ライフサイエンスコーパス: lung injury

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

2 eding protected mice from ventilator-induced lung injury.

3 leads to systemic inflammatory response and lung injury.

4 notype and regulate inflammation in fibrotic lung injury.

5 ute injury, including septic shock and acute lung injury.

6 s in ATII cells and were up-regulated during lung injury.

7 diaphragm activity, in sedated patients with lung injury.

8 injury from a form of patient self-inflicted lung injury.

9 otein alleviated the severity of RSV-induced lung injury.

10 se the major tobacco smoke-induced oxidative lung injury.

11 the development of pulmonary fibrosis after lung injury.

12 re protected from lipopolysaccharide-induced lung injury.

13 ting a unique role for this protein in acute lung injury.

14 t new drug resistance, and prevent permanent lung injury.

15 s and contributes to fibrogenic responses to lung injury.

16 elates with aggravated inflammation and more lung injury.

17 CD14 mediated inflammation in sepsis induced lung injury.

18 pathologic inflammation in murine models of lung injury.

19 eroxia/reactive oxygen species (ROS)-induced lung injury.

20 to oxidative stress-associated inflammatory lung injury.

21 change for host defense and resolution from lung injury.

22 evaluated the effect of adenosine kinase on lung injury.

23 ndecan-1 has an important role in regulating lung injury.

24 tivate ECs and induce EC pyroptosis to cause lung injury.

25 o blocking adenosine kinase on the extent of lung injury.

26 ical importance to patients with IAV-induced lung injury.

27 es fibrogenic responses to bleomycin-induced lung injury.

28 tress is an established model to mimic human lung injury.

29 closed chamber and assessed for survival and lung injury.

30 the extent of pulmonary inflammation during lung injury.

31 ls that proliferate in ventilator associated lung injury.

32 ponse and protects against bleomycin-induced lung injury.

33 sh the harmful effects of ventilator-induced lung injury.

34 antly improved pancreatitis-associated acute lung injury.

35 cigarette smoke that causes edematous acute lung injury.

36 val, increased bacterial burden, and greater lung injury.

37 essential role in host defense against acute lung injury.

38 isruption and cytokine storm in experimental lung injury.

39 artially depleted in mice to create an acute lung injury.

40 are major determinants of ventilator-induced lung injury.

41 inflammation due to traumatic or infectious lung injury.

42 y edema, a devastating complication of acute lung injury.

43 XCR2+ lung neutrophils, culminating in early lung injury.

44 , cigarette smoke, silica, or sepsis-induced lung injury.

45 riteria to include noninvasive surrogates of lung injury.

46 6 abrogates fibrogenesis in murine models of lung injury.

47 ation regulates tissue-sampling during acute lung injury.

48 sure, key determinants of ventilator-induced lung injury.

49 ed as possible therapeutic targets for acute lung injury.

50 mplifies inflammatory signaling during acute lung injury.

51 nts with ARDS by creating ventilator-induced lung injury.

52 flammation, and mitigating LPS-induced mouse lung injury.

53 reduced recovery following bleomycin-induced lung injury.

54 spreading of ATII cells during repair after lung injury.

55 delayed the resolution of permeability after lung injury.

56 tized, mechanically ventilated pigs, without lung injury.

57 reduce the development of acute CAR-induced lung injury.

58 fibroblasts into the alveolar airspace after lung injury.

59 ory distress syndrome and multiple models of lung injury.

60 e animal model of lipopolysaccharide-induced lung injury.

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

62 y of inflammatory disorders, including acute lung injury.-

63 g exosomes; 3) The role of exosomes in acute lung injury; 4) The role of exosomes in acute cardiac in

64 hloric acid in mice, we show that repetitive lung injury activates pulmonary capillary endothelial ce

65 PaO2/FIO2 is used commonly for diagnosis of lung injury (acute respiratory distress syndrome and tra

66 ncreased circulating levels of SPMs and less lung injury after I/R.

67 signaling pathway has been shown to improve lung injury after influenza infection, and future studie

68 ell-mediated IL-17 production and subsequent lung injury after IR.

69 hypothesized that the development of remote lung injury after trauma/hemorrhagic shock requires acti

70 s in lipopolysaccharide (LPS)-mediated acute lung injury (ALI) and assessed the use of DNase I, for t

71 llistatin-encoding plasmid ameliorated acute lung injury (ALI) and reduced cytokine/chemokine levels

72 viral pneumonia, which may progress to acute lung injury (ALI) and respiratory failure with a potenti

73 to compare the impact of feeding from acute lung injury (ALI) diagnosis to hospital discharge, an in

74 racheal injection of PLY caused lethal acute lung injury (ALI) in BLT2-deficient mice, with evident v

75 Acute lung injury (ALI) is a common cause of morbidity in pati

76 Malaria-associated acute lung injury (ALI) is a frequent complication of severe m

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

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

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

80 he molecular mechanisms of NiV-induced acute lung injury (ALI) remain unclear.

