ライフサイエンスコーパス: hyperoxia

1 t decreases in response to increased oxygen (hyperoxia).

2 juvenile and adult mice exposed to neonatal hyperoxia.

3 ent of admission diagnosis and definition of hyperoxia.

4 ds associated with mortality within moderate hyperoxia.

5 ydrogenase (LDH) (68%) following 72 hours of hyperoxia.

6 binding results in increased sensitivity to hyperoxia.

7 n oxidative signaling and protection against hyperoxia.

8 conscious rats during normoxia, hypoxia, or hyperoxia.

9 er, it can also result in varying degrees of hyperoxia.

10 logy in Ndufs4 KO mice exposed to hypoxia or hyperoxia.

11 al apoptosis in the lungs of mice exposed to hyperoxia.

12 to actin S-nitrosylation during exposure to hyperoxia.

13 to a specific FAK inhibitor concurrent with hyperoxia.

14 tivation and autophagy in endothelium during hyperoxia.

15 in neonatal mice lung following exposure to hyperoxia.

16 an important determinant of survival during hyperoxia.

17 mechanism during oxidant challenges, such as hyperoxia.

18 attenuation in prolonged and/or alternating hyperoxia.

19 age of premature infants experience relative hyperoxia.

20 70 from wild-type mice lungs and MLECs after hyperoxia.

21 ng endothelial cells (MLECs) were exposed to hyperoxia.

22 tly diminished by the end of the 3rd week of hyperoxia.

23 resuscitation guidelines recommend avoiding hyperoxia.

24 rbidity and mortality attributed to neonatal hyperoxia.

25 reduced in lungs of mice exposed to neonatal hyperoxia.

26 er each trial was transiently inhibited with hyperoxia.

27 rization, and beta(2) integrin inhibition by hyperoxia.

28 educed in PHD1-depleted mice after 2 days in hyperoxia.

29 n of asthma-like features following neonatal hyperoxia.

30 creased in lungs of neonatal mice exposed to hyperoxia.

31 e in the 3 parafoveal retinal plexuses under hyperoxia.

32 to demonstrate significant change following hyperoxia.

33 y due to oxidative stress caused by neonatal hyperoxia.

34 re larger for severe hyperoxia than for mild hyperoxia.

35 type of EVs found in the early stages after hyperoxia.

36 imilarly biphasically altered in response to hyperoxia.

37 fspring exposed to maternal LPS and neonatal hyperoxia.

38 % arteriolar and 23% total venous area) with hyperoxia (500 mmHg PETCO2; P < 0.001) to the same exten

39 requency reduction (Deltaf(R)) was larger in hyperoxia (65% FiO2), smaller in 15% FiO2, and absent in

40 ection to pregnant dams) and rearing pups in hyperoxia (65% or 85% O2).

41 lyase(+/-) (Sgpl1(+/-)) mice were exposed to hyperoxia (75%) from postnatal day 1 to 7.

42 OR 2.3, 95% CI 1.7-3.0, p<.0001) followed by hyperoxia (80/256 [32%], crude OR 1.5, 95% CI 1.1-2.5, p

43 preexposed to either normoxia (21% O(2)) or hyperoxia (85% O(2)) for up to 21 d.

44 g by exposing mice from 36 inbred strains to hyperoxia (95% O2) for 72 h after birth.

45 ure of pulmonary artery endothelial cells to hyperoxia (95% oxygen and 5% CO2) for 48 h resulted in d

46 were treated with lentivirus and exposed to hyperoxia (95% oxygen).

47 We found that neonatal hyperoxia acutely initially diminished saccular TGF-beta

48 that the retinal autoregulatory response to hyperoxia affects only the deep capillary plexus, but no

49 It was accompanied by tissue reactive hyperoxia, affirming that the post-occlusion oxygen supp

50 application of hypothermia and avoidance of hyperoxia after cardiac arrest and other brain injuries

51 s have shown a worse outcome associated with hyperoxia after resuscitation from cardiac arrest.

52 Although hyperoxia alone attenuated the postshock hyperinflammati

53 Hyperoxia also increased expression of Clec9a, a CD103(+

54 here was also an association with increasing hyperoxia, although not as dramatic as that for hypoxia

55 lysis yielded a relative risk of an SSI with hyperoxia among all surgery patients of 0.84 [95% confid

56 nces in baseline characteristics between the hyperoxia and control group.

