ライフサイエンスコーパス: acute lung injury

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

2 e (female BALB/c strain) with an LPS-induced acute lung injury.

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

4 nt implications for therapeutic targeting in acute lung injury.

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

6 cterizes several vascular diseases including acute lung injury.

7 gnificantly improved pancreatitis-associated acute lung injury.

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

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

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

11 ight into the critical role of C/EBPgamma in acute lung injury.

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

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

14 Exposure to hyperoxia results in acute lung injury.

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

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

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

18 in LPS- and IgG immune complexes-stimulated acute lung injury.

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

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

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

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

23 cterizes acute inflammatory diseases such as acute lung injury.

24 ticosteroids in critically ill patients with acute lung injury.

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

26 ium in mechanically ventilated patients with acute lung injury.

27 recovery and remodeling in a murine model of acute lung injury.

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

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

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

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

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

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

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

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

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

37 pulmonary neutrophilia during pneumonia and acute lung injury.

38 ected lung diseases like cystic fibrosis and acute lung injury.

39 nformation regarding physical recovery after acute lung injury.

40 attenuate lung inflammation and fibrosis in acute lung injury.

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

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

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

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

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

46 ng and protect against P. aeruginosa-induced acute lung injury.

47 l symptoms that rapidly progressed to severe acute lung injury.

48 ation of Pseudomonas (P.) aeruginosa-induced acute lung injury.

49 ms in many inflammatory conditions including acute lung injury.

50 tions required for tissue regeneration after acute lung injury.

51 nd promote resolution of neutrophil-mediated acute lung injury.

52 inflammasome prevented P. aeruginosa-induced acute lung injury.

53 of optimal mechanical ventilator settings in acute lung injury.

54 es life-threatening pneumonia culminating in acute lung injury.

55 contribute to the temperature dependence of acute lung injury.

56 atherosclerosis, diabetes, hypertension, and acute lung injury.

57 ion and inflammation, two major hallmarks of acute lung injury.

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

59 stigated as possible therapeutic targets for acute lung injury.

60 also amplifies inflammatory signaling during acute lung injury.

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

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

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

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

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

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

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

68 5 patients with possible transfusion-related acute lung injury (42%) died and 7 of 164 of controls (4

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

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

71 ve the potential to prevent and to treat the acute lung injury after SARS-CoV-2 infection, especially

72 function linked to pathological features of acute lung injury (ALI) and acute respiratory distress s

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

74 Acute lung injury (ALI) and idiopathic pulmonary fibrosi

75 Acute lung injury (ALI) and its more severe form, acute

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

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

78 4 (PDE4) inhibitor to the lungs for treating acute lung injury (ALI) by intravenous administration.

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

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

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

82 plays a central role in the pathogenesis of acute lung injury (ALI) during both the acute pneumoniti

83 Compared with sham rats, rats a week after acute lung injury (ALI) express more pro-inflammatory cy

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

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

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

87 Acute lung injury (ALI) increases respiratory rate (fR)

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

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

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

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

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

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

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

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

96 Acute lung injury (ALI) occurs in up to 30% of patients

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

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

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

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

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

102 Here, we find that inflicting acute lung injury (ALI) to mice doubles their incidence

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

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

105 Acute lung injury (ALI), a common condition in criticall

106 est in treating respiratory diseases such as acute lung injury (ALI), acute respiratory distress synd

107 Acute lung injury (ALI), endotheliitis, capillary inflam

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

109 n, obese-mouse models suggest that increased acute lung injury (ALI), potentially due to enhanced vir

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

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

112 ne model of lipopolysaccharide (LPS)-induced acute lung injury (ALI), we observed augmented temporal

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

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

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

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

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

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

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

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

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

122 an aerosolized LPS inhalation mouse model of acute lung injury (ALI).

123 evaluated in the 2-hit cell culture model of acute lung injury (ALI).

124 gering pulmonary vascular leak thus inducing acute lung injury (ALI).

125 and increased susceptibility to LPS-induced acute lung injury (ALI).

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

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

128 se model of lipopolysaccharide (LPS)-induced acute lung injury (ALI).

129 ssociated pneumonia, a major risk factor for acute lung injury (ALI)/acute respiratory distress syndr

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

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

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

133 , 130 patients (1.8%) fulfilled criteria for acute lung injury (American European Consensus conferenc

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

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

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

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

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

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

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

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

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

143 into the lungs and were followed by greater acute lung injury and inflammation.

