ライフサイエンスコーパス: acute lung injury

1 injury) or intraperitoneally (extrapulmonary acute lung injury).

2 kg in 0.5 mL of saline/mouse, extrapulmonary acute lung injury).

3 ry injuries, such as after endotoxin-induced acute lung injury.

4 g used to manage smoke inhalation-associated acute lung injury.

5 or equal to 30 cm H2O has been advocated for acute lung injury.

6 roteases are key elements in pathogenesis of acute lung injury.

7 stigated as possible therapeutic targets for acute lung injury.

8 cterizes acute inflammatory diseases such as acute lung injury.

9 ticosteroids in critically ill patients with acute lung injury.

10 nd initiates a feedback loop that attenuates acute lung injury.

11 ium in mechanically ventilated patients with acute lung injury.

12 also amplifies inflammatory signaling during acute lung injury.

13 d mice have more inflammation in response to acute lung injury.

14 elial cell proliferation in a human model of acute lung injury.

15 siglec-9 on human neutrophils in sepsis and acute lung injury.

16 y be used as a treatment in animal models of acute lung injury.

17 l activation and the severity of LPS-induced acute lung injury.

18 improves outcomes in the bleomycin model of acute lung injury.

19 r angiogenesis, pulmonary edema, sepsis, and acute lung injury.

20 th unconstrained NF-kappaB activity, such as acute lung injury.

21 the pathogenesis of influenza virus-induced acute lung injury.

22 pulmonary neutrophilia during pneumonia and acute lung injury.

23 nformation regarding physical recovery after acute lung injury.

24 attenuate lung inflammation and fibrosis in acute lung injury.

25 ar function in a model of ventilator-induced acute lung injury.

26 iables to improve outcomes in the setting of acute lung injury.

27 ficantly reduced in several animal models of acute lung injury.

28 ne model of lipopolysaccharide (LPS)-induced acute lung injury.

29 i-inflammatory agent toward the treatment of acute lung injury.

30 e new therapeutic targets against sepsis and acute lung injury.

31 reased collagen deposition only in pulmonary acute lung injury.

32 e stress occurs, such as pulmonary edema and acute lung injury.

33 lung water (EVLWi) and plasma biomarkers of acute lung injury.

34 ere independent predictors of progression to acute lung injury.

35 yielded endothelial injury in extrapulmonary acute lung injury.

36 in acute injury, including septic shock and acute lung injury.

37 y ill, mechanically ventilated patients with acute lung injury.

38 clinical trials targeting early treatment of acute lung injury.

39 s of baseline health status for survivors of acute lung injury.

40 deposition was only documented in pulmonary acute lung injury.

41 LR ligand, such as LPS, in a murine model of acute lung injury.

42 ling would protect against influenza-induced acute lung injury.

43 ascular tissues mediated this lethal type of acute lung injury.

44 obtained at 14 and 180 days in patients with acute lung injury.

45 ng properties in pulmonary or extrapulmonary acute lung injury.

46 sociated with poor outcomes in patients with acute lung injury.

47 antithrombin III in a large animal model of acute lung injury.

48 mesenchymal stem cells on bacterial-induced acute lung injury.

49 suggesting a unique role for this protein in acute lung injury.

50 gnificantly improved pancreatitis-associated acute lung injury.

51 yde in cigarette smoke that causes edematous acute lung injury.

52 ay an essential role in host defense against acute lung injury.

53 were partially depleted in mice to create an acute lung injury.

54 lmonary edema, a devastating complication of acute lung injury.

55 injury is central to the pathophysiology of acute lung injury.

56 Exposure to hyperoxia results in acute lung injury.

57 nts the early acute inflammatory response in acute lung injury.

58 shown to associate with transfusion-related acute lung injury.

59 l migration regulates tissue-sampling during acute lung injury.

60 a crucial role in allergic inflammation and acute lung injury.

