ライフサイエンスコーパス: hyperoxic

1 1,316 (46%) were hypoxic, and 450 (16%) were hyperoxic.

2 c, 553 (46%) were hypoxic and 256 (21%) were hyperoxic.

3 ly when rabbits breathed air made hypoxic or hyperoxic.

4 Hyperoxic (100% O(2)) and hypercapnic (5% CO(2), 21% O(2

5 ured in diabetic rats housed for 48 hr under hyperoxic (100% O(2)), hypoxic (11% O(2)), or normoxic (

6 0% helium), limitedly and fully aerobic, and hyperoxic (100% oxygen) conditions.

7 In the hyperoxic 140-day fetal baboon BPD model, p66(Shc) expre

8 ted under either physiologic (5%) or chronic hyperoxic (40%) oxygen conditions.

9 immediately placed in normoxic (room air) or hyperoxic (70% oxygen) conditions for 3 days.

10 were then grown in a normoxic (20% O(2)), or hyperoxic (80% O(2)), atmosphere.

11 e considered that Ang2 might be important in hyperoxic acute lung injury (ALI).

12 Hyperoxic acute lung injury (HALI) is characterized by a

13 Prolonged exposure to hyperoxia results in hyperoxic acute lung injury (HALI).

14 A hallmark of hyperoxic acute lung injury is the influx of inflammator

15 the role of genetic imprinting in regulating hyperoxic acute lung injury survival time using a mouse

16 B cell hyperplasia and confers protection in hyperoxic acute lung injury.

17 nstrate that IL-13 has protective effects in hyperoxic acute lung injury.

18 rgic P2X7 receptor to cause inflammation and hyperoxic acute lung injury.

19 inflammation and the inhibition of injury in hyperoxic acute lung injury.

20 pithelial necrosis with an important role in hyperoxic ALI and pulmonary edema.

21 n vitro and neonatal rat ECFCs isolated from hyperoxic alveolar growth-arrested rat lungs mimicking b

22 er transplantation was the same in livers of hyperoxic and control rats.

23 tilatory responses to hypercapnia under both hyperoxic and hypoxic conditions were assessed both with

24 uring superoxide bursts in macrophage cells, hyperoxic and hypoxic conditions, and in responses to H(

25 By subjecting the mouse to alternating hyperoxic and hypoxic conditions, strong and weak functi

26 natively spliced products are produced under hyperoxic and hypoxic conditions.

27 alcium and mitochondrial calcium in both the hyperoxic and hypoxic group.

28 f CCN1 becomes abnormally reduced during the hyperoxic and ischemic phases of ROP modeled in the mous

29 ic neonate group (156+/-14.2) compared to WT hyperoxic animals (255+/-35.1).

30 Chemoafferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia o

31 nd the total number of nuclei was greater in hyperoxic animals.

32 xic animals, there was minimal disruption in hyperoxic animals.

33 s with detachments, but was decreased in the hyperoxic animals.

34 s telomerase and are relatively resistant to hyperoxic apoptosis.

35 higher in untreated cells after growth in a hyperoxic atmosphere than in untreated cells grown in a

36 After 6 days of growth in a hyperoxic atmosphere, the thyroxine-treated cells were 2

37 e hypothesis that BLP mediates BPD using the hyperoxic baboon model.

38 ical evidence of chronic lung disease in the hyperoxic baboon model.

39 gates pulmonary inflammation and fibrosis in hyperoxic baboons, we hypothesized that ionizing radiati

40 cking the protein had the same response to a hyperoxic challenge as did their wild-type siblings.

41 Relative hyperoxic challenge during reoxygenation causes myocardi

42 In vivo, hyperoxic challenge induced p21-dependent differentiatio

43 Exposure of CFs to hyperoxic challenge-induced transcription of smooth musc

44 expression was significantly reduced in both hyperoxic compared to normoxic groups (P<0.05).

45 mice, prolonged survival was observed under hyperoxic condition.

