ライフサイエンスコーパス: ARDS

1 ARDS occurs most often in the setting of pneumonia, seps

2 ARDS swine with high P(PL) demonstrated unchanged transm

3 ARDS was predicted by elevated LDH (P < .0001), while mo

4 As compared with patients with non-COVID-19 ARDS (n = 36), those with COVID-19 (n = 38) were not sig

5 COVID-19 ARDS exhibits a distinct immunologic profile in the lung

6 0-75 years) with moderate-to-severe COVID-19 ARDS were included.

7 ss syndrome (ARDS) with that of non-COVID-19 ARDS, and to identify biomarkers associated with mortali

8 and compared with patients with non-COVID-19 ARDS.

9 emokine signature" were observed in COVID-19 ARDS.

10 de range of Crs was observed in non-COVID-19 ARDS.

11 ted with mortality in patients with COVID-19 ARDS.Methods: Prospective observational monocenter study

12 at baseline (Day 1), Day 4, and Day 8 after ARDS onset (N = 68 total samples).

13 cts alive and extubated within 28 days after ARDS onset (alive/extubated(Day28)) versus those dead or

14 nts were anaemia (four [3%] vs two [4%]) and ARDS (four [3%] vs three [5%]).

15 ide a robust platform for studies of ALI and ARDS to evaluate vaccine and antiviral drug performance,

16 is a major contributor to tissue damage and ARDS(1,2).

17 The association between each exposure and ARDS was determined via multivariable logistic regressio

18 ome coronavirus 2 (SARS-CoV-2) infection and ARDS admitted between March 8 and March 30, 2020, were i

19 an failure, including acute renal injury and ARDS.

20 owed no significant benefit in mortality and ARDS rates.

21 espiratory distress syndrome (ARDS) risk and ARDS outcome.

22 enrolling patients (N = 167) with sepsis and ARDS present for less than 24 hours.

23 lts: A total of 210 patients with sepsis and ARDS were included, of whom 128 had a reactive and 82 an

24 reliminary study of patients with sepsis and ARDS, a 96-hour infusion of vitamin C compared with plac

25 f vitamin C for other outcomes in sepsis and ARDS.

26 brogated PMN priming, PMN sequestration, and ARDS.

27 e first 25 patients with COVID-19 associated ARDS placed on V-V ECMO at our institution.

28 lmonary protection in SARS-CoV-2- associated ARDS.

29 Because ARDS is a heterogeneous syndrome, targeting MSCs to pati

30 ng survivors, 386 (42%) were employed before ARDS (56% male; mean +/- SD age, 45 +/- 13 yr), with sev

31 ide expert consensus that mechanisms causing ARDS in adults and older children-namely complex surfact

32 this study was to develop models to classify ARDS phenotypes using readily available clinical data on

33 and FACTT (P = 0.0072) cohorts.Conclusions: ARDS phenotypes can be accurately identified using machi

34 rgeted inhibition of the SUCNR1 may decrease ARDS development from other disease states to prevent AR

35 of severely injured patients that developed ARDS versus severely injured patients that did not, and

36 d succinate in trauma patients who developed ARDS (p<0.05).

37 associated with a greater risk of developing ARDS after severe trauma and represents a novel and pote

38 emia and Crs was characterized as a distinct ARDS phenotype.Objectives: To determine whether such Crs

39 cellular actors involved in COVID-19-driven ARDS are poorly understood.

40 ess their functions during SARS-CoV-2-driven ARDS.

41 s case, any patient with severe disease (eg, ARDS or pneumonia) requiring hospitalization without an

42 on of pulmonary inflammation in experimental ARDS.

43 (pulmonary) versus indirect (extrapulmonary) ARDS.Conclusions: Clinical outcomes in ARDS are associat

44 principal diagnoses of respiratory failure, ARDS, respiratory arrest, or sepsis with a secondary dia

45 facilitate a precision medicine approach for ARDS.

46 ction of inspired oxygen (Fio2) criteria for ARDS had to be met within a 24-hour period, and the admi

47 ial mortality rates associated with ECMO for ARDS in COVID-19 were high, leading some to believe that

48 lly modifiable environmental risk factor for ARDS.

