ライフサイエンスコーパス: ARDS

1 ARDS outcome depends on the lung injury severity within

2 ARDS represented 0.42 cases per ICU bed over 4 weeks and

3 ARDS seems to be a common and fatal syndrome in a hospit

4 s were consistent with the observed aberrant ARDS PMN survival and functional phenotype that we have

5 haping practice or advancing knowledge about ARDS.

6 At 12 months after ARDS, nearly one-half of previously employed survivors w

7 evaluate the timing of return to work after ARDS, and associated risk factors, lost earnings, and ch

8 or potential therapeutic exploitation in ALI/ARDS.

9 ential of kallistatin for sepsis-related ALI/ARDS.

10 50 km from an air quality monitor and had an ARDS risk factor.

11 sciplinary project which aimed to produce an ARDS consensus definition for neonates that is applicabl

12 study stimulates further work in refining an ARDS definition that can be consistently used in all set

13 poxia, we collected data on demographics and ARDS risk factors, performed lung ultrasonography, and e

14 Associations between pollutant exposure and ARDS risk were evaluated by logistic regression controll

15 monary vascular integrity in lung injury and ARDS-associated GWAS genes remains poorly understood.

16 an failure, including acute renal injury and ARDS.

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

18 Sepsis and ARDS are by definition heterogeneous, and patients vary

19 been able to identify subtypes of sepsis and ARDS that confer different prognoses.

20 d with gut-associated bacteria in sepsis and ARDS, potentially representing a shared mechanism of pat

21 ch 216 showed the same directional change as ARDS PMNs.

22 s and edema in inflammatory diseases such as ARDS.

23 tients with extremely severe H1N1-associated ARDS and positive results of the CESAR trial have led to

24 aO2/FIO2 (150 mm Hg) and PEEP (10 cm H2O) at ARDS onset and at 24 hours, we assigned patients to four

25 Because ARDS diagnosis relies on oxygenation and the chest radio

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

27 Because ARDS is a syndrome (and not a disease), the clinician or

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

29 om ventilated patients fulfilling the Berlin ARDS definition (n=10), in freshly isolated PMNs from ag

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

31 between patients who did and did not develop ARDS (p=0.471 for those at risk of ARDS; p=0.323 for tho

32 Of these, 2377 patients developed ARDS in the first 48 hours and whose respiratory failure

33 y a number of lymphocytes, the source during ARDS being unknown.

34 ypic heterogeneity, and the paucity of early ARDS lung tissue limit some applications of the rapidly

35 h offers unique contributions to elucidating ARDS pathogenesis and the paradigm of precision ARDS med

36 mber of effective treatments for established ARDS, the strategic focus of ARDS research has shifted t

37 del of sepsis and in humans with established ARDS.

38 aTh17 cells were protected from experimental ARDS induced by a single dose of endotracheal LPS.

39 facilitate a precision medicine approach for ARDS.

40 f 1,046 hospital admissions met criteria for ARDS.

41 ria, no patients would have met criteria for ARDS.

42 y unrecognized environmental risk factor for ARDS.

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

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

45 November 17, 2014, 7673 patients at risk for ARDS (Lung Injury Prediction Score >/=4) in the emergenc

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

47 spite advances in mechanical ventilation for ARDS, many interventions have not been successful in red

48 ome (ARDS), the morbidity and mortality from ARDS remains high.

49 ess has been made in reducing mortality from ARDS with lung-protective ventilation, using a tidal vol

50 linical practice, and clinical outcomes from ARDS.

51 o participating ICUs, 3022 (10.4%) fulfilled ARDS criteria.

52 patients enrolled in LUNG SAFE who fulfilled ARDS criteria on day 1 or 2, 1521 (54%) were recruited f

53 The molecular mechanisms governing ARDS PMN function and longevity are incompletely underst

54 Of the 564 patients in our cohort, 48 had ARDS (9%).

55 th the lowest TIE2 expression and 31% higher ARDS risk.

56 wo cohorts in which we previously identified ARDS subphenotypes.

57 lysis showed that 1319 genes were altered in ARDS PMNs relative to healthy volunteer PMNs.

58 owever, the role of adaptive immune cells in ARDS remains largely unknown.