81 in WISP1 contributes to sepsis induced acute lung injury (ALI) via integrin beta6.

82 (TF) is a critical mediator of direct acute lung injury (ALI) with global TF deficiency resulting in

83 hilic lung inflammation, a hallmark of acute lung injury (ALI), in mice, which was not recapitulated

84 ticulum (ER) stress is associated with acute lung injury (ALI), we hypothesized that CIRP causes ALI

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

86 okine gene expression in the lungs and acute lung injury (ALI).

87 minent features in the pathogenesis of acute lung injury (ALI).

88 s protective in two distinct models of acute lung injury (ALI): LPS-induced inflammatory injury and t

89 s isolated from PAI-1-deficient mice without lung injury also showed increased collagen-I and uPA.

90 ces in the pathogenesis of radiation-induced lung injury among murine strains offer a unique opportun

91 -concept study, we enrolled 10 patients with lung injury and a Vt greater than 8 ml/kg under pressure

92 The lung injury and acute cor pulmonale is likely due to pul

93 Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARD

94 acterial pneumonia is a major cause of acute lung injury and acute respiratory distress syndrome, cha

95 ve inflammation after infection precipitates lung injury and an increase in morbidity and mortality.

96 n regulating pulmonary vascular integrity in lung injury and ARDS-associated GWAS genes remains poorl

97 y in the setting of Escherichia coli-induced lung injury and characterize the underlying mechanisms i

98 odulatory effects for the treatment of acute lung injury and chronic lung disease.

99 ry was accompanied by evidence of histologic lung injury and concomitant mobilization of human CD45+

100 ar damage mechanisms governing emphysematous lung injury and demonstrate the potential of vitamin C t

101 13 is a major regulator of radiation-induced lung injury and demonstrates that strategies focusing on

102 To reproduce the lung injury and edema examined in the Webb and Tierney s

103 xpression in multiple animal models of acute lung injury and further elucidate the KLF2-mediated path

104 The mortality was due to enhanced lung injury and greater systemic response.

105 ed in no significant differences between the lung injury and healthy control group before or after he

106 the lungs of mice subjected to experimental lung injury and in cases of human IPF.

107 ion of lung inflammation in a mouse model of lung injury and in human tissues from subjects with lung

108 stress despite low tidal volumes may worsen lung injury and increase risk of death.

109 Subsequently, lung injury and inflammation were evaluated.

110 al epithelial apoptosis, thereby attenuating lung injury and inflammation.

111 standing of the causal relationships between lung injury and kidney injury is not precise.

112 2s are important for AEC2 renewal, repair of lung injury and limiting the extent of fibrosis.

113 markedly augmented LPS-induced inflammatory lung injury and mortality in TSG6(-/-) mice compared wit

114 l instillation of TSG6 prevented LPS-induced lung injury and neutrophil sequestration, and increased

115 (8-iso-PGF2alpha) levels were used to assess lung injury and overall oxidative stress, respectively.

116 t HIF1alpha is activated in ATII cells after lung injury and promotes proliferation and spreading dur

117 -derived EVs (mEVs) are beneficial for acute lung injury and pulmonary fibrosis, mechanisms of mEV up

118 n-survivors, including several implicated in lung injury and repair such as coagulation/thrombosis, a

119 monary margination, which contributes toward lung injury and sepsis mortality.

120 ing the inflammatory changes associated with lung injury and should be pursued as a therapeutic optio

121 IL-17 is rapidly produced during lung injury and significantly contributes to early immun

122 nce the relationship between the severity of lung injury and the degree of hypoxemia and/or the effec

123 tory mediator during poly(I:C)-induced acute lung injury and, in association with HA, generates an EC

124 ophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulati

125 r factor-kappaB activation, animal survival, lung injury, and cytokine profile were assessed.

126 creased intestinal worm burdens, exacerbated lung injury, and increased production of IL-12/23p40, wh

127 nhanced type I IFN production, neutrophilia, lung injury, and lethality, while therapeutic administra

128 ys a critical role in preventing RSV-induced lung injury, and suggest that ACE2 is a promising potent

129 ry TLR4 in the development of NEC-associated lung injury, and they suggest that inhibition of this in

130 Lung injuries are common among those who suffer an impac

131 quish restoration of lung health to enduring lung injury are insufficiently understood.

