ライフサイエンスコーパス: lung injury

1 -17 and miR-548b that are known mediators of lung injury.

2 ale BALB/c strain) with an LPS-induced acute lung injury.

3 likely cellular targets in antibody-mediated lung injury.

4 initiate an immunologic cascade resulting in lung injury.

5 lung diseases like cystic fibrosis and acute lung injury.

6 plays a pivotal role in the pathogenesis of lung injury.

7 s a surrogate outcome for ventilator-induced lung injury.

8 a potential therapeutic adjunct after major lung injury.

9 protect against P. aeruginosa-induced acute lung injury.

10 1) K(+) channels, which results in worsening lung injury.

11 toms that rapidly progressed to severe acute lung injury.

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

13 many inflammatory conditions including acute lung injury.

14 required for tissue regeneration after acute lung injury.

15 ferent levels of atelectasis in experimental lung injury.

16 urther define bioactive pathways relevant to lung injury.

17 mote resolution of neutrophil-mediated acute lung injury.

18 -myofibroblast differentiation and fibrosing lung injury.

19 nary expression of key mediators of neonatal lung injury.

20 ucial role in the resolution of inflammatory lung injury.

21 idal ventilation and PEEP produced the least lung injury.

22 lly activated lung macrophages to exacerbate lung injury.

23 imal mechanical ventilator settings in acute lung injury.

24 e-threatening pneumonia culminating in acute lung injury.

25 and possibly drivers, of ventilator-induced lung injury.

26 ibute to the temperature dependence of acute lung injury.

27 macrophages exhibited reduced sepsis-induced lung injury.

28 sclerosis, diabetes, hypertension, and acute lung injury.

29 d inflammation, two major hallmarks of acute lung injury.

30 y distress syndrome, but can also exacerbate lung injury.

31 mice showed severely defective resolution of lung injury.

32 h couldtherefore decrease ventilator-induced lung injury.

33 masome prevented P. aeruginosa-induced acute lung injury.

34 scular repair and resolution of inflammatory lung injury.

35 equisites for controlling ventilator-induced lung injury.

36 rendered MHC I-deficient mice susceptible to lung injury.

37 enous SP-D levels and overall survival after lung injury.

38 t significantly influence neonatal hyperoxic lung injury.

39 ling in macrophages exacerbated inflammatory lung injury.

40 ophil adaptation, resulting in resolution of lung injury.

41 d most likely related to the severity of the lung injury.

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

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

44 tized, mechanically ventilated pigs, without lung injury.

45 diaphragm activity, in sedated patients with lung injury.

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

47 isruption and cytokine storm in experimental lung injury.

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

49 riteria to include noninvasive surrogates of lung injury.

50 by facilitating resolution of E. coli-evoked lung injury.

51 med at further minimizing ventilator-induced lung injury.

52 y activated phenotype after cadmium-mediated lung injury.

53 lications for therapeutic targeting in acute lung injury.

54 quently improves gas exchange and attenuates lung injury.

55 es several vascular diseases including acute lung injury.

56 lood coagulation presumably in conditions of lung injury.

57 nto the critical role of C/EBPgamma in acute lung injury.

58 rant angiogenesis and impaired resolution of lung injury.

59 S- and IgG immune complexes-stimulated acute lung injury.

60 ry and remodeling in a murine model of acute lung injury.

61 agonist improved outcomes in vivo following lung injury.

62 enues for the treatment of radiation-induced lung injury.

63 tages, was the only tool able to specify the lung injuries.

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

65 Lung injury activates specialized adult epithelial proge

66 potential to prevent and to treat the acute lung injury after SARS-CoV-2 infection, especially for t

67 ion linked to pathological features of acute lung injury (ALI) and acute respiratory distress syndrom

68 Acute lung injury (ALI) and idiopathic pulmonary fibrosis (IPF

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

70 a central role in the pathogenesis of acute lung injury (ALI) during both the acute pneumonitis stag

71 ared with sham rats, rats a week after acute lung injury (ALI) express more pro-inflammatory cytokine

72 Acute lung injury (ALI) increases respiratory rate (fR) and ve

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

74 Acute lung injury (ALI) occurs in up to 30% of patients with s

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

76 Acute lung injury (ALI), a common condition in critically ill

77 treating respiratory diseases such as acute lung injury (ALI), acute respiratory distress syndrome (

78 Acute lung injury (ALI), endotheliitis, capillary inflammation

79 se-mouse models suggest that increased acute lung injury (ALI), potentially due to enhanced viral spr

80 el of lipopolysaccharide (LPS)-induced acute lung injury (ALI), we observed augmented temporal genera

81 osolized LPS inhalation mouse model of acute lung injury (ALI).