59 e if prevention and reduction of delirium in ARDS patients can improve outcomes.

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

61 However, the mechanisms of MSCs' effects in ARDS are not well understood.

62 Transcripts enriched in ARDS PMNs were differentially expressed in known functio

63 treatment, targeting optimal gas exchange in ARDS has become less of a priority compared with prevent

64 ifferences in the BALF protein expression in ARDS survivors vs. non-survivors, including proteins tha

65 Approaches to reducing heterogeneity in ARDS clinical trials include using physiological, radiog

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

67 , a key mediator of alveolar inflammation in ARDS, was significantly correlated with altered lung mic

68 uld improve gas exchange and inflammation in ARDS.

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

70 l understanding of gas exchange mechanism in ARDS is imperative for individualized symptomatic suppor

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

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

73 ostasis and contributes to lung pathology in ARDS.

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

75 blood polymorphonuclear leucocytes (PMNs) in ARDS are basally activated, and exhibit aberrant oxidati

76 ce databases, the gene expression profile in ARDS PMNs showed near-complete correlation to datasets d

77 se 2a clinical trials to establish safety in ARDS are in progress, and two phase 1 trials did not rep

78 ol of the inflammatory dysregulation seen in ARDS, opening up new therapeutic targets.

79 Existing genome-wide studies in ARDS use total blood leucocytes; our study is the first,

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

81 the design of preventive clinical trials in ARDS and to initiate early treatment of patients with ac

82 previous experience with clinical trials in ARDS, we focus in this Review on future opportunities to

83 examines the current practice of NIV use in ARDS, the utility of the PaO2/FiO2 ratio in classifying

84 (ECCO2R) for ultraprotective ventilation in ARDS.

85 the engineered mice against MERS-CoV-induced ARDS.

86 ch for individual factors that may influence ARDS risk, the past 20 years have witnessed the identifi

87 regulating endothelial monolayer integrity, ARDS-associated GWAS genes, and lung pathophysiology.

88 The period prevalence of mild ARDS was 30.0% (95% CI, 28.2%-31.9%); of moderate ARDS,

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

90 was 30.0% (95% CI, 28.2%-31.9%); of moderate ARDS, 46.6% (95% CI, 44.5%-48.6%); and of severe ARDS, 2

91 KLF2 regulates multiple ARDS GWAS genes related to cytokine storm, oxidation, an

92 the first consensus definition for neonatal ARDS (called the Montreux definition).

93 We describe the Neonatal ARDS Project: an international, collaborative, multicent

94 logy of ARDS and present emerging aspects of ARDS pathophysiology that encompass modulators of the in

95 challenges some of the basic assumptions of ARDS prevention and preventive care in the intensive car

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

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

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

99 Each sample, obtained within seven days of ARDS onset, was depleted of high abundance proteins and

100 -European Consensus Conference Definition of ARDS.

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

102 The primary outcome was the development of ARDS by study day 7.

103 e exposure is associated with development of ARDS in at-risk critically ill patients, particularly in

104 arly intervention can prevent development of ARDS remains unclear.

105 The epidemiology of ARDS has not been reported for a low-income country at t

106 The field of ARDS genomics has cycled from candidate gene association

107 for established ARDS, the strategic focus of ARDS research has shifted toward identifying patients wi

108 injury severity within the first 24 hours of ARDS onset.

109 n definition may not allow identification of ARDS in resource-constrained settings.

110 ion is likely to underestimate the impact of ARDS in low-income countries, where resources to meet th

111 id not significantly reduce the incidence of ARDS at 7 days (10.3% vs 8.7%, respectively; odds ratio,

112 id not significantly reduce the incidence of ARDS at 7 days (OR, 1.24; 92.6%CI, 0.67-2.31).

113 The incidence of ARDS increased with increasing ozone exposure: 28% in th

114 The primary outcome was ICU incidence of ARDS.

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

116 ty, clinician recognition, and management of ARDS, and in patients' outcomes.

117 the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which

118 nition, epidemiology, and pathophysiology of ARDS and present emerging aspects of ARDS pathophysiolog

119 her refinements are needed for prediction of ARDS.

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

121 tic insight into the increased prevalence of ARDS in obese humans.