57 ounders, the probability of being exposed to hyperoxia and hospital-specific characteristics, exposur

58 Hyperoxia and hypothermia can attenuate tissue hypoxia d

59 Therefore, we assessed how hyperoxia and hypoxia alter four physiological traits in

60 maturity is whether hyperoxia or alternating hyperoxia and hypoxia creates the disease phenotype in h

61 Alternating hyperoxia and hypoxia in untreated rats led to periphera

62 t for a 10% overlap of patients who had both hyperoxia and hypoxia.

63 in cortical oxygenation induced by systemic hyperoxia and hypoxia.

64 Exposure to a combination of hyperoxia and injurious mechanical ventilation resulted

65 ming injury is induced by the combination of hyperoxia and injurious mechanical ventilation.

66 ples over the course of a 45-min exposure to hyperoxia and iNOS dimers increase in a commensurate fas

67 Exposure to hyperoxia and mechanical ventilation resulted in an incr

68 ere systematically searched for the keywords hyperoxia and mortality or outcome.

69 t data have suggested an association between hyperoxia and mortality; however, this conclusion has no

70 tilator-free days in comparison to both mild hyperoxia and normoxia for all metrics except for the wo

71 -27 +/- 2% baseline) and was attenuated with hyperoxia and PAV (-18 +/- 1 and -17 +/- 2% baseline, P

72 cal adaptation of the retinal vasculature to hyperoxia and reduced pathological angiogenesis followin

73 t of asthma-like features following neonatal hyperoxia and suggest therapeutic potential for targetin

74 ed and newly constructed metrics of arterial hyperoxia and systematically assess their association wi

75 e did not demonstrate an association between hyperoxia and worse outcome, the small proportion of pat

76 ounders, the probability of being exposed to hyperoxia, and hospital-specific effects, exposure to hy

77 ficient mice have increased mortality during hyperoxia, and lung-targeted adenoviral delivery of Hsp7

78 Both severe hypoxia and, to a lesser extent, hyperoxia are associated with an increased risk of death

79 High levels of inspired oxygen, hyperoxia, are frequently used in patients with acute re

80 We studied the use of hyperoxia as an alternative therapeutic strategy for reg

81 Similarly, adult mice exposed to hyperoxia as neonates display alveolar simplification as

82 ed as PaO2 between 120 and 200 mm Hg; severe hyperoxia as PaO2 greater than 200 mm Hg.

83 We show that after hyperoxia-associated oxidative stress, a large amount of

84 NAs are altered the most significantly after hyperoxia-associated oxidative stress.

85 PHD1-deficient mice demonstrated reduced hyperoxia-associated vascular obliteration during oxygen

86 citation from near-lethal hemorrhagic shock, hyperoxia attenuated hyperinflammation, and thereby show

87 Hyperoxia attenuated VE to a similar extent in baseline

88 Although modest hyperoxia attenuates exercise hyperaemia by improving O(

89 production doubles within 10 min exposure to hyperoxia but declines to approximately half-maximum pro

90 us actin increased within 15 min exposure to hyperoxia but then decreased below the control level.

91 ce has shown the potential risks of arterial hyperoxia, but the lack of a clinical definition and met

92 esulted in increased sensitivity of lungs to hyperoxia, but this effect is less prominent if overwhel

93 l growth factor (VEGF), which was reduced by hyperoxia, but to local retinal ganglion cell layer-deri

94 reased the survival of TLR4-deficent mice in hyperoxia by 24 h and decreased LDH release and lung cel

95 Hyperoxia can exacerbate acute respiratory failure, whic

96 olar epithelial cells (AECs) and showed that hyperoxia can induce the expression of this protein.

97 to a vasoactive stimulus such as hypoxia and hyperoxia, can be used to assess the vascular range of a

98 At P8, hyperoxia caused apoptosis of NG2(+)O4(-) progenitor cel

99 Prior work has shown that hyperoxia causes S-nitrosylated actin (SNO-actin) format

100 We show that neonatal hyperoxia causes ultrastructural changes, including: mye

101 nstrated decreased median survival following hyperoxia compared to WT mice.

102 Hyperoxia contributes to lung injury in experimental ani

103 nt of the physiologic phenomenon of reactive hyperoxia could prove clinically beneficial for both dia

104 Episodes of hyperoxia decreased (p < 0.0001), whereas hypoxic episod

105 Hyperoxia decreased BH4 in retinas, lungs, and aortas in

106 Furthermore, hyperoxia decreased cardiac 3-nitrotyrosine formation an

107 In the vasodegenerative phase, during hyperoxia, defective endothelial nitric oxide synthase (

108 Hyperoxia depleted pulmonary immune cells by 67%; howeve

109 Vehicle-injected animals in both levels of hyperoxia developed a severe BPD-like lung disease (alve

110 higher relaxation constant tau at 24 hours, hyperoxia did not affect cardiac function.