61 n array of inflammatory disorders, including acute lung injury.-

62 d; mild acute respiratory distress syndrome acute lung injury, 12 d; moderate acute respiratory dist

63 e 15 of 89 patients with transfusion-related acute lung injury (17%) who died, whereas 61 of 145 pati

64 Of the patients with transfusion-related acute lung injury, 29 of 37 patients (78%) required init

65 ulating exosomes; 3) The role of exosomes in acute lung injury; 4) The role of exosomes in acute card

66 5 patients with possible transfusion-related acute lung injury (42%) died and 7 of 164 of controls (4

67 In pulmonary acute lung injury, a reduction in collagen fiber content

68 This pragmatic definition of early acute lung injury accurately identified patients who pro

69 he incidence of elevated plateau pressure in acute lung injury /acute respiratory distress syndrome p

70 latoxins in the pathogenesis of experimental acute lung injury/acute respiratory distress syndrome (A

71 Limiting the analysis to patients with acute lung injury/acute respiratory distress syndrome di

72 This study elucidates a new mechanism for acute lung injury after severe trauma and proposes that

73 of NETs in lipopolysaccharide (LPS)-mediated acute lung injury (ALI) and assessed the use of DNase I,

74 man kallistatin-encoding plasmid ameliorated acute lung injury (ALI) and reduced cytokine/chemokine l

75 imary viral pneumonia, which may progress to acute lung injury (ALI) and respiratory failure with a p

76 4 (PDE4) inhibitor to the lungs for treating acute lung injury (ALI) by intravenous administration.

77 Although acute lung injury (ALI) contributes significantly to cri

78 While acute lung injury (ALI) contributes significantly to cri

79 signed to compare the impact of feeding from acute lung injury (ALI) diagnosis to hospital discharge,

80 Intratracheal injection of PLY caused lethal acute lung injury (ALI) in BLT2-deficient mice, with evi

81 Using a standard model of acute lung injury (ALI) in mice featuring airway instill

82 nsfer of MSCs after the onset of LPS-induced acute lung injury (ALI) in mice led to improved survival

83 Acute lung injury (ALI) is a common cause of morbidity i

84 Malaria-associated acute lung injury (ALI) is a frequent complication of se

85 Acute lung injury (ALI) is a major component of multiple

86 Acute lung injury (ALI) is an acute inflammatory lung di

87 Acute lung injury (ALI) is an inflammatory disease with

88 Acute lung injury (ALI) is associated with high mortalit

89 Acute lung injury (ALI) is characterized by alveolar inj

90 Acute lung injury (ALI) is characterized by increased en

91 ion of the innate immune response and NiV to acute lung injury (ALI) is still unknown.

92 rts, the molecular mechanisms of NiV-induced acute lung injury (ALI) remain unclear.

93 Acute lung injury (ALI) remains a serious health issue w

94 During sepsis, acute lung injury (ALI) results from activation of innat

95 to 25% of patients with normal lungs develop acute lung injury (ALI) secondary to mechanical ventilat

96 Acute lung injury (ALI) secondary to sepsis is a complex

97 of risk factors for physical impairments in acute lung injury (ALI) survivors were potentially limit

98 protein WISP1 contributes to sepsis induced acute lung injury (ALI) via integrin beta6.

99 toxin-induced mortality in a murine model of acute lung injury (ALI) was associated with increased va

100 Patients with acute lung injury (ALI) who retain maximal alveolar flui

101 factor (TF) is a critical mediator of direct acute lung injury (ALI) with global TF deficiency result

102 eutrophilic lung inflammation, a hallmark of acute lung injury (ALI), in mice, which was not recapitu

103 turation of IL-1beta have been implicated in acute lung injury (ALI), resulting in inflammation and f

104 For development of acute lung injury (ALI), the invasion and regulation of

105 plays a central role in the pathogenesis of acute lung injury (ALI), the precise molecular mechanism

106 mic reticulum (ER) stress is associated with acute lung injury (ALI), we hypothesized that CIRP cause

107 (GPCR) signaling to induce NET formation in acute lung injury (ALI), which is associated with a high

108 he prominent features in the pathogenesis of acute lung injury (ALI).