122 The prevalence of ARDS in patients at risk of ARDS was higher than in indi

123 Us in 50 countries, the period prevalence of ARDS was 10.4% of ICU admissions.

124 use genome-wide transcriptional profiling of ARDS blood PMNs to explore underlying disease mechanisms

125 to reduce the development and progression of ARDS and associated organ failures can be systematically

126 Timely recognition of ARDS and adherence to low tidal volume ventilation is im

127 Clinical recognition of ARDS ranged from 51.3% (95% CI, 47.5%-55.0%) in mild to

128 long-standing existing formal recognition of ARDS syndrome in later life.

129 Clinician recognition of ARDS was associated with higher PEEP, greater use of neu

130 luded assessment of clinician recognition of ARDS, the application of ventilatory management, the use

131 as higher than in individuals not at risk of ARDS (19/260 [7%] vs 17/556 [3%]; p=0.004).

132 critically ill patients, 282 were at risk of ARDS (30%, 95% CI 27-33), representing 0.14 cases per IC

133 ilar for patients at risk and not at risk of ARDS (median 7.6 mL/kg PBW [IQR 6.7-9.1] vs 7.9 mL/kg PB

134 ions occur frequently in patients at risk of ARDS and their clinical outcome is worse compared with t

135 ared with placebo did not reduce the risk of ARDS at 7 days.

136 PEEP was higher in patients at risk of ARDS compared with those not at risk (median 6.0 cm H2O

137 identifying patients with or at high risk of ARDS early in the course of the underlying illness, when

138 als not at risk of ARDS, patients at risk of ARDS had higher in-hospital mortality (86/543 [16%] vs 7

139 , ozone exposure was associated with risk of ARDS in the entire cohort (odds ratio, 1.58 [95% confide

140 ion conferred a 28% reduction in the risk of ARDS independent of other major clinical variables, incl

141 he prevalence of ARDS in patients at risk of ARDS was higher than in individuals not at risk of ARDS

142 gical characteristics of patients at risk of ARDS, describe ventilation management in this population

143 Compared with individuals not at risk of ARDS, patients at risk of ARDS had higher in-hospital mo

144 on Score (LIPS) was used to stratify risk of ARDS, with a score of 4 or higher defining those at risk

145 outcomes compared with people at no risk of ARDS.

146 me was the proportion of patients at risk of ARDS.

147 ore of 4 or higher defining those at risk of ARDS.

148 is worse compared with those not at risk of ARDS.

149 nical ventilation in the ICU were at risk of ARDS.

150 t develop ARDS (p=0.471 for those at risk of ARDS; p=0.323 for those not at risk).

151 pathology consistent with the late stages of ARDS, which is reminiscent of the disease observed in pa

152 hours of care versus survival at the time of ARDS onset.

153 thway is a viable option in the treatment of ARDS.

154 apacity of human MDMs stimulated with LPS or ARDS BALF.

155 l mortality in patients with septic shock or ARDS.

156 Post-ARDS joblessness is associated with readily identifiable

157 se in private health insurance (from 44% pre-ARDS) and a 16% (95% confidence interval, 7-24%; P < 0.0

158 s, averaging $26,949 +/- $22,447 (60% of pre-ARDS annual earnings).

159 S pathogenesis and the paradigm of precision ARDS medicine.

160 al trials indicate an interest in preventing ARDS.

161 ased global genomic profiling of highly pure ARDS blood PMNs in parallel with age-matched and gender-

162 aO2/FiO2 of 114 +/- 39 mm Hg; 40% had severe ARDS (PaO2/FiO2 <100 mm Hg).

163 ild to 78.5% (95% CI, 74.8%-81.8%) in severe ARDS.

164 , 46.6% (95% CI, 44.5%-48.6%); and of severe ARDS, 23.4% (95% CI, 21.7%-25.2%).

165 ngs and evoked symptoms indicative of severe ARDS, including decreased survival, extreme weight loss,

166 For patients with moderate or severe ARDS, the recommendation is strong against routine use o

167 ortality of patients with moderate to severe ARDS compared with a conventional low-PEEP strategy.

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

169 ted in nine patients with moderate to severe ARDS.

170 17, enrolling adults with moderate to severe ARDS.

