ライフサイエンスコーパス: pO2

1 pO2 in the kidney is maintained at relatively stable lev

2 pO2 measurements at 5 locations within the eye were comp

3 pO2 was not significantly related to CCT at any other lo

4 pO2-coupled disulfide formation was identified, whereas

5 pO2-sensitive Cys residues were largely non-overlapping

6 ting Fe(III) (oxyhydr)oxides under 21 and 1% pO2 at pH 6.

7 rgeted pathway inhibition between 21% and 1% pO2.

8 ments except the mineral-free systems at 21% pO2, and SRFA decreased Fe(III) phase crystallinity, fac

9 sponsive to mTOR kinase inhibitors near 1.5% pO2, but will respond at higher or lower pO2 values.

10 We find that near 1.5% pO2, the signaling network associated with mammalian tar

11 gradients throughout the tumor mass (0.1-6% pO2).

12 However, the magnitude of 9L pO2 fluctuations was approximately eight times greater t

13 ts predominantly oxide ion conduction over a pO2 range from 10(-20) to 1 atm with a bulk conductivity

14 etime microscopy, we determined the absolute pO2 of the bone marrow to be quite low (<32 mm Hg) despi

15 Additionally, pO2 was measured at a single location for 90 to 120 minu

16 ings grown in PEG solutions of above-ambient pO2 (alanine and proline accumulation are responses to h

17 osition in the water column at which ambient pO2 is equal to species-specific blood P50 values) from

18 nificant inverse correlation between CCT and pO2 in the anterior chamber angle (P = .048).

19 Associations between glaucoma risk, CCT, and pO2 in the AC angle suggest that exposure of the outflow

20 e basis of the location of track markers and pO2 probe measurement depth.

21 gnificant difference in extracellular pH and pO2 between tumor and normal mammary gland tissues, as w

22 microns) measurements of interstitial pH and pO2 profiles between adjacent vessels in a human tumor x

23 found (1) heterogeneity in shapes of pH and pO2 profiles; (2) a discordant relation between local pH

24 yet a strong correlation between mean pH and pO2 profiles; (3) no correlation between perivascular pH

25 RCF and pO2 were temporally coordinated, and there were linear r

26 The effects of reaction temperature and pO2 were investigated on a series of (Ba,Ca,Nd)FeO3-delt

27 led O2 starting 15 min after dMCAO, arterial pO2 312 +/- 10 mmHg).

28 O2 supply and function to maintain arterial pO2 within physiological limits.

29 dMCAO) in normoxic (30% inhaled O2, arterial pO2 134 +/- 9 mmHg), or hyperoxic mice (100% inhaled O2

30 s of cardiopulmonary resuscitation, arterial pO2 (mm Hg) and mixed venous O2 saturation (%) were sign

31 As pO2 rises, the concentration of up- and down-regulating

32 AT pO2 was lower in overweight/obese subjects than lean sub

33 AT pO2 was negatively correlated with percent body fat (R =

34 Of clinical importance, AT pO2 negatively correlated with CD68 mRNA and macrophage

35 pheric level), but that stability is lost at pO2<0.01 PAL.

36 arefaction might lie upstream of both low AT pO2 and inflammation in obesity.

37 = -0.79, P < 0.05), suggesting that lower AT pO2 could drive AT inflammation in obesity.

38 Oxygen partial pressure (AT pO2) and AT temperature in abdominal AT (9 lean and 12 o

39 VI mRNA expression, which correlated with AT pO2 (P < 0.05).

40 ected in a world with much lower atmospheric pO2 than at present, resulting in severe ecological cons

41 f of Earth history regardless of atmospheric pO2 If recent pO2 constraints from Cr isotopes are corre

42 Average pO2 levels in tumor tissue were found to be 3-fold lower

43 In the intestine, for example, baseline pO2 levels are uniquely low due to counter-current blood

44 wave" of angiogenesis and increases in both pO2 and Q(O2).

45 From before to after arrest, jugular bulb pO2 changed by -21.67 mm Hg (26.4) in the HCA group vers

46 ke is dependent on the oxygen concentration (pO2).