46 wn for 2 weeks in physiological (5% O(2)) or hyperoxic conditions (40% O(2)) in the presence or absen

47 C57BL/6J mice were transiently exposed to hyperoxic conditions (75% O2) between postnatal day 7 (P

48 Gigantism has been linked to hyperoxic conditions because oxygen concentration is a k

49 In this study, we show that exposure to hyperoxic conditions during the evolution of pneumonia r

50 The reduction under hyperoxic conditions from 0.75 +/- 0.34 to 0.49 +/- 0.09

51 The lack of change in the ASL signal under hyperoxic conditions is consistent with the hypothesis t

52 Expression is optimal in hyperoxic conditions or in air and is reduced under hypo

53 sults demonstrate that culturing cells under hyperoxic conditions reduces their ability to efficientl

54 Hyperoxic conditions were established by ventilating the

55 Under hyperoxic conditions, overexpressors had increased longe

56 abolic lesions, exacerbated by storage under hyperoxic conditions, were ameliorated by hypoxic storag

57 ression of YHB1 is optimal under normoxic or hyperoxic conditions, yet respiring yeast cells have low

58 on of pulmonary blood flow under hypoxic and hyperoxic conditions.

59 dy labeling in the detachments maintained in hyperoxic conditions.

60 ty to isoprenaline seen under these slightly hyperoxic conditions.

61 ately 0.11), separated by 30 min of control, hyperoxic conditions.

62 ed to evaluate HRMVECs following hypoxic and hyperoxic conditions.

63 ROS, SA-beta-gal, and AF normally induced by hyperoxic conditions.

64 cultured cells and intact animals die under hyperoxic conditions.

65 ubated, and exposed to normoxic, hypoxic, or hyperoxic conditions.

66 has a shorter lifespan under both normal and hyperoxic conditions; (iii) develops an atypical (tip-to

67 t CO protects cultured epithelial cells from hyperoxic damage.

68 rference (RNAi) knockdown of Bcl-XL enhanced hyperoxic death of cells expressing p21, whereas overexp

69 two components would be expected, and under hyperoxic (end-tidal PO2 = 200 Torr) conditions, when th

70 aurantiacus since this bacterium lives in a hyperoxic environment and is subject to high UV radiatio

71 Prolonged exposure of porcine TM cells to a hyperoxic environment led to an increase in ROS producti

72 be a behavioural strategy for responding to hyperoxic environments.

73 , using the modified Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic h

74 nt increase of MVD in the TG group following hyperoxic exposure (85+/-12) in comparison to the WT hyp

75 After hyperoxic exposure (O2 > 95%), neonatal (<12 hours old)

76 sion is increased from P7 to P17, altered by hyperoxic exposure and relative hypoxic recovery and mod

77 ivity or chelation of cellular iron prior to hyperoxic exposure decreased reactive iron levels in the

78 In HPAECs, a 3-h hyperoxic exposure enhanced the tyrosine phosphorylation

79 idant enzymes in preventing lung injury from hyperoxic exposure has been implicated in a number of ea

80 Hyperoxic exposure increases the activation of CD103(+),

81 preventing oxidant-mediated lung injury from hyperoxic exposure is negligible, and other cellular ant

82 petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal perio

83 h GM-CSF (9 micro g/kg/day) during 4 days of hyperoxic exposure resulted in decreased apoptosis in th

84 rth, indicating that even a relatively short hyperoxic exposure was sufficient to derange normal chem

85 We hypothesized that hyperoxic exposure, a predisposing factor to bronchopulm

86 Two to four months after the hyperoxic exposure, treated rats were compared with untr

87 ell viability in lung primary cultures after hyperoxic exposure.

88 increased markers of oxidative injury before hyperoxic exposure.

89 number of myelinated axons was unaffected by hyperoxic exposure.

90 is massively up-regulated in the lungs after hyperoxic exposure.

91 gocytic activity for yeast; however, similar hyperoxic exposures in iron-supplemented media significa

92 eatment-limiting consequence of therapy with hyperoxic gas mixtures.

93 k rate, but with EIAH prevented by inspiring hyperoxic gas or work of breathing reduced via a proport

94 c exposure (85+/-12) in comparison to the WT hyperoxic group (62+/-8.4), (P<0.05).

95 EPC's showed significant reduction in WT hyperoxic group compared to others (P>0.05).

96 Among the hyperoxic groups, both RNA and protein of VEGF expressio

97 hrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO(2)), and during peripheral

98 n with cyanide, but only mildly activated by hyperoxic hypercapnia (central chemoreceptor stimulation

99 We studied the effect of hyperoxic hypercapnia (CO2) on the variational activity

100 hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above

101 tivation of central chemoreceptors with mild hyperoxic hypercapnia also causes resetting of the arter

102 experiments in fourteen rats, we found that hyperoxic hypercapnia and poikilocapnic hypoxia also res

103 f experiments, the animals were subjected to hyperoxic hypercapnia and poikilocapnic hypoxia.