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

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

84 ncreased susceptibility to LPS-induced acute lung injury (ALI).

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

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

87 el of lipopolysaccharide (LPS)-induced acute lung injury (ALI).

88 ted pneumonia, a major risk factor for acute lung injury (ALI)/acute respiratory distress syndrome (A

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

90 s an emerging illness associated with severe lung injury and constitutional and gastrointestinal symp

91 al models, indicate that platelets may drive lung injury and contribute to dysregulated host defense

92 Lung injury and development and PH were quantified at di

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

94 Histologic lung injury and fibroproliferation scores were positivel

95 phatics have an overall protective effect in lung injury and fibrosis and fit with a mechanism whereb

96 ) by inhalation to treat different models of lung injury and fibrosis.

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

98 r epithelial type 2 cells (AT2s), leading to lung injury and impaired gas exchange, but the mechanism

99 ) to offset pleural pressure might attenuate lung injury and improve patient outcomes in acute respir

100 function, reduced myocardial damage, shock, lung injury and improved survival independent of pancrea

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

102 ls of fibrosis, lung dysbiosis precedes peak lung injury and is persistent.

103 Acute lung injury and its more severe form, acute respiratory

104 near-apneic ventilation decreased histologic lung injury and matrix metalloproteinase activity, and p

105 nly the removal of endothelial MHC I reduced lung injury and mortality, related mechanistically to ab

106 e, whereas complement depletion reduced both lung injury and NETs.

107 ate appears in several independent models of lung injury and persists in human lung fibrosis, creatin

108 (HL) but carries risks of bleomycin-induced lung injury and radiation toxicity.

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

110 ng that may lead to increased likelihood for lung injury and respiratory failure.

111 en paid to the evolving interactions between lung injury and response and to the timing of interventi

112 in, authors representing the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network He

113 science researchers from the Pediatric Acute Lung Injury and Sepsis Investigators Network, the EBMT,

114 e in pulmonary innate immune TLR4 signaling, lung injury and subsequent abnormal lung development is

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

116 orticoids may modulate inflammation-mediated lung injury and thereby reduce progression to respirator

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

118 ish TACO and TRALI from underlying causes of lung injury and/or fluid overload as well as from each o

119 culatory overload, transfusion-related acute lung injury, and acute and delayed hemolytic transfusion

120 seases in mouse models of peritonitis, acute lung injury, and atherosclerosis.

121 ve cell types, typically seen in response to lung injury, and by striking infidelity among transcript

122 ce restores surfactant homeostasis, prevents lung injury, and improves lung physiology.

123 resulting in decreased viral spread, reduced lung injury, and increased survival.

124 hat normoxic HC increases viral replication, lung injury, and mortality in mice infected with influen

125 rdial infarction, acute kidney injury, acute lung injury, and others are among the leading causes of

126 is of lung diseases, including asthma, acute lung injury, and pulmonary fibrosis, and thus suggest a

127 perthermia worsens and hypothermia mitigates lung injury, and temperature dependence of lung injury i

128 Elevated End-Expiratory Pressure to Obviate Lung Injury], and FACTT [Fluids and Catheter Treatment T

129 antly attenuated P. aeruginosa-induced acute lung injury, as assessed by lung wet-to-dry weight ratio

130 An ongoing outbreak of lung injury associated with e-cigarettes or vaping (also

131 60 patients presented with lung injury associated with e-cigarettes or vaping at 13

132 Lung injury associated with e-cigarettes or vaping is an

133 Lung injury associated with e-cigarettes or vaping remai

134 tudy, we collected data on all patients with lung injury associated with e-cigarettes or vaping seen

135 Two patients died and lung injury associated with e-cigarettes or vaping was t

136 oposed diagnosis and treatment guideline for lung injury associated with e-cigarettes or vaping.