111 ) Attenuation of peripheral chemoreflexes by hyperoxia does not abolish the augmented CO2 chemoreflex

112 tially rescued the immune cell population in hyperoxia (doubling the viable cells), reduced the perce

113 Following hyperoxia DTI was unchanged in controls.

114 d for meta-analyses and showed that arterial hyperoxia during admission increases hospital mortality:

115 Avoidance of hyperoxia during perfusion may prevent postreperfusion s

116 Hyperoxia during resuscitation from hemorrhagic shock in

117 Investigation of the effects of hyperoxia during resuscitation from hemorrhagic shock in

118 On day 3, perinatal inflammation and hyperoxia each triggered a distinct pulmonary immune res

119 Exposure of neonatal mice to hyperoxia enhanced sphingosine-1-phosphate (S1P) levels

120 In addition, IRAK-M(-/-) AECs exposed to hyperoxia experienced a decrease in cell death.

121 Comparison of transcriptome changes in hyperoxia-exposed animals (WT versus knock-out) identifi

122 Treatment of hyperoxia-exposed mice with either IL1 receptor antagoni

123 Hyperoxia-exposed neonatal mice have increased caspase-1

124 y, alveolar-capillary structural deficits in hyperoxia-exposed pups were accompanied by a significant

125 pression of GSNO reductase, was decreased in hyperoxia-exposed pups.

126 Hyperoxia-exposed RV-infected mice showed further increa

127 Induced IL-12 expression in hyperoxia-exposed, RV-infected mice was associated with

128 hydrogen peroxide into the supernatant after hyperoxia exposure (mean +/- SEM, 1,879 +/- 278 vs. 842

129 Hyperoxia exposure accentuated lung injury in TREK-1-def

130 oping retinal vasculature during therapeutic hyperoxia exposure and later ischemia-induced neovascula

131 Our data suggest that neonatal hyperoxia exposure causes detrimental effects on airway

132 e have previously demonstrated that neonatal hyperoxia exposure in the mouse disrupts development of

133 Neonatal hyperoxia exposure inhibited alveolar-capillary septal d

134 Hyperoxia exposure resulted in a 74% increase in (99m)Tc

135 At baseline and after hyperoxia exposure, bronchoalveolar lavage cytokine leve

136 We were unable to verify any harm from hyperoxia exposure.

137 servational studies have suggested harm from hyperoxia exposure.

138 antly reduced the number of live cells after hyperoxia exposure.

139 toxicity is neonatal lung injury induced by hyperoxia exposure.

140 k, C57BL/6J background) mice were exposed to hyperoxia (FiO2 > 0.95) for 48 hours.

141 at rest and in all conditions with alveolar hyperoxia (FIO2 = 1.0).

142 for arterial oxygen saturation >/= 90%) and "hyperoxia" (FIO2 1.0 for 24 hr) groups.

143 Mice were exposed to neonatal hyperoxia followed by a period of room air recovery.

144 n, 2) 95% hyperoxia for 24 hours, and 3) 95% hyperoxia for 24 hours followed by mechanical ventilatio

145 room air, no mechanical ventilation, 2) 95% hyperoxia for 24 hours, and 3) 95% hyperoxia for 24 hour

146 by the exposure of wild-type newborn mice to hyperoxia for 24 hours, or by APC specific deficiency in

147 ng uptake of these agents in rats exposed to hyperoxia for prolonged periods, a common model of acute

148 Mortality was higher in the hyperoxia group as compared with normoxia (crude odds ra

149 Plasma creatinine values were lower in the hyperoxia group during resuscitation coinciding with sig

150 The hyperoxia group had a higher incidence of DCI (p<0.001)

151 al rates were 50% and 89% in the control and hyperoxia groups, respectively (p = 0.077).

152 e; wild-type mice, which induced PINK1 after hyperoxia, had intermediate susceptibility; and NLRP3(-/

153 ex vivo retina from 34 to 548 mm Hg, whereas hyperoxia has been reported to increase retinal pO(2) in

154 cause few trials assessed potential harms of hyperoxia, hazards were not included.

155 We recently demonstrated that hyperoxia (HO) activates lung endothelial cell NADPH oxi

156 i is also effective in a 24-hour alternating hyperoxia-hypoxia model.