109 c endothelial injury, and the development of acute lung injury (ALI).

110 ice in bacterial LPS- and bleomycin-mediated acute lung injury (ALI).

111 of toxic oxidants and proteases, a cause of acute lung injury (ALI).

112 r are crucial factors in the pathogenesis of acute lung injury (ALI).

113 nnate immune responses in conditions such as acute lung injury (ALI).

114 adenosine has been implicated in attenuating acute lung injury (ALI).

115 al determinant of morbidity and mortality in acute lung injury (ALI).

116 a critical determinant of oxygenation during acute lung injury (ALI).

117 ed to be major pathogenic components driving acute lung injury (ALI).

118 ry cytokine gene expression in the lungs and acute lung injury (ALI).

119 mation, endothelial barrier dysfunction, and acute lung injury (ALI).

120 hallmark of several disease states including acute lung injury (ALI).

121 GA2 was protective in two distinct models of acute lung injury (ALI): LPS-induced inflammatory injury

122 lung injury and possible transfusion-related acute lung injury also had a statistically significant i

123 may limit their usefulness in patients with acute lung injury, alternative compounds are needed for

124 , 130 patients (1.8%) fulfilled criteria for acute lung injury (American European Consensus conferenc

125 ting enzyme 2 was shown to protect mice from acute lung injury, an effect attributed to reduced bioav

126 ro-inflammatory stimulus that contributes to acute lung injuries and to chronic lung disease includin

127 LRTIs are also an important cause of acute lung injury and acute exacerbations of chronic obs

128 publication of the Respiratory Management of Acute Lung Injury and Acute Respiratory Distress Syndrom

129 erous studies have focused on biomarkers for acute lung injury and acute respiratory distress syndrom

130 Acute lung injury and acute respiratory distress syndrom

131 pressure improves mortality in patients with acute lung injury and acute respiratory distress syndrom

132 Bacterial pneumonia is a major cause of acute lung injury and acute respiratory distress syndrom

133 mmunomodulatory effects for the treatment of acute lung injury and chronic lung disease.

134 et activation, exacerbated influenza-induced acute lung injury and death.

135 rhMG53 reduces symptoms in rodent models of acute lung injury and emphysema.

136 KLF2 expression in multiple animal models of acute lung injury and further elucidate the KLF2-mediate

137 plicated in reactive oxygen species-mediated acute lung injury and in Th2 immune responses.

138 eratrol might be an option for prevention of acute lung injury and inflammatory responses observed in

139 Inflammatory diseases such as acute lung injury and ischaemic tissue injury are caused

140 Risk of transfusion-related acute lung injury and mortality in plasma recipients exp

141 therapies aimed at reducing the severity of acute lung injury and other inflammatory situations in w

142 ences of NS1-mediated alteration of c-Abl on acute lung injury and pathogenicity in an in vivo mouse

143 Patients with transfusion-related acute lung injury and possible transfusion-related acute

144 Patients with transfusion-related acute lung injury and possible transfusion-related acute

145 -mediated blockade of c-Abl signaling drives acute lung injury and primes for bacterial coinfections

146 gh MSC-derived EVs (mEVs) are beneficial for acute lung injury and pulmonary fibrosis, mechanisms of

147 gnificantly associated with the incidence of acute lung injury and SOFA scores, as well as markers of

148 to IAV infection, as evidenced by attenuated acute lung injury and spleen atrophy and consequently in

149 flammatory mediator during poly(I:C)-induced acute lung injury and, in association with HA, generates

150 n macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-re

151 s profile could serve both as a biomarker of acute lung injury and, potentially, as a mediator of sys

152 t model of lipopolysaccharide (LPS)-mediated acute lung injury, and a combination of primary human le

153 with chronic obstructive pulmonary disease, acute lung injury, and critical care illness may develop

154 te epithelial cell growth and recovery after acute lung injury, and individualize ventilator care on

155 Acute lung injury/ARDS developed in the CMV group (mean

156 Mechanically ventilated patients with acute lung injury are at especially high risk for deep s

157 f the impact of mTORC1 on the development of acute lung injury are conflicting.