47 liter) under normoxic or hypoxic conditions (pO2 = 35 mm of Hg) and measured the indices of apoptotic

48 Under normoxic conditions, pO2 ranges from 90 to <3 torr in mammalian organs with t

49 which produces oxidative stress; muscle core pO2 approximately 400 mmHg), force production is enhance

50 between local pH profiles and corresponding pO2 profiles, yet a strong correlation between mean pH a

51 arison of PET tracer uptake to corresponding pO2 values.

52 parietal cortex of the animals and cortical pO2 was measured optically by phosphorescence quenching.

53 The hypoxic insult (cortical pO2 = 3-10 mmHg) induced expression of hsp72 mRNA in reg

54 tion between the rate of decline of cortical pO2 and baseline FiO2 levels.

55 The cortical pO2 decreased from control values of 24.1, 32.3 and 38.3

56 With reventilation, the cortical pO2 reached maximal values of 42.8, 51.9 and 57.2 Torr a

57 duration of apnea necessary for the cortical pO2 to drop below 20.3 Torr was 18, 44 and 81 s at 15%,

58 characterized by constant Q(O2) and elevated pO2.

59 umbilical vein ECs to a hypoxic environment (pO2 approximately 20 torr) stimulated release of von Wil

60 EPR pO2 image voxel distributions in these approximately 0.5

61 These data confirm the significance of EPR pO2 hypoxic fractions.

62 dents and discovered a severe hypoxic event (pO2 < 10 mmHg) after the termination of seizures.

63 In the nonsurgical (control) eye, pO2 did not change significantly from the first to secon

64 For G(pO2), G(pCO2) and G(cC O2), but not the sensitivity of P

65 sensitivities to acute isocapnic hypoxia (G(pO2)) and hyperoxic hypercapnia, the latter divided into

66 Additionally, the change in G(pO2) during acclimatization to hypoxia correlated well w

67 bsequent rise in ventilation and change in G(pO2) during acclimatization.

68 etized, rats at low pO2, but similar at high pO2.

69 mical emulsions combined with breathing high pO2 gases.

70 using synchrotron X-ray diffraction on high-pO2 floating zone-grown single crystals that this transi

71 ntilated with an FIO2 of 0.21) and/or higher pO2 values (animals ventilated with an FIO2 of 0.5 or 1.

72 observed an expected increase in hippocampal pO2 (15 +/- 4% from baseline) in response to tail pinch

73 Hypoxia (pO2 = 25 mmHg) reversibly depressed the K current by 22%

74 Moderate hypoxia (pO2, 79+/-4 mmHg) stimulated SP release by approximately

75 %, whereas SP release during severe hypoxia (pO2, 11+/-6 mmHg) was 2-fold higher than the normoxic co

76 omus cells increased in response to hypoxia (pO2 = 35 +/- 8 mmHg; 5 min), whereas hypoxia induced dec

77 hat cultured monocytes subjected to hypoxia (pO2 approximately 12 torr) displayed increased Egr-1 exp

78 MPs and HeLa cells subjected to hypoxia (pO2 approximately 13 torr) had increased levels of tissu

79 o, HepG2 cells were incubated under hypoxia (pO2 = 2%) and normoxia (pO2 = 20%).

80 Our results implicate pO2 as an important factor in climate forcing throughout

81 Wildfire is highly responsive to changes in pO2 implying that fire-activity should vary across OAEs.

82 n of pilocarpine induced biphasic changes in pO2 in the hippocampus.

83 e sensitivity to relatively small changes in pO2, which have evolved to modulate respiratory and circ

84 is one of the main causes of the decline in pO2 observed after irradiation.

85 tumor regression followed by an increase in pO2 coincident with regrowth.

86 lar stasis, can cause temporal variations in pO2 that extend from perivascular regions to the maximum

87 e of PtTCHP-C307 was demonstrated in vivo in pO2 measurements through the intact mouse skull into the

88 argue this was primarily driven by increased pO2.

89 tissue hypoxia markers, suggesting increased pO2.