49 variations in demographics, risk factors for ARDS, and comorbid diseases.

50 effort, however, pharmacological options for ARDS remain scarce.

51 re whole-genome genotyped and phenotyped for ARDS.

52 with improved pharmacological properties for ARDS is possible.

53 irculating metabolites and clinical risk for ARDS.

54 of success of pharmacological therapies for ARDS, however, presents a continued challenge in the fie

55 at CNI103 is a promising novel treatment for ARDS and other inflammatory diseases.

56 fore, HCA may adversely impact recovery from ARDS at the cellular level, whereas MSCs may not be ther

57 wo cohorts in which we previously identified ARDS subphenotypes.

58 P = 0.035), and a significant difference in ARDS in squamous cell carcinoma with 14% versus 2% in ad

59 , current evidence, and future directions in ARDS prevention.

60 tigate the role of proteasome dysfunction in ARDS pathogenesis.

61 post-injury may serve as the first event in ARDS.

62 une response in the lung is a key feature in ARDS pathophysiology.

63 In view of the heterogeneity in ARDS, both prognostic and predictive enrichment strategi

64 from a cohort study of myocardial injury in ARDS and performed survival analysis with primary outcom

65 ing how various mechanisms of lung injury in ARDS may potentially be mitigated by ultra-lung-protecti

66 ned about the pathogenesis of lung injury in ARDS, with an emphasis on the mechanisms of injury to th

67 ate plasma sRAGE as a causal intermediate in ARDS by Mendelian randomization (MR), a statistical meth

68 notion that the macromolecule is involved in ARDS caused by SARS-CoV-2.

69 mprove physiological or clinical outcomes in ARDS and might be harmful to patient health.

70 nary) ARDS.Conclusions: Clinical outcomes in ARDS are associated with highly distinct AM transcriptio

71 Income per person and outcomes in ARDS are independently associated.

72 ostasis and contributes to lung pathology in ARDS.

73 We sought to identify biological pathways in ARDS that differentiate survivors from non-survivors.

74 biological patterns that are also present in ARDS, suggesting that generalizable patterns exist in di

75 ate disease endotypes previously reported in ARDS.

76 opolysaccharide, a second event, resulted in ARDS in vivo requiring PMNs.

77 on was associated with increased survival in ARDS; hospital survival was significantly lower in Middl

78 do not support PES-guided PEEP titration in ARDS.

79 ple bedside index of impaired ventilation in ARDS.

80 (ECCO2R) for ultraprotective ventilation in ARDS.

81 tilatory ratio correlates well with Vd/Vt in ARDS, and higher values at baseline are associated with

82 ing severe disease manifestations, including ARDS.

83 at increased plasma sRAGE leads to increased ARDS risk, suggesting plasma sRAGE acts as a causal inte

84 stigate the pathogenesis of COVID-19-induced ARDS and evaluate therapeutic strategies.

85 lavage fluid from patients with IAV-induced ARDS.

86 he National Heart, Lung, and Blood Institute ARDS Clinical Trials Network recommends a target partial

87 Methods: ARDS was induced by saline lung lavage followed by injur

88 therapy in a model of ARDS and ECMO.Methods: ARDS was induced in 14 sheep, after which they were esta

89 3-68) reached criteria for mild and moderate ARDS between t = 90-120 min and t = 120-180 min, respect

90 min, respectively, and remained in moderate ARDS until t = 300 min.

91 PaO2/FiO2 among patients with mild-moderate ARDS, and the possibility of decreased mortality in pati

92 verified in secondary analyses of two NHLBI ARDS Network randomized controlled trials.

93 acid warrants further validation as a novel ARDS biomarker.

94 injury, and impaired oxygenation on Day 1 of ARDS, and conferred fourfold increased odds of mortality

95 age, which is the histopathological basis of ARDS.

96 We report two cases of ARDS in two aged African green monkeys (AGMs) infected w

97 e whether, during NIV, the categorization of ARDS severity based on the PaO2/FiO2 Berlin criteria is

98 Classification of ARDS severity based on PaO2/FiO2 ratio was associated wi

99 cs analysis to an existing patient cohort of ARDS in patients with sepsis admitted to two ICUs during

100 e interactions in the lung in the context of ARDS are poorly understood.

