ライフサイエンスコーパス: hyperoxia

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

2 oxygen ( FI,O2 ) concentrations of 60-100% (hyperoxia).

3 campal mitochondrial dysfunction by neonatal hyperoxia.

4 re larger for severe hyperoxia than for mild hyperoxia.

5 ds associated with mortality within moderate hyperoxia.

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

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

8 n of asthma-like features following neonatal hyperoxia.

9 creased in lungs of neonatal mice exposed to hyperoxia.

10 e in the 3 parafoveal retinal plexuses under hyperoxia.

11 to demonstrate significant change following hyperoxia.

12 y due to oxidative stress caused by neonatal hyperoxia.

13 es and GSH as assessed immediately following hyperoxia.

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

15 imilarly biphasically altered in response to hyperoxia.

16 fspring exposed to maternal LPS and neonatal hyperoxia.

17 juvenile and adult mice exposed to neonatal hyperoxia.

18 ent of admission diagnosis and definition of hyperoxia.

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

20 should decline as AT2 cells are depleted by hyperoxia.

21 binding results in increased sensitivity to hyperoxia.

22 n oxidative signaling and protection against hyperoxia.

23 conscious rats during normoxia, hypoxia, or hyperoxia.

24 structure and prevented RVH after postnatal hyperoxia.

25 creased glutamine consumption in response to hyperoxia.

26 notype and PH in rodents exposed to neonatal hyperoxia.

27 the BPD transcriptomic phenotype induced by hyperoxia.

28 stnatally but had opposing effects following hyperoxia.

29 populations on the innate immune response to hyperoxia.

30 and EOPE TB lines did not differ, but, under hyperoxia (20% O(2)), invasiveness of EOPE TB was reduce

31 % arteriolar and 23% total venous area) with hyperoxia (500 mmHg PETCO2; P < 0.001) to the same exten

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

33 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

34 PD-PH model, rat pups exposed to room air or hyperoxia (85% O(2)) were randomly assigned to receive e

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

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

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

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

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

40 Although hyperoxia alone attenuated the postshock hyperinflammati

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

42 In hyperoxia, anaplerotic catabolism of glutamine by Muller

43 ducibility, were respectively 9% and 24% for hyperoxia and 35% and 28% for hypoxia.

44 Our study suggests that exposure to both hyperoxia and antibiotics early in life may cause long-t

45 chemoreflex inhibition elicited by transient hyperoxia and chemoreflex excitation produced by exposur

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

47 Hyperoxia and hypothermia can attenuate tissue hypoxia d

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

49 lear statistical differences of O(2) between hyperoxia and hypoxia states in tissue.

50 Ventilatory and MSNA responsiveness to hyperoxia and hypoxia were not significantly correlated

51 in cortical oxygenation induced by systemic hyperoxia and hypoxia.

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

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

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

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

56 ike multimodal sensory neurons, are inert to hyperoxia and other TRPA1 activators (carbon dioxide, el

57 ning to justify strategies using respiratory hyperoxia and oxygenation agents in cancer treatment.

58 -27 +/- 2% baseline) and was attenuated with hyperoxia and PAV (-18 +/- 1 and -17 +/- 2% baseline, P

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

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

61 mitochondrial disease models display tissue hyperoxia and that disease pathology can be reversed by

62 chemoreflex inhibition elicited by transient hyperoxia and to chemoreflex excitation produced by stea

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

64 for 20 min during and after 10 min systemic hyperoxia; and on day 3, electroretinography (ERG) was p

65 cancer and the administration of respiratory hyperoxia as a means to improve tumor oxygenation, we pr

66 r findings also support the use of transient hyperoxia as a reliable, sensitive, measure of the carot

67 that 14-week-old young adult mice exposed to hyperoxia as newborns had spatial and learning deficits

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

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

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

71 Hyperoxia at birth increases the severity of influenza A

72 Acute hyperoxia at HA had minimal effect on baroreflex control

73 D-19 because their early exposure to oxygen (hyperoxia) at birth increases the severity of respirator

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

75 t endothelial cells from apoptosis caused by hyperoxia but increased endothelial proliferation and lu

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

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

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

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

80 Hyperoxia can exacerbate acute respiratory failure, whic

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

82 Additionally, hyperoxia caused a shift in the phenotype of alveolar ma

83 t frequency (+55 +/- 31%), whereas transient hyperoxia caused marked reductions in these variables (-

84 Placental DeltaR2* during maternal hyperoxia changed with GA in healthy control fetuses and

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

86 r simplification in neonatal mice exposed to hyperoxia.Conclusions: Cell therapy involving c-KIT(+) E

87 Hyperoxia contributes to lung injury in experimental ani

88 that changes in blood flow during hypoxia or hyperoxia could be explained by altered NO degradation i

89 This limits our understanding of whether hyperoxia could lower the brain's threshold of tolerance

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

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

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

93 Furthermore, hyperoxia decreased cardiac 3-nitrotyrosine formation an

94 In the mouse, neonatal hyperoxia decreased the number of c-KIT(+) EC progenitor

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

96 fficient (wild type) newborn mice exposed to hyperoxia develop hypoalveolarization, which phenocopies

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

98 Hyperoxia disrupted pulmonary alveolarization and vascul

99 ed that ventilatory responses to hypoxia and hyperoxia do not predict MSNA responses and it is recomm

100 steady-state, eucapnic hypoxia and transient hyperoxia do not predict MSNA responsiveness.