157 fy gene orthologues responding to hypoxia or hyperoxia in both mice and drosophila.

158 present results suggest a higher benefit of hyperoxia in comorbid swine due to an increased suscepti

159 cohort studies investigating the effects of hyperoxia in critically ill adults.

160 l changes during chronic moderate normobaric hyperoxia in mice.

161 moderately high probability of a benefit to hyperoxia in reducing SSIs in colorectal surgery patient

162 kin-1beta gene expression was not altered by hyperoxia in TREK-1-deficient mice compared with control

163 contrast, human fetal lung ECFCs exposed to hyperoxia in vitro and neonatal rat ECFCs isolated from

164 The role of lung endothelial HO-1 during hyperoxia in vivo is not well defined.

165 Hyperoxia increased levels of ATP metabolites and expres

166 Hyperoxia increased lung IL-12 expression, which persist

167 a neonatal mouse model of BPD, we show that hyperoxia increases activity and expression of a mediato

168 Hyperoxia increases synthesis of reactive species leadin

169 We have previously reported that hyperoxia increases the formation of NO and peroxynitrit

170 Neonatal hyperoxia induced asthma-like features including airway

171 Hyperoxia induced significant reduction in the flow inde

172 Furthermore, SphK1 deficiency attenuated hyperoxia-induced accumulation of IL-6 in bronchoalveola

173 Hyperoxia-induced acute lung injury (HALI) is a key cont

174 resent study, we address the question of how hyperoxia-induced alterations in WM development affect o

175 ysis to provide comprehensive information on hyperoxia-induced biomolecular modifications in neonatal

176 beta-LGND2 inhibited in vitro hypoxia- or hyperoxia-induced cell death and the formation of endoth

177 nia seemed to nonsignificantly attenuate the hyperoxia-induced changes.

178 ient in liver-specific HIF-1alpha experience hyperoxia-induced damage even with DMOG treatment, where

179 P326TAT inhibited hyperoxia-induced disruption of monolayer barrier integr

180 Functionally, the hyperoxia-induced epithelial MVs promote macrophage acti

181 esidues 326-333 has been shown to reduce the hyperoxia-induced formation of NO and peroxynitrite in l

182 bstitution (P265L) had significantly reduced hyperoxia-induced inflammation compared to strains witho

183 Hyperoxia-induced intracellular pH changes and subsequen

184 promote cell growth and thereby exaggerating hyperoxia-induced lung epithelial cell death.

185 showed that TLR4 confers protection against hyperoxia-induced lung injury and mortality.

186 ignaling-regulated ROS in the development of hyperoxia-induced lung injury in a murine neonatal model

187 e the relationship between TLR4 and Hsp70 in hyperoxia-induced lung injury in vitro and in vivo and t

188 Hyperoxia-induced lung injury was evaluated by using bro

189 Further, hyperoxia-induced lung injury was significantly reduced

190 Sgpl1(+/-), mice offered protection against hyperoxia-induced lung injury, with improved alveolariza

191 role of TREK-1 in vivo in the development of hyperoxia-induced lung injury.

192 opment of novel treatment strategies against hyperoxia-induced lung injury.

193 Hyperoxia-induced oxidative stress is an established mod

194 nd NLRP3(-/-) mice, which had high basal and hyperoxia-induced PINK1, were the least susceptible.

195 namics and underlying mechanisms involved in hyperoxia-induced PWMI will allow for future targeted th

196 To identify the causes of hyperoxia-induced PWMI, we characterized cellular change

197 e results suggest a novel role for nmMLCK in hyperoxia-induced recruitment of cytoskeletal proteins a

198 coupling when raised sufficiently high, the hyperoxia-induced rise in retinal pO(2) in vivo is not s

199 iRNA, or inhibitor against SphK1, attenuated hyperoxia-induced S1P generation.

200 ia-induced pathologic angiogenesis, but also hyperoxia-induced vaso-obliteration, which suggests a no

201 nd hph1(-/-) groups did not show exacerbated hyperoxia-induced vessel closure, but exhibited greater

202 is study, we made the novel observation that hyperoxia induces intracellular acidification in nMLF, w

203 We hypothesize that hyperoxia is common and associated with worse outcome af

204 A pathogenic consequence of hyperoxia is endothelial injury.

205 ut suggest that a short period of normobaric hyperoxia is not beneficial in this context.