101 ective, we discuss the historical context of ARDS description and attempts at its definition.

102 has been explored in the clinical context of ARDS, its effect upon alveolar epithelial cell (AEC) wou

103 proinflammatory programs over the course of ARDS.

104 -European Consensus Conference Definition of ARDS.

105 strongly associated with the development of ARDS (OR 7.72; 95% CI: 1.64-36.28, P = 0.03).

106 e followed for 6 days for the development of ARDS according to Berlin Criteria.

107 ant risk factors both for the development of ARDS and for important patient-centered outcomes like mo

108 XCR4 protein agonists prevent development of ARDS and reduce mortality in a rat model, and that devel

109 and 28- and 90-day mortality; development of ARDS, pneumonia, pneumothorax, severe atelectasis, sever

110 to occur within 48 hours of the diagnosis of ARDS.

111 nt in patients with the most severe forms of ARDS.

112 We update the current knowledge of ARDS trends in incidence and mortality, risk factors, an

113 the use of IFN-beta-1a in the management of ARDS.

114 obronchial hMSC therapy in an ovine model of ARDS and ECMO can impair membrane oxygenator function an

115 ty and efficacy of MSC therapy in a model of ARDS and ECMO.Methods: ARDS was induced in 14 sheep, aft

116 s were tested in a two-event animal model of ARDS to identify a molecular link between circulating me

117 ulmonary sequestration in an animal model of ARDS.

118 f the AC-cAMP axis in experimental models of ARDS.

119 ly been examined but none exist for onset of ARDS nor in patients with burn injury.

120 athway contributes to the pathophysiology of ARDS, whereas activation of the ACE-2-angiotensin(1-7)-a

121 lly expressed between biologic phenotypes of ARDS supporting the observation that the subgroups of AR

122 These findings support the presence of ARDS subtypes that may require different treatment appro

123 atients for both the study and prevention of ARDS in patients with burn injury.

124 eroids were associated with a higher rate of ARDS (P = .0003).

125 efforts to facilitate earlier recognition of ARDS, identifying responsive subsets of patients and ong

126 e-center, prospective observational study of ARDS, we tested the association of Vd/Vt with ventilator

127 orting the observation that the subgroups of ARDS are incomparable in terms of pathophysiology.

128 uld be effective for prevention/treatment of ARDS.

129 asma sRAGE had a consistent causal effect on ARDS risk with a beta estimate of 0.50 (95% confidence i

130 (ARDS) is limited, and most studies focus on ARDS onset.

131 ates of the causal effect of plasma sRAGE on ARDS risk.Measurements and Main Results: There were 393

132 The causal effect of plasma sRAGE on ARDS was inferred using the top variants with significan

133 Whether pediatric ARDS (PARDS) is similarly associated with altered neutro

134 ers and clinical risk factors for predicting ARDS mortality have recently been examined but none exis

135 lopment from other disease states to prevent ARDS globally.

136 n, CXCL12, CXCL12(1) and CXCL12(2) prevented ARDS development.

137 ECMO has a role in severe, refractory ARDS associated with COVID-19.

138 al injury compared with non-COVID-19-related ARDS (odds ratio, 0.55 [95% CI, 0.36-0.84]; P=0.005).

139 After adjustment, COVID-19-related ARDS was associated with lower odds of myocardial injury

140 s as a causal intermediate in sepsis-related ARDS.

141 Among adults with moderate or severe ARDS, intravenous IFN-beta-1a administered for 6 days, c

142 atients with COVID-19 and moderate or severe ARDS, use of intravenous dexamethasone plus standard car

143 d 16 years and older with moderate to severe ARDS (Pao2:Fio2 <=200 mm Hg) were enrolled between Octob

144 ventilated patients with moderate to severe ARDS (ratio of partial pressure of oxygen to fractional

145 included 301 adults with moderate to severe ARDS according to the Berlin definition.