90 The increased pO2 during anti-VEGFR-2 mAb and hormone ablation therapy

91 ce was paralleled by an increase of lesional pO2.

92 sed a persistent suppression of the lesional pO2 and a concurrent increase of the parasite load.

93 infected tissue displayed low oxygen levels (pO2 approximately 21 Torr).

94 des were inserted into the tumor, and linear pO2 measurements were recorded in 50-microm steps along

95 raphy, coagulation panels, lactate and local pO2, there is an opportunity for frontline trauma clinic

96 e can simultaneously report changes in local pO2 and LFP-related currents during pilocarpine-induced

97 e further uncovered heterogeneities in local pO2, with the lowest pO2 ( approximately 9.9 mm Hg, or 1

98 gh-frequency amperometric recording of local pO2 and local field potential (LFP)-related currents dur

99 We found Fe(II) oxidation was slower at low pO2 and resulted in higher-crystallinity Fe(III) phases.

100 awake, relative to anesthetized, rats at low pO2, but similar at high pO2.

101 A good correlation between low pO2 and high Cu-ATSM accumulation was observed.

102 results in lung damage characterized by low pO2 and albumin leakage into the bronchoalveolar lavage

103 tion of triacylglycerol (TAG) storage by low pO2 and LPS.

104 prolonged TAG storage induced by either low pO2 or LPS.

105 tion of 2-nitroimidazole drug binding in low pO2 tumors is a technique that can allow the assessment

106 9L had more low pO2 measurements < or =2.5 mm Hg than did FSA, whereas b

107 s was observed, consistent with areas of low pO2.

108 explain why cervical tumors that possess low pO2 values are more aggressive.

109 Noting that cells responding to low pO2 or agonistic bacterial molecules often decrease pHo

110 cellular changes currently attributed to low pO2 or bacterial agonists may be promoted, at least in p

111 Under low pO2 and a reduced-density atmosphere, shortwave scatteri

112 ersibly oxidized at high (21% O2) versus low pO2 (1% O2), but their identity among the 100 Cys residu

113 Cys residues are oxidized at high versus low pO2 only when NADPH levels are supplemented to enhance N

114 s in NO reactivity, especially at a very low pO2.

115 system but increased at least 10-fold in low-pO2 conditions.

116 .5% pO2, but will respond at higher or lower pO2 values.

117 The lower pO2 levels in tumor compared to normal tissue may explai

118 eterogeneities in local pO2, with the lowest pO2 ( approximately 9.9 mm Hg, or 1.3%) found in deeper

119 um pO2 and a recovery at the time of maximum pO2 in each tumor.

120 Mean pO2 measured intraoperatively was 7.2 +/- 0.6 mm Hg (n =

121 -invasive in vivo method was used to measure pO2 profiles and to calculate oxygen consumption rates (

122 Median pO2 was 7.5 mm Hg for metastasizing tumors versus 20 mm

123 Median pO2 was inversely related to radial distance from microv

124 re pO2 fluctuations were <2 mm Hg and median pO2 was <5 mm Hg.

125 O2 breathing significantly increased median pO2 in FSA from 3 to 8 mm Hg (P < 0.005) and caused a si

126 FSA and 9L tumors had spatial median pO2 measurements of 4 and 1 mm Hg, respectively.

127 >10 mm Hg but only 35% for those with median pO2 values of <10 mm Hg (P=0.01).

128 in uptake of Gd-DTPA at the time of minimum pO2 and a recovery at the time of maximum pO2 in each tu

129 ats, hemorrhage-induced reductions in muscle pO2 were corrected by SNO-Hb-repleted RBCs, but not by c

130 ion of banked RBCs decreased skeletal muscle pO2, but infusion of renitrosylated cells maintained tis

131 ormocapnic (pCO2=35 Torr, pHo=7.4) normoxia (pO2=100 Torr), high pCO (>300 Torr) causes Ca2+-dependen

132 bated under hypoxia (pO2 = 2%) and normoxia (pO2 = 20%).