104 Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia

105 tivation of central chemoreceptors with mild hyperoxic hypercapnia does not affect arterial pressure,

106 In the FD group, whereas hyperoxic hypercapnia induced normal cardiovascular and

107 threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral

108 tilatory and occlusion pressure responses to hyperoxic hypercapnia with and without added resistive l

109 g progressive isocapnic hypoxia, progressive hyperoxic hypercapnia, and during recovery from moderate

110 Heart rate is elevated during hyperoxic hypercapnia, but this response is not differen

111 ties to acute isocapnic hypoxia (G(pO2)) and hyperoxic hypercapnia, the latter divided into periphera

112 mined the closed- and open-loop responses to hyperoxic hypercapnia.

113 ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia, and exercise; breath-hold toleran

114 did not have any worsening in symptoms, her hyperoxic hypercapnic rebreathing ventilatory response w

115 ation was sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being n

116 Under hyperoxic/hyperoxic incubation (control), hepatocytes we

117 Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tida

118 Under conditions of hyperoxic, hypocapnic apnoea, the mean threshold for ind

119 ormoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxi

120 antly decreased after 2 continuous cycles of hyperoxic-hypoxic-hyperoxic treatments compared with wil

121 Mean respiratory variables (baseline, hyperoxic/hypoxic responses) were not severely influence

122 Replicating the hyperoxic in vivo pO(2) of 53 mm Hg in the ex vivo retin

123 Under hypoxic/hyperoxic incubation (reoxygenation), however, loss of t

124 extracellular lung compartment contribute to hyperoxic-induced lung damage and that overexpression of

125 To study the biologic role of EC-SOD in hyperoxic-induced pulmonary disease, we created transgen

126 room air value, or deltaPO(2), in mm Hg) to hyperoxic inhalation challenge.

127 , DA restored lung ability to clear edema in hyperoxic-injured rat lungs.

128 ial cells (HLMVEC) are a principal target of hyperoxic injury (hyperoxia).

129 n, and proliferation during remodeling after hyperoxic injury also require FGF signaling.

130 IRAK-M may potentiate hyperoxic injury by suppression of key antioxidant pathw

131 data suggest that: (1) iron uptake promotes hyperoxic injury to AM; and (2) hyperoxia impairs the ca

132 erve to protect the neonatal lung from acute hyperoxic injury via inhibition of apoptosis.

133 the importance of the endothelium in lethal hyperoxic injury, 2) HO-1 and CO require endothelial STA

134 ects the neonatal pulmonary vasculature from hyperoxic injury.

135 ge and promotes proper vascular repair after hyperoxic insult in the OIR model.

136 in the neonatal dog, revascularization after hyperoxic insult involves a period of marked vasoprolife

137 ditions and to the pulmonary defense against hyperoxic insult is very limited.

138 However, glutathione supplementation during hyperoxic insult restored the ability of Nrf2(-/-) cells

139 als at different time points during or after hyperoxic insult were analyzed.

140 sed mortality following a normally sublethal hyperoxic insult, accompanied by alveolar epithelial cel

141 ls and intravitreal neovascularization after hyperoxic insult.

142 t mortality following an otherwise nonlethal hyperoxic insult.

143 ibited using dopamine (5 to 10 microg/kg) or hyperoxic lactated Ringer's solution.

144 date the specific roles of HO-1 and STAT3 in hyperoxic lung and endothelial cell injury.

145 e P326TAT ameliorates barrier dysfunction of hyperoxic lung endothelial monolayer and attenuates eNOS

146 P450 (CYP)1A enzymes are protective against hyperoxic lung injury (HLI).

147 e-8/Bid pathway in signaling associated with hyperoxic lung injury and cell death in vivo and in vitr

148 f GM-CSF in the lung would protect mice from hyperoxic lung injury by limiting alveolar epithelial ce

149 -6, which results in increased resistance to hyperoxic lung injury in Foxp1/HDAC2 compound mutant ani

150 remarkable effectiveness of MR1 in blunting hyperoxic lung injury in this preclinical model may be r

151 essing hEC-SOD in the airways attenuated the hyperoxic lung injury response, showed decreased morphol

152 s in the transcriptome and proteome of acute hyperoxic lung injury using the omics platforms: microar

153 Employing a mouse model of hyperoxic lung injury, a monoclonal anti-CD40 ligand (L)

154 nes causes increased fluid resorption during hyperoxic lung injury.

155 zymes by hyperoxia may have implications for hyperoxic lung injury.