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

102 Following hyperoxia DTI was unchanged in controls.

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

104 the coral diffusive boundary layer revealed hyperoxia during daytime and hypoxia at nighttime result

105 Avoidance of hyperoxia during perfusion may prevent postreperfusion s

106 Hyperoxia during resuscitation from hemorrhagic shock in

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

108 ing it important to understand mechanisms of hyperoxia effects.

109 In WT mice, hyperoxia elicited tyrosine nitration and inhibition of

110 Our finding that hyperoxia enhances the age-dependent expression of SARS-

111 Hyperoxia evoked a rapid reduction in gCBF, yet cognitiv

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

113 rough postnatal days (PNDs) 1 to 14, and the hyperoxia-exposed mice were allowed to recover in normox

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

115 Hyperoxia-exposed neonatal mice have increased caspase-1

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

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

118 Early Klotho supplementation in neonatal hyperoxia-exposed rodents preserved lung alveolar and va

119 Hyperoxia-exposed RV-infected mice showed further increa

120 Comparisons of normoxia- and hyperoxia-exposed samples were made by real-time quantit

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

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

123 Neonatal hyperoxia exposure altered intestinal beta diversity and

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

125 conclude that the proinflammatory effects of hyperoxia exposure are, at least in part, because of the

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

127 Proteomic analysis revealed that hyperoxia exposure decreased complex I NDUFB8 and NDUFB1

128 Neonatal hyperoxia exposure inhibited alveolar-capillary septal d

129 We found that hyperoxia exposure reduced mitochondrial ATP-linked oxyg

130 At the tested time point, hyperoxia exposure resulted in decreased abundance of im

131 nhibition improved alveolarization following hyperoxia exposure, and treatment with recombinant Wnt5a

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

133 toxicity is neonatal lung injury induced by hyperoxia exposure.

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

135 servational studies have suggested harm from hyperoxia exposure.

136 tal lung and characterize their responses to hyperoxia exposure.

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

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

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

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

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

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

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

144 and Keap1(f/f) pups at PND1 were exposed to hyperoxia for 72 h and then allowed to recover at room a

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

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

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

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

149 Prolonged exposure to hyperoxia has deleterious effects on the lung, provoking

150 No targeted therapies exist to counteract Hyperoxia (HO)-induced Acute Lung Injury (HALI).

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

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

153 es with TV CHD but increased during maternal hyperoxia in fetuses with SV or AO CHD (mean DeltaR2*, 0

154 Placental DeltaR2* increased during maternal hyperoxia in healthy fetuses and fetuses with CHD, but i

155 response to flicker stimulation and systemic hyperoxia in mice using a laser speckle flowgraphy (LSFG

156 mospheric normoxia may constitute a cellular hyperoxia in mitochondrial disease.

157 nd determined sO(2) responses to hypoxia and hyperoxia in the different retinal capillary beds.

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

159 bronchodilation following supplemental O(2) (hyperoxia) in early life, making it important to underst

160 the cells most affected by sEH deletion, and hyperoxia increased astrocyte apoptosis.

161 Hyperoxia increased levels of ATP metabolites and expres

162 Hyperoxia increased lung IL-12 expression, which persist

163 Conclusion Six minutes of maternal hyperoxia increased placental oxygenation in healthy fet

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

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

166 cker stimulation and decreased with systemic hyperoxia, independent of age.

167 Neonatal hyperoxia induced asthma-like features including airway

168 Hyperoxia induced significant reduction in the flow inde

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

170 Hyperoxia-induced apoptosis and PH resolved by PND14 and

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

172 NOS3 expression decreased and the extent of hyperoxia-induced BPD and PH increased in ADM(+/-) mice

173 nsequently, we hypothesized that AM resolves hyperoxia-induced BPD and PH via endothelial nitric oxid

174 Collectively, this work suggests hyperoxia-induced brain hypoperfusion is accompanied by

175 on, we defined the magnitude and duration of hyperoxia-induced changes in CBF, cortical electrical ac

176 The collective hyperoxia-induced changes in gCBF, cognitive performance

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 ng the mitochondrial membrane to prevent the hyperoxia-induced dissociation of presenilin-1 and prese

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

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

183 pups were protected against prolonged (96 h) hyperoxia-induced hypoalveolarization.