133 CO (pCO approximately 550 Torr) in normoxic (pO2 approximately 100 Torr) normocapnia (pCO2 approximat

134 ypoxic core [</=0.1% partial pressure of O2 (pO2)] whereas smaller tumors possessed hypoxic gradients

135 mHg or approximately 400 mG/mM); accuracy of pO2 measurement, approximately 1 mmHg).

136 we have observed an initial fast decrease of pO2 after irradiation, followed by a slow increase.

137 Here we report on the dynamics of pO2 and oxygen consumption in a hormone-dependent tumor

138 eoxygenation-dependent relative elevation of pO2 results in perceived hyperoxia.

139 Fluctuations of pO2 of the type reported herein are predicted to signifi

140 NOS (nNOS)-deficient mice, the influence of pO2 on whole-muscle contractility and on myocyte calcium

141 vs. 55 +/- 9.1 mmHg); however, this level of pO2 did not activate the classic hypoxia targets (pyruva

142 tumor pO2, and it decreased the magnitude of pO2 fluctuations with borderline significance.

143 icant increase in frequency and magnitude of pO2 fluctuations.

144 creased Fe(II) oxidation rates regardless of pO2 levels, with goethite being the stronger catalyst.

145 tein levels remained constant, regardless of pO2.

146 fluorescence intensity in response to pH or pO2 changes.

147 atmospheric oxygen concentration is of order pO2 approximately 0.1 PAL (present atmospheric level), b

148 environment (TME) parameters such as oxygen (pO2), extracellular acidosis (pHe), and concentration of

149 l should drive a rise in atmospheric oxygen (pO2) leading to termination of an OAE after approximatel

150 Changes of partial pressure of oxygen (pO2) and blood perfusion were studied in MTG-B and RIF-1

151 The partial pressure of oxygen (pO2) and pH play critical roles in tumor biology and the

152 the kinetics of partial pressure of oxygen (pO2) fluctuations in fibrosarcoma (FSA) and 9L tumors un

153 The partial pressure of oxygen (pO2) of FSaII tumors grown in the leg of C3H mice signif

154 re compared with partial pressure of oxygen (pO2) probe measurements.

155 odulation of the partial pressure of oxygen (pO2), as a result of its contribution to atmospheric mas

156 oxygen tension [partial pressure of oxygen (pO2)] that can interfere with NO signaling (95% O2).

157 xygen levels (FiO2) on cortical oxygenation (pO2) during and after recovery from apnea, was investiga

158 Blood parameters (pH, Na(+), iCa, pCO2, pO2, glucose, Hct, lactate) and muscle pH confirm a step

159 perfusate gases and electrolytes (pH, pCO2, pO2, O2 saturation, Na(+), K(+), Cl(-), Ca(2+), HCO3(-),

160 e measured the intraluminal and perivascular pO2 in rat mesenteric arterioles in vivo by using noninv

161 ovessel red cell flux (RCF) and perivascular pO2 were measured simultaneously and continuously in dor

162 mple to each lung block was analyzed for pH, pO2, pCO2, and hematocrit to follow alterations in suppo

163 itative and discriminative assessment of pH, pO2, and concentrations of the probe and inorganic phosp

164 ; (3) no correlation between perivascular pH/pO2 and nearest vessel blood flow; and (4) well-perfused

165 At physiological pO2, nanomolar NO activates the channel by S-nitrosylati

166 inhibitory influence at higher physiological pO2, which depend on endogenous nNOS.

167 s of muscle performance at low physiological pO2 and an inhibitory influence at higher physiological

168 Correlation analysis between [Pi], pO2, pHe and tumor volumes reveal an association of high

169 Pre-PPV pO2 was also measured intraoperatively using a polarogra

170 e occurred across the timescale of predicted pO2 variations, and we argue this was primarily driven b

171 poxia, characterized by low oxygen pressure (pO2) and decreased O2 intracellular perfusion.

172 patients with tumor median oxygen pressure (pO2) values of >10 mm Hg but only 35% for those with med

173 ints on atmospheric oxygen partial pressure (pO2) before 2.2 Gyr ago.

174 ons at ambient solution O2 partial pressure (pO2) had decreased steady-state root elongation rates, i

175 mpact of changes in oxygen partial pressure (pO2) on the state of signaling networks is less clear.