132 dels of noninfectious, tissue damage-induced lung injury are needed to understand the signals and res

133 populations as therapeutic targets in acute lung injury as well as fibrotic and degenerative disease

134 prove the association between the underlying lung injury, as detected by CT, and PaO2/FIO2-derived se

135 Our analyses demonstrate that acute lung injury associated with systemic hypoxia is characte

136 d receiving mechanical ventilation for acute lung injury at nine participating hospitals were include

137 biomarkers for predicting radiation-induced lung injury before symptoms develop.

138 tiate early treatment of patients with acute lung injury before the need for endotracheal intubation.

139 planation for the differences in severity of lung injury between different age groups.

140 After major lung injuries, BSCs are activated and recruited to sites

141 proteins, contributing to the major share of lung injury, but also activate Rtp801, a key proinflamma

142 totaxin activity increases locally following lung injury, but is not required for pulmonary lysophosp

143 a and inflammation in preclinical studies of lung injury, but its therapeutic effects have never been

144 and atelectrauma promote ventilator-induced lung injury, but their relative contribution to inflamma

145 the development of TGF-beta1-mediated acute lung injury by promoting pulmonary edema via regulation

146 formaldehyde contributes to edematous acute lung injury by reducing transalveolar Na(+) transport, t

147 ely, our animal studies show that a specific lung injury can induce Treg alterations, which can augme

148 led trial in which transfusion-related acute lung injury cases only involved plasma transfusions.

149 catrienoic acid (12-HHT), protects mice from lung injury caused by a pneumococcal toxin, pneumolysin

150 l cells are critical for prevention of acute lung injury caused by bacterial pathogens or excessive m

151 OxPAPC administration in the model of acute lung injury caused by intratracheal injection of LPS.

152 After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired to rega

153 stem/stromal cells on physiologic indices of lung injury, cellular infiltration, and E. coli colony c

154 CM or by genetic down-regulation, diminished lung injury, collagen production, and transforming growt

155 ium, indicating a role for pulmonary TLR4 in lung injury development.

156 Attenuated viruses induced minimal lung injury, diminished limited neutrophil influx, and i

157 ts for clinical use to prevent patients from lung injury during MV treatment.

158 4 weeks, can engulf neutrophils during acute lung injury, enhance pulmonary tissue repair, and promot

159 murine CIRP (rmCIRP) in C57BL/6 mice causes lung injury, evidenced by vascular leakage, edema, incre

160 g plays a central role in the development of lung injury following blood transfusion.

161 rgy, regulates type 2 immunity and restricts lung injury following hookworm infection.

162 tress syndrome and transfusion-related acute lung injury), for assessment of pulmonary disease course

163 tive therapy, to minimize the progression of lung injury from a form of patient self-inflicted lung i

164 data to support their potential efficacy for lung injury from both infectious and noninfectious cause

165 direct lung injury; however, in the indirect lung injury group, the odds of mortality in the obese we

166 Survivors with direct lung injury had no difference in the duration of mechani

167 Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pathogene

168 In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-e

169 )1A enzymes are protective against hyperoxic lung injury (HLI).

170 e between body mass index groups with direct lung injury; however, in the indirect lung injury group,

171 sh the harmful effects of ventilator-induced lung injury if used as an alternative to conventional MV

172 ng physiological (heart rate), pathological (lung injury), immuno-histochemical (oxidative/nitrosativ

173 t diet protects mice from ventilator-induced lung injury in a manner independent of neutrophil recrui

174 mechanisms by which VZV infection can cause lung injury in an immune competent host.

175 h has been learned about the pathogenesis of lung injury in ARDS, with an emphasis on the mechanisms

176 Hyperoxia contributes to lung injury in experimental animals and diseases such as

177 e presence of endotoxemia does not result in lung injury in humans.

178 ith MSC-derived EVs reduced inflammation and lung injury in LPS-injured mice.

179 hen compared with viral activation pathways, lung injury in lung contusion demonstrated increased p38

180 ced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a

181 d CXCL5 upregulation and blocked NEC-induced lung injury in mice.

182 Hydrogen sulfide reduces ventilator-induced lung injury in mice.

183 ate the role of C1P during LPS-induced acute lung injury in mice.

184 KLF2 overexpression ameliorates LPS-induced lung injury in mice.

185 hat promotes sickle vaso-occlusion and acute lung injury in murine models of sickle cell disease.

186 ctive ventilation is used to prevent further lung injury in patients on invasive mechanical ventilati

187 pharmacologic treatments directly targeting lung injury in patients with the acute respiratory distr

188 responsible for AM pyroptosis and augmented lung injury in response to LPS.