137 artment of Public Health received reports of lung injury associated with the use of e-cigarettes (als

138 l stem cells (MSC) protect against hyperoxic lung injury at least in part by increasing the number of

139 graft dysfunction (PGD), a syndrome of acute lung injury, attenuates improvements in patient-reported

140 ecule 79-6 is able to treat and even reverse lung injury attributable to experimental chronic graft-v

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

142 re found in the alveoli with aging and after lung injury, but go undetected since they express alveol

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

144 tigated the ferroptotic damage in IR-induced lung injury by reducing lipid peroxidation and increasin

145 on, reduces pulmonary function, and enhances lung injury by respiratory syncytial virus.

146 Epithelial cells in the field of lung injury can give rise to distinct premalignant lesio

147 fect of low tidal volume ventilation against lung injury caused by lipopolysaccharides and ventilatio

148 The Pediatric Acute Lung Injury Consensus Conference (PALICC) definition was

149 erior ventilation defects secondary to acute lung injury could be re-inflated by applying positive en

150 In an experimental model of inflammatory lung injury, deletion of cGas in mice restored endotheli

151 y distress, asynchronies, ventilator-induced lung injury, diaphragmatic injury, and cardiovascular co

152 geneity may contribute to ventilator-induced lung injury during high-frequency oscillatory ventilatio

153 The potential for ventilator-induced lung injury during high-frequency oscillatory ventilatio

154 y rate per se may promote ventilator-induced lung injury, dynamic hyperinflation, ineffective efforts

155 cigarette, or vaping, product use-associated lung injury (EVALI) had been reported to the Centers for

156 cigarette, or vaping, product use associated lung injury (EVALI) have been reported in the USA.

157 cigarette, or vaping, product use-associated lung injury (EVALI) have not been established.

158 c cigarette or vaping product use-associated lung injury (EVALI) is a serious public health concern w

159 e-cigarette or vaping-product use-associated lung injury (EVALI) is alarming.

160 c cigarette or vaping product use-associated lung injury (EVALI).

161 cigarette, or vaping, product use associated lung injury (EVALI).

162 e-cigarette or vaping product use-associated lung injury (EVALI).

163 clinically in five human patients with acute lung injury, experimentally in five mice ventilated befo

164 t to counteract Hyperoxia (HO)-induced Acute Lung Injury (HALI).

165 birth led to severe acute hyperoxia-induced lung injury (HILI) and significant mortality.

166 )1A enzymes are protective against hyperoxic lung injury (HLI).

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

168 Treatment with RvD1 mitigated I/R lung injury in aging, promoted efferocytosis, and preven

169 broproliferation following bleomycin-induced lung injury in alcohol-fed mice.

170 ether flow-controlled ventilation attenuates lung injury in an animal model of acute respiratory dist

171 , there were no differences in the degree of lung injury in antibiotic treated mice compared to vehic

172 but also regarding how various mechanisms of lung injury in ARDS may potentially be mitigated by ultr

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

174 nosa (strain: PA103) infection induced acute lung injury in C57BL/6 mice in a dose- and time-dependen

175 let activation and calcium flux, and reduced lung injury in CF mice after intratracheal LPS or Pseudo

176 To better understand the mechanism of lung injury in CIP, we prospectively collected bronchoal

177 terial pathogens, resulting in a more severe lung injury in COVID-19.

178 for predicting symptomatic radiation-induced lung injury in human.

179 ting that ILCs may be involved in regulating lung injury in lung transplant recipients.

180 ation and reduced histopathological signs of lung injury in mice exposed to E. coli.

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

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

183 get for the treatment of ventilation-induced lung injury in newborns.

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

185 pothesis of genetic predisposition to severe lung injury in patients with coronavirus disease 2019.

186 lation strategy mitigates ventilator-induced lung injury in patients with severe acute respiratory di

187 ysiologic, hematologic, and imaging basis of lung injury in severe COVID-19 pneumonia.Methods: Clinic

188 to modulate the immune response and abrogate lung injury in severe COVID-19.