146 In patients with moderate to severe ARDS, a strategy with lung recruitment and titrated PEEP

147 atients with COVID-19 and moderate to severe ARDS, according to the Berlin definition, were enrolled

148 Among patients with moderate to severe ARDS, PES-guided PEEP, compared with empirical high PEEP

149 lled trial in adults with moderate to severe ARDS.

150 of MSCs to patients with moderate to severe ARDS.

151 was safe in patients with moderate to severe ARDS.

152 17, enrolling adults with moderate to severe ARDS.

153 ly assigned patients with moderate-to-severe ARDS (defined by a ratio of the partial pressure of arte

154 early after the onset of moderate-to-severe ARDS (median, 7.6 hours after onset).

155 omized within 24 hours of moderate-to-severe ARDS onset to receive either intravenous midazolam or in

156 Among patients with moderate-to-severe ARDS who were treated with a strategy involving a high P

157 eased mortality in patients with very severe ARDS.

158 ariable for survival in patients with severe ARDS due to pneumonia.

159 with proven SARS-CoV-2 infection with severe ARDS requiring PP.

160 ge of admitted COVID-19 patients with severe ARDS.

161 membrane oxygenation in patients with severe ARDS.

162 aeruginosa-induced pneumonia and subsequent ARDS.

163 t research targets, as many patients survive ARDS only to have ongoing functional and/or psychologica

164 0.001), acute respiratory distress syndrome (ARDS) (OR: 10.142, 95% CI 1.611-63.853, p = 0.014), redu

165 ence of acute respiratory distress syndrome (ARDS) among all predisposing conditions, but few studies

166 ion and acute respiratory distress syndrome (ARDS) and may have the appearance of liquid jelly.

167 stem in acute respiratory distress syndrome (ARDS) and respiratory failure in patients with coronavir

168 induced acute respiratory distress syndrome (ARDS) at a single US academic hospital between March and

169 Acute respiratory distress syndrome (ARDS) caused by SARS-CoV-2 is largely the result of a dy

170 ts with acute respiratory distress syndrome (ARDS) could identify cell-specific biological programs t

171 cted on acute respiratory distress syndrome (ARDS) Day 1 from 235 children at five hospitals between

172 Acute respiratory distress syndrome (ARDS) due to coronavirus disease 2019 (COVID-19) is asso

173 reating acute respiratory distress syndrome (ARDS) experienced initial success followed by failures.

174 ypes of acute respiratory distress syndrome (ARDS) have been identified based on plasma protein marke

175 prevent acute respiratory distress syndrome (ARDS) in coronavirus disease 2019 (COVID-19) and discuss

176 ts with acute respiratory distress syndrome (ARDS) in the emergency room (ER) is distinguishing betwe

177 ress to acute respiratory distress syndrome (ARDS) in the most severe form, while children are largel

178 isease, acute respiratory distress syndrome (ARDS) is a common and often fatal presentation.

179 The acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critic

180 Acute respiratory distress syndrome (ARDS) is a common feature of severe forms of COVID-19 an

181 Acute respiratory distress syndrome (ARDS) is a devastating disorder characterized by diffuse

182 Acute respiratory distress syndrome (ARDS) is a heterogeneous condition characterized by the

183 Acute respiratory distress syndrome (ARDS) is an inflammatory lung disease with a high morbid

184 IONALE: Acute respiratory distress syndrome (ARDS) is caused by widespread endothelial barrier disrup

185 tion on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset.

186 ionale: Acute respiratory distress syndrome (ARDS) lacks known causal biomarkers.

187 n a rat acute respiratory distress syndrome (ARDS) model utilizing the PaO(2)/FiO(2)-ratio as a clini

188 dentify acute respiratory distress syndrome (ARDS) patient subgroups with differential outcomes from

189 IONALE: Acute respiratory distress syndrome (ARDS) remains a major cause of respiratory failure in cr

190 osis to acute respiratory distress syndrome (ARDS) requiring ventilator support.

191 explain acute respiratory distress syndrome (ARDS) risk and ARDS outcome.