206 onflicting findings is important, given that hyperoxia is often used in the clinic in the treatment o

207 The ability to resist hyperoxia is proportional to PINK1 expression.

208 Confirmation following a longer period of hyperoxia is required.

209 nistering high levels of inspired oxygen, or hyperoxia, is commonly used as a life-sustaining measure

210 Hyperoxia lowered LG from a median of 3.4 [interquartile

211 We have previously shown that normobaric hyperoxia may benefit peri-lesional brain and white matt

212 Ventilation-induced hyperoxia may decrease myocardial oxygenation and lead t

213 Oxygen is vital during critical illness, but hyperoxia may harm patients.

214 , produced more superoxide after exposure to hyperoxia (mean +/- SEM, 89,807 +/- 16,616 vs. 162,706 +

215 In patients following hyperoxia, mean diffusivity (MD) was unchanged despite b

216 rotective effect of MIF, including decreased hyperoxia-mediated AKT phosphorylation and a 20% reducti

217 Treatment with MIF decreased hyperoxia-mediated H2AX phosphorylation in a CD74-depend

218 separate nights, subjects were submitted to hyperoxia (n = 9; FiO2 approximately 0.5) or hypoxia (n

219 Macrophages were exposed to hyperoxia (O2) for 24 h and LPS for 6 h or 24 h.

220 to test the hypothesis that tissue reactive hyperoxia occurs following release of hind-limb tourniqu

221 ratio, 1.68; 95% CI, 1.09-2.57) and moderate hyperoxia (odds ratio, 1.66; 95% CI, 1.11-2.50) were ass

222 strain (hph1)] to investigate the impact of hyperoxia on BH4 bioavailability and retinal vascular pa

223 This study seeks to assess the effects of hyperoxia on myocardia oxygenation in the presence of se

224 ublications assessing the effect of arterial hyperoxia on outcome in critically ill adults (>/= 18 yr

225 Little is known about the impact of hyperoxia on the ischemic heart.

226 y demonstrates that the beneficial effect of hyperoxia on the severity of OSA is primarily based on i

227 udy of retinopathy of prematurity is whether hyperoxia or alternating hyperoxia and hypoxia creates t

228 mulated with recombinant VEGF and exposed to hyperoxia or hydrogen peroxide.

229 avoid the harms associated with inadvertent hyperoxia or hypoxia through careful and precise control

230 r equal to 300, and normoxia, not defined as hyperoxia or hypoxia.

231 ratio </= 300, and normoxia, not defined as hyperoxia or hypoxia.

232 O2 ratio </=300 and normoxia, not defined as hyperoxia or hypoxia.

233 Neonatal mouse pups were exposed to >90% hyperoxia or room air during postnatal days 0 to 7, and

234 t was inhibited under hypoxia (P<0.0001) and hyperoxia (P=0.0006) compared with normoxia.

235 e first arterial gas, 207 patients (11%) had hyperoxia (Pa(O)(2) >/=300 mm Hg) and 448 (24%) had hypo

236 erate hyperoxia (PaO2 101-300mm Hg), extreme hyperoxia (PaO2 > 300 mm Hg), and mortality were evaluat

237 m Hg), normoxia (PaO2 60-100mm Hg), moderate hyperoxia (PaO2 101-300mm Hg), extreme hyperoxia (PaO2 >

238 core temperature 34 degrees C), or "combi" (hyperoxia plus hypothermia) (n = 9 each).

239 In addition, neonatal hyperoxia promoted allergic TH responses to house dust m

240 the underlying mechanisms by which neonatal hyperoxia promotes asthma development.

241 greatest quadriceps fatigue attenuation with hyperoxia (r(2) = 0.79, P < 0.0001).

242 known as linc1623 in mice, in the setting of hyperoxia/reactive oxygen species (ROS)-induced lung inj

243 clinical data suggesting potential harm with hyperoxia remain compelling, and further investigation,

244 However, in vivo, hyperoxia reportedly has no effect on blood flow.

245 However, sustained hyperoxia resulted in a biphasic response and subsequent

246 mean fractional flow reserve of 0.64+/-0.02, hyperoxia resulted in a significant decrease of myocardi

247 y increased H(2)O(2) emission in response to hyperoxia, resulting in substantial loss of Ca(2+) buffe

248 Exposure to hyperoxia results in acute lung injury.

249 During hyperoxia, RTN activation maintains breathing despite th

250 to antagonize negative effects of the GCY-35 hyperoxia sensor on spermatogenesis.