171 were included if they had moderate-to-severe ARDS as defined by the acute onset of the need for posit

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

173 ved MSCs in patients with moderate-to-severe ARDS.

174 eased mortality in patients with very severe ARDS.

175 0.0144) exclusively in patients with severe ARDS due to pneumonia.

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

177 The proportion of patients with severe ARDS or with ratios of the partial pressure of arterial

178 PEEP observed in these patients with severe ARDS under extracorporeal membrane oxygenation reinforce

179 For patients with severe ARDS, the recommendation is strong for prone positioning

180 moderate, and 47.1% of patients with severe ARDS.

181 (95% CI, 41.9%-50.4%) for those with severe ARDS.

182 95% CI, 13.7%-19.2%) of patients with severe ARDS.

183 membrane oxygenation in patients with severe ARDS.

184 ght the epidemiologic challenges of studying ARDS, as well as other intensive care syndromes, and pro

185 cluding acute respiratory distress syndrome (ARDS) and acute renal failure, requiring mechanical vent

186 during acute respiratory distress syndrome (ARDS) and correlate with severity and prognosis.

187 risk of acute respiratory distress syndrome (ARDS) and how ventilation is managed in these individual

188 lthough acute respiratory distress syndrome (ARDS) and progressive pulmonary endothelial damage are k

189 and the acute respiratory distress syndrome (ARDS) are major causes of mortality without targeted the

190 esis in acute respiratory distress syndrome (ARDS) by enhancing neutrophil recruitment.

191 apy for acute respiratory distress syndrome (ARDS) exists, and mortality remains high.

192 risk of acute respiratory distress syndrome (ARDS) in an intensive care unit cohort of 1,614 subjects

193 Acute respiratory distress syndrome (ARDS) is a common, lethal, and morbid respiratory compli

194 Acute respiratory distress syndrome (ARDS) is a devastating disorder characterized by increas

195 of the acute respiratory distress syndrome (ARDS) is above 40%.

196 Acute respiratory distress syndrome (ARDS) is associated with high mortality.

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

198 Acute respiratory distress syndrome (ARDS) is characterized by severe impairment of gas excha

199 Acute respiratory distress syndrome (ARDS) is undefined in neonates, despite the long-standin

200 risk of acute respiratory distress syndrome (ARDS) is unknown.

201 tone of acute respiratory distress syndrome (ARDS) management.

202 severe acute respiratory distress syndrome (ARDS) on extracorporeal membrane oxygenation receiving m

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

204 ts with acute respiratory distress syndrome (ARDS) remain uncertain.

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

206 ment of acute respiratory distress syndrome (ARDS) remains largely supportive.

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

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

209 ts with acute respiratory distress syndrome (ARDS) use information and guidance from a wide array of

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

211 such as acute respiratory distress syndrome (ARDS), characterized by edema and inflammatory cell infi

212 ts with acute respiratory distress syndrome (ARDS), early successes were followed by failures.

213 related acute respiratory distress syndrome (ARDS), indicating a compensatory mechanism.

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

215 n cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortali

216 causing acute respiratory distress syndrome (ARDS), severe pneumonia-like symptoms and multi-organ fa

217 ies for acute respiratory distress syndrome (ARDS), the average treatment effect in the study populat

218 ts with acute respiratory distress syndrome (ARDS), the morbidity and mortality from ARDS remains hig

219 ause of acute respiratory distress syndrome (ARDS), we aimed to investigate the effect of the FER pol

220 ury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessi

221 tion of acute respiratory distress syndrome (ARDS).

222 ts with acute respiratory distress syndrome (ARDS).

223 sis and acute respiratory distress syndrome (ARDS).

224 ts with acute respiratory distress syndrome (ARDS).

225 ith the acute respiratory distress syndrome (ARDS).

226 ts with acute respiratory distress syndrome (ARDS).

227 ts with acute respiratory distress syndrome (ARDS).

228 ated in acute respiratory distress syndrome (ARDS).

229 cial in acute respiratory distress syndrome (ARDS).

230 ts with acute respiratory distress syndrome (ARDS).

231 died as acute respiratory distress syndrome (ARDS).

232 tic for acute respiratory distress syndrome (ARDS).

233 ts with acute respiratory distress syndrome (ARDS).