158 hanisms underlying inflammatory responses in acute lung injury are poorly understood, and therapeutic

159 leic acid administration protected rats from acute lung injury as evident by reduced lung edema, myel

160 chymal populations as therapeutic targets in acute lung injury as well as fibrotic and degenerative d

161 cally, MKK3(-/-) mice were protected against acute lung injury, as assessed by reduced inflammation,

162 Our analyses demonstrate that acute lung injury associated with systemic hypoxia is ch

163 (through first 72 hr or up to 6 hr prior to acute lung injury) associated with progression to acute

164 Furthermore we studied ten pigs with acute lung injury at multiple airway pressures, as well

165 ars old receiving mechanical ventilation for acute lung injury at nine participating hospitals were i

166 to initiate early treatment of patients with acute lung injury before the need for endotracheal intub

167 iction Score identifies patients at risk for acute lung injury but may be limited for routine clinica

168 chanical ventilation settings can exacerbate acute lung injury by causing a secondary ventilator-indu

169 the protective role of MD-2s in LPS-induced acute lung injury by delivering intratracheally an adeno

170 ole in the development of TGF-beta1-mediated acute lung injury by promoting pulmonary edema via regul

171 t that formaldehyde contributes to edematous acute lung injury by reducing transalveolar Na(+) transp

172 Rats were also protected from acute lung injury by the AT1 antagonist irbesartan; howe

173 ontrolled trial in which transfusion-related acute lung injury cases only involved plasma transfusion

174 l course and outcomes in transfusion-related acute lung injury cases.

175 thelial cells are critical for prevention of acute lung injury caused by bacterial pathogens or exces

176 Previous studies reported that acute lung injury caused by chemical or microbial insult

177 venous OxPAPC administration in the model of acute lung injury caused by intratracheal injection of L

178 After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired t

179 rtality in patients with transfusion-related acute lung injury compared with transfused controls.

180 ecific definitions proposed by the Pediatric Acute Lung Injury Consensus Conference utilizing oxygena

181 In extrapulmonary acute lung injury, CPAP-30 and STEP-30/30 increased vasc

182 In pulmonary acute lung injury, CPAP-30 yielded lower surfactant prot

183 In a mouse model of acute lung injury, dual targeting reduces both the expre

184 least 4 weeks, can engulf neutrophils during acute lung injury, enhance pulmonary tissue repair, and

185 Patients meeting consensus criteria for acute lung injury enrolled in one of three recent Acute

186 reduced static lung elastance independent of acute lung injury etiology.

187 immune cells to the lung and development of acute lung injury following influenza virus infection.

188 ry distress syndrome and transfusion-related acute lung injury), for assessment of pulmonary disease

189 In both acute lung injury groups, recruitment maneuvers improved

190 were similar in pulmonary and extrapulmonary acute lung injury groups.

191 lung injury and possible transfusion-related acute lung injury had an increased duration of mechanica

192 Patients with possible transfusion-related acute lung injury had even higher in-hospital morbidity

193 Patients with transfusion-related acute lung injury had evidence of more systemic inflamma

194 Patients with transfusion-related acute lung injury had fever, tachycardia, tachypnea, hyp

195 Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pat

196 Acute lung injury has been associated with increases in

197 alcohol misuse) on outcomes in patients with acute lung injury have been inconsistent, and there are

198 In LPS-induced acute lung injury, humanized resistin mice demonstrated

199 4 in a mouse model of immune complex-induced acute lung injury (IC-ALI).

200 Evaluation of prevalence and outcomes of acute lung injury in a large cohort of critically ill pa

201 Furthermore, active immunization reduced acute lung injury in a lung infection model.

202 stromal) cells (MSCs) reduce the severity of acute lung injury in animal models and in an ex vivo per

203 0 fails to protect against bleomycin-induced acute lung injury in mice, while FTY720 (S)-phosphonate

204 vestigate the role of C1P during LPS-induced acute lung injury in mice.