192 ed from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 ag

193 ied two acute respiratory distress syndrome (ARDS) subphenotypes in two separate randomized controlle

194 n cause acute respiratory distress syndrome (ARDS) that is rapidly progressive, severe, and refractor

195 torm or acute respiratory distress syndrome (ARDS) that often causes severe morbidity.

196 sses to acute respiratory distress syndrome (ARDS) triggered by a cytokine storm.

197 ed with acute respiratory distress syndrome (ARDS) unrelated to COVID-19.

198 s since acute respiratory distress syndrome (ARDS) was first described, substantial progress has been

199 ty, and acute respiratory distress syndrome (ARDS) were 10.9%, 4.3%, and 18.4%, respectively.

200 related acute respiratory distress syndrome (ARDS) were associated with increased mortality and delay

201 ts with acute respiratory distress syndrome (ARDS) where they acquire an activated pro-survival pheno

202 seen in acute respiratory distress syndrome (ARDS) which is currently a growing challenge for intensi

203 ts with acute respiratory distress syndrome (ARDS) who are receiving mechanical ventilation remain un

204 ypes of acute respiratory distress syndrome (ARDS) with differential clinical outcomes and responses

205 OVID-19 acute respiratory distress syndrome (ARDS) with that of non-COVID-19 ARDS, and to identify bi

206 sult in acute respiratory distress syndrome (ARDS)(1).

207 ion for acute respiratory distress syndrome (ARDS), although trials to date have not investigated its

208 (ALI), acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and

209 llowing acute respiratory distress syndrome (ARDS), joblessness is common but poorly understood.

210 Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is ass

211 ts with acute respiratory distress syndrome (ARDS), the National Heart, Lung, and Blood Institute ARD

212 severe acute respiratory distress syndrome (ARDS), the use of prone and supine positioning procedure

213 in the acute respiratory distress syndrome (ARDS).

214 ts with acute respiratory distress syndrome (ARDS).

215 VID-19) acute respiratory distress syndrome (ARDS).

216 LI) and acute respiratory distress syndrome (ARDS).

217 prevent acute respiratory distress syndrome (ARDS).

218 lity of acute respiratory distress syndrome (ARDS).

219 without acute respiratory distress syndrome (ARDS).

220 atening acute respiratory distress syndrome (ARDS).

221 of the acute respiratory distress syndrome (ARDS).

222 dies of acute respiratory distress syndrome (ARDS).

223 lity in acute respiratory distress syndrome (ARDS).

224 omes in acute respiratory distress syndrome (ARDS).

225 ting in acute respiratory distress syndrome (ARDS).

226 sis and acute respiratory distress syndrome (ARDS).

227 dels of acute respiratory distress syndrome (ARDS).

228 lethal acute respiratory distress syndrome (ARDS).

229 ts with acute respiratory distress syndrome (ARDS).

230 on with acute respiratory distress syndrome (ARDS).

231 ts with acute respiratory distress syndrome (ARDS).

232 ts with acute respiratory distress syndrome (ARDS).

233 ated in acute respiratory distress syndrome (ARDS).

234 cial in acute respiratory distress syndrome (ARDS).

235 ts with acute respiratory distress syndrome (ARDS).

236 died as acute respiratory distress syndrome (ARDS).

237 atening acute respiratory distress syndrome (ARDS).

238 OVID-19 acute respiratory distress syndrome (ARDS).

239 y (ALI)/acute respiratory distress syndrome (ARDS).

240 ts with acute respiratory distress syndrome (ARDS).Objectives: To determine whether a maximal lung re

241 ts were acute respiratory distress syndrome (ARDS; four [4%] vs two [4%]), allergic transfusion react

242 whether plasma sRAGE contributes causally to ARDS remains unknown.Objectives: Evaluate plasma sRAGE a

243 d respiratory burst thought to contribute to ARDS pathophysiology.

244 subsets of dendritic cells and monocytes to ARDS is still poorly understood.

245 A Streptococcus coinfection, progressing to ARDS and shock.

246 icropuncture model of AEC injury relevant to ARDS.

247 em organ dysfunction, similar to traditional ARDS.

248 ays and gradually increased afterwards until ARDS occurred with following death events (R(2) = 0.711,

249 phils isolated from the blood of adults with ARDS have elevated expression of interferon (IFN) stimul

250 ith conventional ventilation for adults with ARDS.