189 We found worsened outcomes and lung injury in Sdc1(-/-) mice compared with WT mice afte

190 owed clear attenuation of ventilator-induced lung injury in terms of respiratory mechanics, blood gas

191 ed RBCs can induce transfusion-related acute lung injury in the presence of a "first hit" (e.g., seps

192 her maximally stored RBCs are able to induce lung injury in the presence of a "first hit" in humans (

193 ic acidosis reduced E. coli inflammation and lung injury in vivo and reduced nuclear factor-kappaB ac

194 bitor of the contact phase, may protect from lung injury in vivo and to decipher the possible underly

195 d ATII cell proliferation in vitro and after lung injury in vivo.

196 AMs treated with MSC-derived EVs ameliorate lung injury in vivo.

197 For transfusion-related acute lung injury incidence, final analysis was restricted to

198 ed to a control group (n = 5) and a model of lung injury induced by bacterial products (lipopolysacch

199 chetype model of oxygen toxicity is neonatal lung injury induced by hyperoxia exposure.

200 Following lung injury induced by polysorbate lavage, a higher PEEP

201 Following lung injury induced by polysorbate lavage, the APRV grou

202 Following lung injury induced by polysorbate lavage, the LTVV grou

203 ing enzyme-2 (ACE2) protected against severe lung injury induced by RSV infection in an experimental

204 In its acute phase lung injury induced by tissue or bacterial products is c

205 The degree of lung injury, inflammation, and macrophage apoptosis was

206 in the protection against ventilator-induced lung injury involves cyclooxygenase 2/15-deoxy Delta-pro

207 Acute lung injury is a life-threatening condition caused by di

208 Acute lung injury is a life-threatening inflammatory response

209 Acute lung injury is characterized by rapid alveolar injury, l

210 diatric acute respiratory distress syndrome, lung injury is mediated by immune activation and severe

211 Although NEC-associated lung injury is more severe than the lung injury that occ

212 bution to inflammation in ventilator-induced lung injury is not well established.

213 RATIONALE: Fibrosis after lung injury is related to poor outcome, and idiopathic p

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

215 en interleukin-17A and inflammation in human lung injury is unknown.

216 for mechanically ventilated patients without lung injury, it is unclear whether a similar relationshi

217 ts were stratified by direct versus indirect lung injury leading to pediatric acute respiratory distr

218 re, administration of MEKi after LPS-induced lung injury led to improved recovery of weight, fewer ne

219 ventilation of the left (ventilator-induced lung injury) lung with tidal volume of approximately 3 m

220 Ventilator-induced lung injury may arise from heterogeneous lung microanato

221 were analyzed in a mouse ventilator-induced lung injury model in vivo as well as in a cell stretch m

222 dema in mice induced by bleomycin exposure-a lung injury model in which TGF-beta1 plays a critical ro

223 We aimed to create a reproducible lung injury model utilizing injection of mitochondrial d

224 Using an acid inhalation-induced lung injury model, we explored the mechanisms by which a

225 Data from in-vitro, animal, and human lung injury models suggest that keratinocyte growth fact

226 ated the cellular function of miR-150 in our lung injury models.

227 the Prevention and Early Treatment of Acute Lung Injury network.

228 ry that is similar to the ventilator-induced lung injury observed in mechanically ventilated patients

229 ether a similar relationship holds for acute lung injury or altered hemodynamics.

230 tory rate might not be dependent on moderate lung injury or cardiac output but on the metabolic produ

231 leukocyte lineage, inflammatory and induced lung injury pathways.

232 60-month follow-up (Improving Care of Acute Lung Injury Patients).

233 CI: -7.64 to -0.18, P = 0.04, I(2) = 95%) in lung injury patients.

234 Obese children with indirect lung injury pediatric acute respiratory distress syndrom

235 er 17, 2014, 7673 patients at risk for ARDS (Lung Injury Prediction Score >/=4) in the emergency depa

236 The Lung Injury Prediction Score (LIPS) was used to stratify

237 rgency department hospitalized patients, the Lung Injury Prediction Score and Lung Injury Prediction

238 A Lung Injury Prediction Score greater than or equal to 4

239 operating characteristic curve of 0.70 and a Lung Injury Prediction Score greater than or equal to 4

240 tients, the Lung Injury Prediction Score and Lung Injury Prediction Score greater than or equal to 4

241 spiratory distress syndrome development, the Lung Injury Prediction Score has an area under the recei

242 We aimed to evaluate whether Lung Injury Prediction Score identifies non-emergency de

243 The Lung Injury Prediction Score identifies patients at risk

244 Lung Injury Prediction Score was calculated using the wo

245 Increasing Lung Injury Prediction Score was significantly associate

246 3l1 to inhibit oxidant-induced apoptosis and lung injury, promote melanoma metastasis and stimulate T

247 R7 agonist or PCEC-targeted Jag1 shRNA after lung injury promotes alveolar repair and reduces fibrosi

248 zed that aging shifts the balance toward the lung injury-promoting angiotensin-converting enzyme, whi

249 ative pulmonary complications (postoperative lung injury, pulmonary infection, or barotrauma).