205 tate that promotes sickle vaso-occlusion and acute lung injury in murine models of sickle cell diseas

206 novel therapeutic agent to treat or prevent acute lung injury in oxygen toxicity.

207 is that human MSCs promote the resolution of acute lung injury in part through the effects of a speci

208 hat aged RBCs can induce transfusion-related acute lung injury in the presence of a "first hit" (e.g.

209 We established acute lung injury in wild-type and Nlrc4(-/-) mice using

210 , is unlikely to produce transfusion-related acute lung injury, in contrast to antibodies reacting to

211 y reduces plasma-related transfusion-related acute lung injury incidence and possibly mortality.

212 re all studies reporting transfusion-related acute lung injury incidence, all-cause mortality (primar

213 For transfusion-related acute lung injury incidence, final analysis was restrict

214 Among survivors of acute lung injury, increasing chest high-resolution comp

215 before the emergence of disease symptoms for acute lung injury, influenza and breast cancer.

216 Acute lung injury is a common complication after severe

217 Acute lung injury is a life-threatening condition caused

218 Acute lung injury is a life-threatening inflammatory res

219 Acute lung injury is characterized by rapid alveolar inj

220 hallmarks of severe pneumonia and associated acute lung injury is neutrophil recruitment to the lung.

221 Transfusion-related acute lung injury is the leading cause of transfusion-re

222 Transfusion-related acute lung injury is the leading cause of transfusion-re

223 hway in many dangerous conditions, including acute lung injury, ischemia-reperfusion, and inflammatio

224 Compared with extrapulmonary acute lung injury, mesenchymal stem cell decreased colla

225 Acute lung injury mice received Escherichia coli lipopol

226 , two hypoxic mouse models were assessed, an acute lung injury model and mice exposed to 10% O2 for 3

227 eir virulence in olive plants and in a mouse acute lung injury model respectively.

228 sed to enhance resolution in an experimental acute lung injury model with the potential for therapeut

229 y and pro-inflammatory cytokine levels in an acute lung injury model.

230 within the Prevention and Early Treatment of Acute Lung Injury network.

231 on of acute neurologic illness and may mimic acute lung injury of other etiology.

232 effects of pleural effusion in patients with acute lung injury on lung volume, respiratory mechanics,

233 fe support tripled in the first 3 days after acute lung injury onset, increased again after day 5, an

234 During the first 5 days after acute lung injury onset, limitations were significantly

235 ficantly lower during the first 5 days after acute lung injury onset.

236 anges in organ failure status and time since acute lung injury onset.

237 ESIGN, SETTING, AND PATIENTS: A total of 129 acute lung injury or acute respiratory distress syndrome

238 Pleural effusion in acute lung injury or acute respiratory distress syndrome

239 ear whether a similar relationship holds for acute lung injury or altered hemodynamics.

240 mg/kg in 0.05 mL of saline/mouse, pulmonary acute lung injury) or intraperitoneally (20 mg/kg in 0.5

241 saccharide either intratracheally (pulmonary acute lung injury) or intraperitoneally (extrapulmonary

242 edicted body weight are necessary to improve acute lung injury outcome.

243 our understanding of the pathophysiology of acute lung injury, patient-ventilator interaction, and w

244 Sedative use and delirium status in acute lung injury patients after implementation of the q

245 acute lung injury patients receiving lower tidal volume

246 tive cohort study evaluating 490 consecutive acute lung injury patients recruited from 11 ICUs at thr

247 -, and 60-month follow-up (Improving Care of Acute Lung Injury Patients).

248 Early identification of acute lung injury prior to onset of respiratory failure

249 rately identified patients who progressed to acute lung injury prior to requiring positive pressure v

250 In conclusion, transfusion-related acute lung injury produced a condition resembling the sy

251 Importantly, it suppressed acute lung injury provoked by LPS inhalation by suppress

252 tral to the pathogenesis of diseases such as acute lung injury, pulmonary fibrosis, and pulmonary ade

253 tic effects of MVs in an infectious model of acute lung injury remain unknown.