251 lar traps (NETs) are elevated in adults with ARDS.

252 cation end products) strongly associate with ARDS risk.

253 g-term exposures (3 yr) were associated with ARDS (P < 0.01) in adjusted models, despite exposure lev

254 esentation was significantly associated with ARDS (P < 0.05).

255 ablish a metabolic signature associated with ARDS development.

256 Plasma sRAGE was strongly associated with ARDS risk in both populations (odds ratio, 1.86; 95% con

257 days before presentation was associated with ARDS, except sulfur dioxide, which demonstrated a nonlin

258 a role in the pathobiology of children with ARDS.

259 ion and 28-day mortality in individuals with ARDS.Methods: We performed genome-wide transcriptional p

260 tively collected cohort of 441 patients with ARDS admitted to three intensive care units at the Unive

261 to recruit lung atelectasis in patients with ARDS and class III obesity but causes minimal overdisten

262 Additionally, patients with ARDS and class III obesity tolerate hemodynamically LRM

263 for biologic heterogeneity in patients with ARDS and suggests that a personalized approach to interv

264 Long-term outcomes of patients with ARDS are increasingly recognized as important research t

265 eight approach is imperfect in patients with ARDS because the amount of aerated lung varies considera

266 based phenotypes existed among patients with ARDS before the COVID-19 pandemic and to closely examine

267 V increases mortality for most patients with ARDS but may improve survival among patients with severe

268 Medical Centre identified 274 patients with ARDS due to pneumonia.

269 Pathological specimens from patients with ARDS frequently reveal diffuse alveolar damage, and labo

270 Pediatric patients with ARDS have specific plasma MMP profiles associated with i

271 ve validation of this range in patients with ARDS is lacking.

272 s toward specific subgroups of patients with ARDS on the basis of both severity and biology.

273 evidence supporting NIV use in patients with ARDS remains relatively sparse.

274 randomized trial, we assigned patients with ARDS to receive either conservative oxygen therapy (targ

275 therapeutically beneficial in patients with ARDS who develop HCA.

276 and Main Results: Among 1,117 patients with ARDS who met inclusion criteria, the median Crs was 30 (

277 us syndrome, targeting MSCs to patients with ARDS with a more hyperinflammatory endotype may further

278 Compared with patients with ARDS without COVID-19, patients with COVID-19 were older

279 Among patients with ARDS, early exposure to a conservative-oxygenation strat

280 NIV was used in 15% of patients with ARDS, irrespective of severity category.

281 In more severely hypoxaemic patients with ARDS, neuromuscular blockade and prone positioning have

282 s include the heterogeneity of patients with ARDS, the potential for a differential response to drugs

283 In patients with ARDS, use of inhaled sevoflurane improved oxygenation an

284 ertook a secondary analysis of patients with ARDS, who were invasively ventilated on controlled modes

285 tion of MSCs in critically ill patients with ARDS.

286 dy described the management of patients with ARDS.

287 nchoalveolar lavage fluid from patients with ARDS.

288 reased ventilator-free days in patients with ARDS.

289 ity in a preexisting cohort of patients with ARDS.

290 cs, management, and outcome of patients with ARDS.

291 ange would improve outcomes in patients with ARDS.

292 shown to improve outcomes for patients with ARDS.

293 educes ventilator-free days in patients with ARDS.Methods: A phase II, multicenter randomized control

294 ional crossover trial in adult subjects with ARDS and BMI >=35 kg/m(2) (n=21) was performed to explor

295 Measurements and Main Results: Subjects with ARDS and obesity (BMI=57+/-12 kg/m(2)), following LRM, r

296 om BAL fluid collected from 35 subjects with ARDS.

297 ring low/high PEEPs in a model of swine with ARDS and high P(PL) (n=9) versus healthy swine with norm

298 Among patients in the ICU without ARDS who were expected not to be extubated within 24 hou

299 n the Netherlands among 980 patients without ARDS expected not to be extubated within 24 hours after

300 rt the use of lower PEEP in patients without ARDS.