234 tion of acute respiratory distress syndrome (ARDS).

235 Collectively our results show that ARDS PMNs display important de-novo transcriptional acti

236 of human MSCs on macrophage function in the ARDS environment and to elucidate the mechanisms of thes

237 In the ARDS environment, MSCs promote an antiinflammatory and h

238 ociated in the subgroup with trauma as their ARDS risk factor (odds ratio, 2.26 [95% confidence inter

239 To identify these subphenotypes in a third ARDS cohort, to test whether subphenotypes respond diffe

240 studies (GWAS) have linked multiple genes to ARDS.

241 e of some of these sources as they relate to ARDS and review examples of when they have succeeded (an

242 Our findings could be relevant to ARDS in humans, because we found significant elevation o

243 Although many modalities to treat ARDS have been investigated over the past several decade

244 present promising new approaches to treating ARDS, including combination therapies, cell-based therap

245 This analysis confirms the presence of two ARDS subphenotypes that can be accurately identified wit

246 Current mechanisms underlying ARDS focus on alveolar endothelial and epithelial injury

247 verage Over 12-month longitudinal follow-up, ARDS survivors from 43 U.S.

248 ith conventional ventilation for adults with ARDS.

249 NO2 exposure was also associated with ARDS but not independently of ozone exposure.

250 nd genetic variants that are associated with ARDS.

251 d change in serum biomarkers associated with ARDS.

252 er less than 10 mum were not associated with ARDS.

253 ronchoalveolar lavage fluid from humans with ARDS, gut-specific bacteria (Bacteroides spp.) were comm

254 ar lavage fluid (BALF) from 36 patients with ARDS (20 survivors, 16 non-survivors).

255 a sRAGE correlated with AFC in patients with ARDS (Spearman's rho = -0.59; P < 10(-3)).

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

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

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

259 the high mortality observed in patients with ARDS by creating ventilator-induced lung injury.

260 7796 on the 90-day survival in patients with ARDS due to pneumonia.

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

262 lyze individual data from 3562 patients with ARDS enrolled in nine previously reported randomized tri

263 y therefore rescue the sickest patients with ARDS from the high risk for death associated with severe

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

265 Less than two-thirds of patients with ARDS received a tidal volume 8 of mL/kg or less of predi

266 attractive, the use of ECLS in patients with ARDS remains controversial, and high-quality research is

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

268 andomized clinical trial of 83 patients with ARDS requiring NIV delivered by face mask for at least 8

269 Clinicians managing patients with ARDS should personalize decisions for their patients, pa

270 Median age for patients with ARDS was 37 years, and infection was the most common ris

271 Only 30.9% of patients with ARDS were admitted to an ICU, and hospital mortality was

272 site, prospective study of 482 patients with ARDS with 11,558 twice-daily tidal volume assessments (e

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

274 Of 2,813 patients with ARDS, 436 (15.5%) were managed with NIV on Days 1 and 2

275 nchoalveolar lavage fluid from patients with ARDS, and rIL-17A directly increased permeability across

276 recommended for routine use in patients with ARDS, but can be used to improve oxygenation in patients

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

278 In 22 patients with ARDS, lung recruitment was assessed at 5 and 15 cm H2O P

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

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

281 For all patients with ARDS, the recommendation is strong for mechanical ventil

282 Among patients with ARDS, treatment with helmet NIV resulted in a significan

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

284 latory interventions for adult patients with ARDS.

285 eolar lavage fluid (BALF) from patients with ARDS.

286 provement in the management of patients with ARDS.

287 ollected urine samples from 70 patients with ARDS.

288 dy described the management of patients with ARDS.

289 and is crucial for survival of patients with ARDS.

290 e consecutive time points from patients with ARDS.

291 o prospectively assessed in 30 patients with ARDS.

292 nchoalveolar lavage fluid from patients with ARDS.

293 reased ventilator-free days in patients with ARDS.

294 ity in a preexisting cohort of patients with ARDS.

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

296 ualized symptomatic support of patients with ARDS.

297 vestigate the effect of KGF in patients with ARDS.

298 ease, but are not recommended for those with ARDS.

299 NTilation in critically ill patients without ARDS at onset of ventilation) is an international, multi

300 vement in the management of patients without ARDS.