251 Analytical metrics of arterial hyperoxia should be judiciously considered when interpre

252 Time spent in hyperoxia showed a linear and positive relationship with

253 Furthermore, cultured astrocytes exposed to hyperoxia showed a reduced capacity to protect oligodend

254 maintain arterial oxygen saturation > 90%), "hyperoxia" (standard resuscitation, but FIO2, 1.0), "hyp

255 There was no significant difference between hyperoxia TG and control group (P>0.05).

256 conditional mortality were larger for severe hyperoxia than for mild hyperoxia.

257 sustained hypopnoea post-CBD than before; in hyperoxia, the responses were identical.

258 ygen from postnatal day 7 to 12 (P7 to P12) (hyperoxia), then returned to normal air (relative hypoxi

259 s) under respiration challenges ranging from hyperoxia to hypoxia (10 levels of oxygenation, 100%-10%

260 ates the potential of BOLD MRI with maternal hyperoxia to quantify regional placental function in viv

261 ion-Level-Dependent (BOLD) MRI with maternal hyperoxia to quantitatively assess mismatch in placental

262 Use of hyperoxia to reduce SSIs is controversial.

263 ian methods to evaluate the effectiveness of hyperoxia to reduce surgical site infections (SSIs) and/

264 bout 270 d, likely from cardiac disease, and hyperoxia-treated mice die within days from acute pulmon

265 After hyperoxia-treated neonatal mice were returned to ambient

266 Hyperoxia treatment (HT, 40%-75% oxygen) was initiated o

267 Hyperoxia treatment (HT, 75% oxygen) was initiated on po

268 dantly, the treatment of SMNDelta7 mice with hyperoxia treatment increased the inclusion of SMN2 exon

269 We further confirmed that hyperoxia up-regulates the levels of certain specific mi

270 udy examined the impact of brief exposure to hyperoxia using diffusion tensor imaging (DTI) to identi

271 tence of IL-1alpha and IL-1beta on day 28 in hyperoxia/vehicle-treated lungs.

272 lung endothelium increased susceptibility to hyperoxia via alterations in autophagy/mitophagy, protea

273 ge in functional MRI signal intensity due to hyperoxia was 16% +/- 3% in BR-d0 vs. 4% +/- 3% in hemor

274 A shorter protocol with normoxia to hyperoxia was also performed (five levels of oxygenation

275 In SAH patients, exposure to hyperoxia was associated with DCI.

276 Severe hyperoxia was associated with higher mortality rates and

277 Moderate hyperoxia was associated with increased mortality during

278 Moderate hyperoxia was associated with increased mortality in pat

279 subsets of critically ill patients, arterial hyperoxia was associated with poor hospital outcome.

280 The difference in R1 (DeltaR1) after hyperoxia was converted to change in partial pressure of

281 nts were divided into three exposure groups: hyperoxia was defined as PaO2 >/= 300 mm Hg (39.99 kPa),

282 Hyperoxia was defined as PaO2 >/=300 mm Hg (39.99 kPa),

283 Mild hyperoxia was defined as PaO2 between 120 and 200 mm Hg;

284 nts were divided into three exposure groups: hyperoxia was defined as PaO2 more than or equal to 300

285 Hyperoxia was defined as the highest quartile of an area

286 Hyperoxia was frequent, affecting 54% of patients.

287 anial pressure crisis, pneumonia and sepsis, hyperoxia was independently associated with DCI (OR, 3.1

288 spital-specific characteristics, exposure to hyperoxia was independently associated with higher in-ho

289 d TBI patients admitted to the ICU, arterial hyperoxia was independently associated with higher in-ho

290 , and hospital-specific effects, exposure to hyperoxia was independently associated with in-hospital

291 troke patients admitted to the ICU, arterial hyperoxia was independently associated with in-hospital

292 II score, rebleeding, pneumonia and sepsis, hyperoxia was independently associated with poor outcome

293 ntly associated with worse outcome; however, hyperoxia was not (odds ratio for good outcome, 1.02 [0.

294 cohort study, we tested the hypothesis that hyperoxia was not associated with higher in-hospital cas

295 the antioxidant, catalase, these effects of hyperoxia were abolished.

296 Similarly, effects of hyperoxia were abrogated in cells depleted of focal adhe

297 e of 23 to 24 weeks and (2) inflammation and hyperoxia were associated with prominent increases in ri

298 g and newly constructed metrics for arterial hyperoxia were examined, and the associations with hospi

299 imed at the prevention of harm by iatrogenic hyperoxia while preserving adequate tissue oxygenation.

300 sis whether mild therapeutic hypothermia and hyperoxia would attenuate postshock hyperinflammation an