189 have been shown to decrease the severity of lung injury in some patients.

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

191 Dexamethasone use might attenuate lung injury in these patients.

192 phil proteases may reduce the progression of lung injury in these patients.

193 te passage cells to clonal density, to mimic lung injury in vivo, selects for rare subsets of HBECs t

194 Other less common forms of lung injury, including acute eosinophilic pneumonia and

195 ntions likely to decrease ventilator-induced lung injury, including low tidal volume, prone position,

196 sed LTB(4) levels in C57BL/6 mice with acute lung injury, increasing overall antimicrobial activity.

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

198 The imaging sequence was repeated after lung injury induced by whole-lung lavage and injurious v

199 culatory overload, transfusion-related acute lung injury, infection transmission, alloimmunization, a

200 bleomycin treatment, they exhibited enhanced lung injury, inflammation, and fibrosis compared with co

201 esence within blood and lungs, as well as in lung injury, inflammation, and oxidative stress.

202 -19b oligo inhibitor significantly decreased lung injury, inflammation, and permeability and improved

203 r activity-modifying protein 2 and modulates lung injury initiation.

204 osis of acute ischemic stroke, septic shock, lung injuries, insulin resistance in diabetic patients,

205 ltaneously examined for evidence of BPD-like lung injury, investigating both the short- and long-term

206 Radiation-induced lung injury is a highly complex combination of pathologi

207 s lung injury, and temperature dependence of lung injury is blunted by inhibitors of p38 mitogen-acti

208 c cigarette or vaping product use-associated lung injury is characterized by bilateral symmetric grou

209 promote metabolic reprogramming to regulate lung injury is essential.

210 y adaptation during oxidative stress-induced lung injury is mediated by a novel subset of forkhead bo

211 ndrome (ARDS), the most severe form of acute lung injury, is associated with reduced lung compliance

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

213 e is a major contributing factor in neonatal lung injury leading to bronchopulmonary dysplasia.

214 However, histological evidence of lung injury (lung injury score mean difference = -0.07;

215 egulation of Sftpc(I73T) initiated a diffuse lung injury marked by increases in bronchoalveolar lavag

216 physiological, histological, and biochemical lung injury markers.

217 Ventilator-induced lung injury may occur in acute respiratory distress synd

218 with histological and gene markers of early lung injury.Measurements and Main Results: DynPEEP signi

219 tions of the lung; and 2) resultant regional lung injury.Methods: Preterm lambs (125 +/- 1 d gestatio

220 ced pulmonary hypertension and monocrotaline lung injury model).

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

222 -series single cell RNA-seq of the bleomycin lung injury model, we resolved transcriptional dynamics

223 d macrophage efferocytosis in a murine acute lung injury model.

224 eceived a saline-lavage surfactant depletion lung injury model.

225 both zebrafish tail injury and murine acute lung injury models of neutrophilic inflammation, overexp

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

227 c cigarette or vaping product use-associated lung injury most frequently presents with an acute lung

228 overload (n = 7), transfusion-related acute lung injury (n = 11), and severe allergic transfusion re

229 Following lung injury, NE cells proliferate and generate other cel

230 r gradual lung aeration at birth causes less lung injury.Objectives: To examine the effect of gradual

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

232 signaling plays a dual role, driving severe lung injury on the one hand, yet restricting systemic vi

233 EVALI most commonly show a pattern of acute lung injury on the spectrum of organizing pneumonia and

234 rats CLEN, DEX or CLEN + DEX did not induce lung injury or inflammation, however DEX and CLEN + DEX

235 e-derived adipokine, has been shown to limit lung injury originating from endothelial cell (EC) damag

236 objective of the current study was to define lung injury, pathology, and associated behavioral change

237 njury most frequently presents with an acute lung injury pattern at CT, manifesting as multifocal gro

238 ll strategies generated similar nondependent lung injury patterns.

239 f pathogen-specific CD4 T-cell function, and lung injury prior to and after ART initiation in adults

240 potentially accelerating ventilator-induced lung injury process.

241 ls of endotoxin, insufficient to cause donor lung injury, promoted TRAM-dependent production of CXCL2

242 al lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.