250 of Pf phage was also associated with reduced lung injury, reduced neutrophil recruitment, and lower c

251 In patients with existing lung injury, regional forces generated by the respirator

252 elial cell populations are controlled during lung injury repair in adults.

253 he biology of endogenous stem cells in adult lung injury repair.

254 mong survivors, the overweight with indirect lung injury requires longer duration of mechanical venti

255 Successful recovery from lung injury requires the repair and regeneration of alve

256 o mediate macrophage phagocytic function and lung injury resolution.

257 mental in early wound healing in response to lung injury, restoring epithelial integrity through spre

258 Radiation-induced lung injury (RILI) is a delayed effect of acute radiatio

259 Lung injury scoring of histological sections was signifi

260 s heparin anticoagulant activity without the lung injury seen with protamine.

261 from IPF lungs or mice with diverse types of lung injuries showed increased p53 acetylation and miR-3

262 ized mice; however, the extent of NA-induced lung injury (shown as volume fraction of damaged cells)

263 end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to l

264 The majority of acute lung injury survivors had clinically significant general

265 NGPT2, a gene previously implicated in acute lung injury syndromes, with nocturnal SaO2, suggesting t

266 ratory distress syndrome is a multifactorial lung injury that continues to be associated with high le

267 es a novel regulatory role for ILC2 in acute lung injury that could be targeted in trauma patients pr

268 data suggest that these patients may develop lung injury that is similar to the ventilator-induced lu

269 sociated lung injury is more severe than the lung injury that occurs in premature infants without NEC

270 e colleagues identified a syndrome of severe lung injury that united a group of patients with dispara

271 length of stay; however, those with indirect lung injury, the overweight required longer duration of

272 ression and contribute to ventilator-induced lung injury through alveolar overdistention.

273 r trial INTACT (Intensive Nutrition in Acute Lung Injury Trial) was designed to compare the impact of

274 mesenteric lymph are key mediators of acute lung injury triggering the macrophage activation via Tol

275 When stratified by lung injury type, there was no mortality difference betw

276 ranscriptome and proteome of acute hyperoxic lung injury using the omics platforms: microarray and Re

277 oxyglucose uptake rate in ventilator-induced lung injury versus control lung (0.017 [0.014-0.025] vs

278 d into the circulation during sepsis, causes lung injury via an as yet unknown mechanism.

279 cation of C1INH alleviates bleomycin-induced lung injury via direct interaction with extracellular hi

280 jected into a rat model of radiation-induced lung injury via endotracheal (ET) or intravascular (IV)

281 However, MV causes ventilator-induced lung injury (VILI), a condition characterized by increas

282 iance are used to prevent ventilator-induced lung injury (VILI).

283 owever, MV can also cause ventilator-induced lung injury (VILI).

284 ated with 0.2 g/kg intratracheal silica, and lung injury was assessed 1, 3, or 14 days post-exposure.

285 ated male mice were treated with silica, and lung injury was assessed.

286 as also performed in vivo, and the effect on lung injury was assessed.

287 Moderate lung injury was induced by injection of oleic acid in 10

288 Lung injury was induced by intratracheal administration

289 Lung injury was induced in wild-type (C57BL/6) and IL-17

290 oxide administration in children with acute lung injury was not associated with improved mortality.

291 In a rat model of acute lung injury, we investigated whether age affects the bal

292 ether NPD can be applied to diagnose hypoxic lung injury, we searched PubMed, EMBASE, Scopus, Web of

293 nal 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high Vt with

294 , whereas signatures associated with induced lung injury were less enriched in adult-onset severe ast

295 Animal and in vitro models of acute lung injury were used to characterize KLF2 expression an

296 ased inflammatory mediator response and more lung injury (wet-to-dry ratio and histology) in elderly

297 d patients is the risk of ventilator-induced lung injury, which is partially prevented by lung-protec

298 dematous pancreatitis accompanied by minimal lung injury, while L-arginine induced extremely severe p

299 infected with Klebsiella pneumoniae develop lung injury with accumulation of cardiolipin.

300 w T cell migration in a mouse model of acute lung injury with two-photon imaging of intact lung tissu