomized into 3 groups in which ALI was induced by HCl inhalation: pigs studied in the s

289 od, in both control animals and animals with ALI.

290 PBF in both normal animals and animals with ALI.

291 gic conditions, which sharply increased with ALI.

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

293 clearance or resistance to IPD in mice with ALI.

294 ssociated with impaired AFC in patients with ALI.

295 rovide a survival advantage in patients with ALI.

296 ssociated with poor outcome in patients with ALI/ALF as evidenced by higher grades of encephalopathy,

297 ted levels of VWF in plasma of patients with ALI/ALF support platelet adhesion, despite a relative lo

298 better supported by plasma of patients with ALI/ALF when compared with control plasma.

299 levels were highly elevated in patients with ALI/ALF.

300 Amputation occurred in 17.6% presenting with ALI.