254 Mortality associated with acute lung injury remains high.

255 ents with severe smoke inhalation-associated acute lung injury requiring mechanical ventilation.

256 ts enrolled, 62 patients (25%) progressed to acute lung injury requiring positive pressure ventilatio

257 rately identified patients who progressed to acute lung injury requiring positive pressure ventilatio

258 associated with smoke inhalation-associated acute lung injury results from airway damage, mucosal dy

259 roup are mainly influenced by the underlying acute lung injury risk factor(s).

260 r age, severity of illness, pneumonia as the acute lung injury risk factor, and length of time on mec

261 A simple three-component early acute lung injury score (1 point for oxygen requirement

262 An early acute lung injury score greater than or equal to 2 ident

263 data, no studies dedicated to patients with acute lung injury, sepsis, shock, or multiple trauma cou

264 For clinicians treating acute lung injury since 2000, achieving VT less than or

265 at (cm H2O) practices reported in studies of acute lung injury since ARMA using a systematic literatu

266 Despite decreasing mortality rates in acute lung injury, studies of long-term physical functio

267 nhibitor of metalloproteinase-1 in pulmonary acute lung injury, suggesting that mesenchymal stem cell

268 The majority of acute lung injury survivors had clinically significant g

269 y, studies of long-term physical function in acute lung injury survivors have consistently reported p

270 n of ANGPT2, a gene previously implicated in acute lung injury syndromes, with nocturnal SaO2, sugges

271 reported worse baseline health status before acute lung injury than population norms and better statu

272 defines a novel regulatory role for ILC2 in acute lung injury that could be targeted in trauma patie

273 plays a central role in the pathogenesis of acute lung injury, the molecular mechanisms underlying i

274 bronchopulmonary dysplasia (BPD) from one of acute lung injury to a disease of disrupted lung develop

275 criteria for a pragmatic definition of early acute lung injury to identify patients with lung injury

276 Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory d

277 Transfusion-related acute lung injury (TRALI) is the leading cause of transf

278 Transfusion-related acute lung injury (TRALI) remains a significant cause of

279 In a model of transfusion-related acute lung injury (TRALI), Boc2 also reversed ASA protec

280 severe, sometimes fatal transfusion-related acute lung injury (TRALI).

281 Our trial INTACT (Intensive Nutrition in Acute Lung Injury Trial) was designed to compare the imp

282 tshock mesenteric lymph are key mediators of acute lung injury triggering the macrophage activation v

283 Muscle weakness is common after acute lung injury, usually recovering within 12 months.

284 Acute lung injury was induced by Escherichia coli lipopo

285 Acute lung injury was induced in C57BL/6 mice with bleom

286 In our population, prevalence of acute lung injury was low, most cases were diagnosed 2 d

287 nitric oxide administration in children with acute lung injury was not associated with improved morta

288 Using a model of acute lung injury, we demonstrate that TGF-beta1 decreas

289 In a rat model of acute lung injury, we investigated whether age affects t

290 lung injury) associated with progression to acute lung injury were analyzed by backward regression.

291 r bacterial or H1N1 pneumonia and associated acute lung injury were immunostained for leptin.

292 Animal and in vitro models of acute lung injury were used to characterize KLF2 express

293 otential epithelial cell damage in pulmonary acute lung injury, whereas both CPAP-30 and STEP-30/30 y

294 This study aimed at determining during early acute lung injury whether local (18)F-FDG phosphorylatio

295 l to 2 identified patients who progressed to acute lung injury with 89% sensitivity and 75% specifici

296 mice varied from mild pneumonitis to severe acute lung injury with extensive pneumonia and bronchiol

297 ry tract and resulted in pulmonary edema and acute lung injury with hyaline membrane formation, leadi

298 we show T cell migration in a mouse model of acute lung injury with two-photon imaging of intact lung

299 Using animal models of acute lung injury with vascular hyperpermeability, we ob

300 pothesized that DAD, the most severe form of acute lung injury, would lead to the highest risk of chr