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

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

146 Acute lung injury and its more severe form, acute respir

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

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

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

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

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

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

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

154 Herein, authors representing the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Netw

155 basic science researchers from the Pediatric Acute Lung Injury and Sepsis Investigators Network, the

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

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

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

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

160 ed circulatory overload, transfusion-related acute lung injury, and acute and delayed hemolytic trans

161 ory diseases in mouse models of peritonitis, acute lung injury, and atherosclerosis.

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

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

164 myocardial infarction, acute kidney injury, acute lung injury, and others are among the leading caus

165 ogenesis of lung diseases, including asthma, acute lung injury, and pulmonary fibrosis, and thus sugg

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

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

168 gnificantly attenuated P. aeruginosa-induced acute lung injury, as assessed by lung wet-to-dry weight

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

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

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

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

173 imary graft dysfunction (PGD), a syndrome of acute lung injury, attenuates improvements in patient-re

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

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

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

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

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

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

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

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

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

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

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

185 The Pediatric Acute Lung Injury Consensus Conference (PALICC) definiti

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

187 , posterior ventilation defects secondary to acute lung injury could be re-inflated by applying posit

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

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

190 essed clinically in five human patients with acute lung injury, experimentally in five mice ventilate

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

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

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

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

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

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

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

198 s exist to counteract Hyperoxia (HO)-induced Acute Lung Injury (HALI).

199 Acute lung injury has been associated with increases in

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

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

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

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

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

205 aeruginosa (strain: PA103) infection induced acute lung injury in C57BL/6 mice in a dose- and time-de

206 0 fails to protect against bleomycin-induced acute lung injury in mice, while FTY720 (S)-phosphonate

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

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

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

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

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

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

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

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

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

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

217 increased LTB(4) levels in C57BL/6 mice with acute lung injury, increasing overall antimicrobial acti

218 In a model of acute lung injury induced by LPS, C6(-/-) mice showed re

219 ed circulatory overload, transfusion-related acute lung injury, infection transmission, alloimmunizat

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

221 Acute lung injury is a life-threatening condition caused

222 Acute lung injury is a life-threatening inflammatory res

223 Acute lung injury is characterized by rapid alveolar inj

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

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

226 ess syndrome (ARDS), the most severe form of acute lung injury, is associated with reduced lung compl

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

228 drome is propelled by inflammation producing acute lung injury, large-vessel thrombosis, and in situ

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

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

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

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

233 sis and macrophage efferocytosis in a murine acute lung injury model.

234 In both zebrafish tail injury and murine acute lung injury models of neutrophilic inflammation, o

235 latory overload (n = 7), transfusion-related acute lung injury (n = 11), and severe allergic transfus

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

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

238 ngs in EVALI most commonly show a pattern of acute lung injury on the spectrum of organizing pneumoni

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

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

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

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

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

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

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

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

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

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

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

250 lung injury most frequently presents with an acute lung injury pattern at CT, manifesting as multifoc

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

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

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

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

255 Mortality associated with acute lung injury remains high.

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

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

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

259 entification of SNPs Predisposing to Altered Acute Lung Injury Risk; n=882), Copenhagen General Popul

260 onodular lesions of organizing pneumonia and acute lung injury seen at histopathologic findings in th

261 In a model of acute lung injury, selective deletion of EC MIF decrease

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

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

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

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

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

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

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

269 target organ for COVID-19; patients develop acute lung injury that can progress to respiratory failu

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

271 After acute lung injury, they are preferentially localized in

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

273 accessibility and gene expression following acute lung injury to elucidate repair mechanisms.

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

275 tory overload (TACO) and transfusion-related acute lung injury (TRALI) are syndromes of acute respira

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

277 Transfusion-related acute lung injury (TRALI) is one of the leading causes o

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

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

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

281 roducts can cause lethal transfusion-related acute lung injury (TRALI).

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

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

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

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

286 SA was associated with increased leukopenia, acute lung injury, vasopressor use, extracorporeal life

287 ade protected against P. aeruginosa -induced acute lung injury via activation of A(2A)R and A(2B)R.

288 ffects; adenosine can either protect against acute lung injury via adenosine receptors or cause lung

289 Acute lung injury was induced by Escherichia coli lipopo

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

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

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

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

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

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

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

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

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

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

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