184 premature lung are insufficient to mitigate hyperoxia-induced hypoalveolarization.

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

186 Hyperoxia-induced intracellular pH changes and subsequen

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

188 Hyperoxia-induced lung hypoalveolarization was remarkabl

189 However, there were no differences in hyperoxia-induced lung inflammatory response immediately

190 lear phagocytes at birth led to severe acute hyperoxia-induced lung injury (HILI) and significant mor

191 Further, hyperoxia-induced lung injury was significantly reduced

192 A mouse model of perinatal hyperoxia-induced lung injury was used to identify molec

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

194 Hyperoxia-induced oxidative stress is an established mod

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

196 Our findings suggest hyperoxia-induced reductions in gCBF evoke enhanced leve

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

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

199 Hyperoxia induces glutamine-fueled anaplerosis that reve

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

201 ased mesenchymal Wnt5A during saccular-stage hyperoxia injury contributes to the impaired alveolariza

202 f activated Wnt/beta-catenin signaling after hyperoxia injury.Methods: Three hyperoxia models were us

203 dings demonstrate that pulmonary response to hyperoxia involves marked changes in specific subsets of

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 Transient hyperoxia is recommended as a sensitive and reliable mea

207 Confirmation following a longer period of hyperoxia is required.

208 mote survival of severely premature infants, hyperoxia is simultaneously harmful to premature develop

209 ms driving BPD remain uncertain, exposure to hyperoxia is thought to contribute to disease pathogenes

210 In addition, increased oxygen supply (hyperoxia) is a pathological factor also critical in bac

211 Hyperoxia lowered LG from a median of 3.4 [interquartile

212 response to flicker stimulation and systemic hyperoxia may be useful indexes for noninvasive monitori

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

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

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

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

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

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

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

220 ), and in a postnatal model due to prolonged hyperoxia.Methods: ETX or sFlt-1 were administered into

221 11-7082 reduced Wnt5a expression in the PCLS hyperoxia model and in vivo mouse hyperoxia model, with

222 n the PCLS hyperoxia model and in vivo mouse hyperoxia model, with improved alveolarization in the PC

223 ncreased alveolar simplification in a murine hyperoxia model.

224 cut lung slices (PCLS), and a murine in vivo hyperoxia model.

225 naling after hyperoxia injury.Methods: Three hyperoxia models were used: A three-dimensional organoty

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

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

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

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

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

231 l oxygen administration, effects of maternal hyperoxia on blood oxygenation of the placenta and fetal

232 Here we report the effect of hyperoxia on central carbon metabolism in primary mouse

233 esis.Objectives: To determine the effects of hyperoxia on epithelial-mesenchymal interactions and to

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

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

236 are important in the effects of hypoxia and hyperoxia on placental syncytialization.

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

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

239 ted HVS regression might result from retinal hyperoxia or dopamine abnormality due to retinal remodel

240 he magnitudes of ventilatory inhibition with hyperoxia or excitation with eucapnic hypoxia were not c

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

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

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

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

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

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

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

248 In conclusion, neonatal hyperoxia permanently impairs hippocampal mitochondrial

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

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

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

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

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

254 Hyperoxia reduces global cerebral perfusion (gCBF), incr

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

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

257 Exposure to hyperoxia results in acute lung injury.

258 During hyperoxia, RTN activation maintains breathing despite th

259 However, an understanding of hyperoxia's effect on cortical activity and concomitant

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

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

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

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

264 Neonatal hyperoxia stimulated expression of ACE2 in Club cells an

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

266 Further, under hyperoxia, the baseline blood volume and saturation of a

267 endent neuroprotective approaches-normobaric hyperoxia, the free radical scavenger alpha-phenyl-butyl

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

269 (ADM(+/-)) mice were exposed to normoxia or hyperoxia through postnatal days (PNDs) 1 to 14, and the

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

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

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

273 veolar space of mice, exposed to 48 hours of hyperoxia together with normoxic controls.

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

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

276 This study aimed to quantify the impact of hyperoxia upon global cerebral perfusion (gCBF), cogniti

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

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

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

280 Severe hyperoxia was associated with higher mortality rates and

281 Moderate hyperoxia was associated with increased mortality during

282 Moderate hyperoxia was associated with increased mortality in pat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

297 thin days after birth in newborns exposed to hyperoxia who later developed chronic lung disease.

298 line (room air); phase II, 6-minute maternal hyperoxia with 100% oxygen; and phase III, 5.6-minute re

299 NaHS and GYY4137 in the context of moderate hyperoxia, with intracellular calcium regulation as a re

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