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

244 errupting the POOR-get-POORer progression of lung injury relies on two principles: 1) open the lung t

245 Ventilator-induced lung injury remains a key contributor to the morbidity a

246 The etiology of susceptibility to severe lung injury remains unclear.

247 However, its role in lung injury resolution and the mechanisms by which it re

248 phoid organ formation, and then decreased as lung injury resolved by 56 days.

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

250 cation of SNPs Predisposing to Altered Acute Lung Injury Risk; n=882), Copenhagen General Population

251 wever, histological evidence of lung injury (lung injury score mean difference = -0.07; P = 0.04) and

252 ompliance, 33.7 +/- 14.7 ml/cm H(2)O; Murray lung injury score, 3.14 +/- 0.53; mean ventilatory ratio

253 of pulmonary function, such as histological lung injury score, wet/dry ratio, and oxygenation index,

254 L1249 improved lung compliance, histological lung injury scores, broncho-alveolar lavage protein leve

255 Lung injury scoring of histological sections was signifi

256 ar lesions of organizing pneumonia and acute lung injury seen at histopathologic findings in these pa

257 In a model of acute lung injury, selective deletion of EC MIF decreases neut

258 t organ for COVID-19; patients develop acute lung injury that can progress to respiratory failure, al

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

260 to mechanical ventilation (MV) are prone to lung injury that may result in bronchopulmonary dysplasi

261 in mice resulteds in hypoxia and features of lung injury that resemble emphysema.

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

263 ause MK2 participates in the pathogenesis of lung injury, the observed changes in the structure and f

264 After acute lung injury, they are preferentially localized in regene

265 y modeled to define the military standard 1% lung injury threshold.

266 orts to understand fundamental mechanisms of lung injury to design specific treatments.

267 sibility and gene expression following acute lung injury to elucidate repair mechanisms.

268 TNF-alpha challenge-augmented lung injury to the levels observed in aged mice stimulat

269 of ACE2, a tissue-protective mediator during lung injury, to enhance infection.

270 verload (TACO) and transfusion-related acute lung injury (TRALI) are syndromes of acute respiratory d

271 Transfusion-related acute lung injury (TRALI) is one of the leading causes of tran

272 s can cause lethal transfusion-related acute lung injury (TRALI).

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

274 havioral changes from primary repeated blast lung injury under appropriate exposure conditions and co

275 entilated rabbits, at baseline and following lung injury, using high-resolution synchrotron phase-con

276 associated with increased leukopenia, acute lung injury, vasopressor use, extracorporeal life suppor

277 otected against P. aeruginosa -induced acute lung injury via activation of A(2A)R and A(2B)R.

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

279 lung injury via adenosine receptors or cause lung injury via adenosine receptors or equilibrative nuc

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

281 results indicate that AM resolves hyperoxic lung injury via NOS3.

282 thermore, how to minimize ventilator-induced lung injury (VILI) for any given lung remains controvers

283 perimentally to influence ventilator-induced lung injury (VILI).

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

285 This "ventilator-induced lung injury vortex" of the shrinking baby lung is oppose

286 The extent of lung injury was identified at 24 h following BOP by asse

287 Blast lung injury was identified in one patient and tympanic m

288 In 18 animals lung injury was induced by a double-hit consisting of re

289 Lung injury was induced with saline lung lavage followed

290 Lung injury was mathematically modeled to define the mil

291 A mouse model of perinatal hyperoxia-induced lung injury was used to identify molecular mechanisms th

292 hways by which RAGE mediates smoking related lung injury we performed unbiased gene expression profil

293 onary adaptation to oxidative stress-induced lung injury, we exposed mice to repeated nose-only chlor

294 hind limb ischemia-reperfusion (I/R) remote lung injury, we present evidence that aging is associate

295 Lung injuries were assessed by histologic analysis.

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

297 ts of PAFAH2 inhibition on TNF-alpha-induced lung injury were observed in vivo.

298 IRF also caused vagus nerve, esophageal, and lung injury while PFA did not.

299 which aims at minimizing ventilator-induced lung injury (with low Vt/high positive end-expiratory pr

300 irefighters, stratified by resistance to WTC-Lung Injury (WTC-LI) to determine metabolite pathways si