156 hrome P4501A enzymes have been implicated in hyperoxic lung injury.

157 s demonstrate that IL-11 markedly diminishes hyperoxic lung injury.

158 ath, resulting in enhanced susceptibility to hyperoxic lung injury.

159 In certain conditions, such as in the hyperoxic lung, this process may be deleterious.

160 sion in all segments of room air control and hyperoxic lungs infected with either dose of adbeta-gal.

161 Net transgene expression in hyperoxic lungs was not different from room air controls

162 ion of Apo E and transferrin was observed in hyperoxic lungs.

163 inhaled O2, arterial pO2 134 +/- 9 mmHg), or hyperoxic mice (100% inhaled O2 starting 15 min after dM

164 sections demonstrated increased apoptosis in hyperoxic mice, predominantly in macrophages and alveola

165 l apoptosis, and pulmonary edema in lungs of hyperoxic mice.

166 Using a hyperoxic model of premature brain injury, we have previ

167 ronic oxidative stress was applied using the hyperoxic model; acute oxidative stress was applied with

168 ere was a significant reduction of ROS in TG hyperoxic neonate group (156+/-14.2) compared to WT hype

169 ge significantly in response to apnea during hyperoxic or hypercapnic baseline conditions with both a

170 lated rat hepatocytes were incubated under a hyperoxic or hypoxic atmosphere for 60 min.

171 A4 cells also exhibited marked resistance to hyperoxic oxidant insult.

172 d-rank test was used to compare baseline and hyperoxic parameters.

173 e periods of hypoxia were followed by 8 h of hyperoxic perfusion.

174 At the hyperoxic phase, caffeine reduced oxygen-induced neural

175 ypoxic phase and negatively with that of the hyperoxic phase.

176 comprising a primary hypoxic and a secondary hyperoxic phase.

177 These data indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.

178 subnormal retinal oxygenation response to a hyperoxic provocation (DeltaPo2) is strongly associated

179 gene transfer techniques protects mice from hyperoxic pulmonary damage and delays death of mice.

180 athways may contribute to the development of hyperoxic pulmonary edema, lung injury, and respiratory

181 eceiving the same graft size, so the area in hyperoxic rats receiving 700 islets was not significantl

182 Lungs of hyperoxic rats showed increase in the expression of CYP1

183 islet area and number of islets engrafted in hyperoxic rats was significantly increased when compared

184 s, preserved alveolar and vascular growth in hyperoxic rats, and attenuated pulmonary hypertension.

185 of DA on active Na+ transport in control and hyperoxic rats, whereas the isomer beta-lumicolchicine,

186 via multi-wavelength irradiation in behaving hyperoxic rats.

187 ever, hypocalcemia acts synergistically with hyperoxic reoxygenation to produce more severe damage.

188 During the ensuing 60-min hyperoxic reoxygenation, medium [Ca2+]ex was varied from

189 The hyperoxic response in rats (n = 9) injected with 10(-4)

190 a surrogate of blood flow, from physiologic hyperoxic responses (20% increase) to pathological hypox

191 tly decreased in blood vessels isolated from hyperoxic retinas compared with those from normoxic cont

192 tality in P. murina-infected mice exposed to hyperoxic stress by inhibition of inflammation and apopt

193 so exhibited increased survivability against hyperoxic stress when compared with rats receiving AdV-b

194 ility, locomotor activity, and resistance to hyperoxic stress, compared with wild-type controls.

195 ional culture conditions is a consequence of hyperoxic stress.

196 and heme oxygenase were induced by the same hyperoxic stress.

197 tional role of secreted Cyr61 in response to hyperoxic stress.

198 iapoptotic effects of carbon monoxide during hyperoxic stress.

199 Hyperoxic subacute lung injury was induced by 95 % oxyge

200 ter 2 continuous cycles of hyperoxic-hypoxic-hyperoxic treatments compared with wild-type (WT) BM cel

201 in the mice tumor subjected to normoxic and hyperoxic treatments.

202 cantly reduced in sVlow subregions that were hyperoxic under 80% O2 conditions.

203 ogical responses of hypoxic vasodilation and hyperoxic vasconstriction in the human respiratory cycle

204 (CNS O2 toxicity) is preceded by release of hyperoxic vasoconstriction, which increases regional cer

205 HBO2 exposure is responsible for escape from hyperoxic vasoconstriction.

206 dies are conducted in atmospheric O2 levels, hyperoxic with respect to the physiologic milieu.