176 The oxygen partial pressure, pO2 , at which blood is 50% saturated (P50 ) is a measur

177 tory regardless of atmospheric pO2 If recent pO2 constraints from Cr isotopes are correct, we predict

178 fts, (64)Cu-ATSM but not (64)CuCl2 reflected pO2 measurements, indicating that (64)Cu-ATSM is a hypox

179 Decreases of renal pO2 promote hypoxia-inducible factor 2-mediated (HIF-2-m

180 nce suggesting that fire-feedbacks to rising pO2 may have aided in terminating the T-OAE.

181 increased solution pO2 did not increase root pO2 above physiological levels.

182 Measurements of root pO2 were made using an O2 microsensor to ensure that inc

183 igh solution pO2 was necessary to raise root pO2 to the levels found in vermiculite-grown roots.

184 hat gave maximal root elongation rates, root pO2 was similar to or less than (depending on depth in t

185 After completion of the CT scan, pO2 probe measurements were performed along each track.

186 ted T1 times indicated that the mean (+/-SD) pO2 increased significantly following PPV, from 13.2 +/-

187 Even without PEG, high solution pO2 was necessary to raise root pO2 to the levels found

188 icrosensor to ensure that increased solution pO2 did not increase root pO2 above physiological levels

189 interpretation of the temporal data, spatial pO2 distributions were measured in 10 FSA and 8 9L tumor

190 us and aqueous, respectively, for a suitable pO2 range (5-70 mm Hg).

191 Red cell fluxes in microvessels surrounding pO2 measurement locations were measured using fluorescen

192 Temporal pO2 instability was observed in all experiments during a

193 Temporal pO2 instability was observed in all experiments.

194 Temporal pO2 records were evaluated for their potential radiobiol

195 n studied extensively in ambient O2 tension (pO2), whereas tissue PO2 is much lower.

196 imaging technology, that low oxygen tension (pO2) impairs NO-mediated anti-leishmanial immunity, lead

197 n vivo measurements of local oxygen tension (pO2) in the bone marrow of live mice.

198 sel regression should reduce oxygen tension (pO2) in tumors, decreasing the effectiveness of radiothe

199 flow rate can modify vessel oxygen tension (pO2) sufficiently to cause intermittent hypoxia (IH; tis

200 of RyR1 is coupled to muscle oxygen tension (pO2) through O2-dependent production of hydrogen peroxid

201 e RBCs respond to changes in oxygen tension (pO2) with graded vasodilator and vasoconstrictor activit

202 on vascular density, partial oxygen tension (pO2), and apoptosis was also measured.

203 ge lipid storage: low tissue oxygen tension (pO2), low extracellular pH (pHo), and exposure to agonis

204 This study was undertaken to confirm the pO2 dependence of this selective uptake in vivo by corre

205 No significant differences were noted in the pO2 of the pulmonary effluent blood or the Kf; analyzed

206 O2, even in marginal relative excess of the pO2 to which cells are adjusted, results in the activati

207 Raising the pO2 (100% O2) slowed the release of NO bioactivity from

208 ermic cardiac preservation, during which the pO2 within the cardiac vasculature declines to similarly

209 These pO2 values change markedly after radiation and chemother

210 During moderate hypoxemia, average tissue pO2 decreased but oxygen utilization was sustained when

211 ly to cause intermittent hypoxia (IH; tissue pO2 < 3 mmHg) in the tumor parenchyma supplied by such v

212 litates oxygen release, and increases tissue pO2.

213 as assumed to be supported with local tissue pO2 greater than 1 mmHg.

214 a needle oxygen electrode to measure tissue pO2.

215 The distribution of tissue pO2 was also calculated during moderate hypoxemia (paO2=

216 ed O2 consumption, and elevated renal tissue pO2.

217 n tissues in vivo is dependent on the tissue pO2, and that significantly greater uptake and retention

218 less than (depending on depth in the tissue) pO2 of roots growing in vermiculite at the same psiw.

219 In addition, responsivity to pO2 is altered significantly in nNOS mutant muscle.

220 th, </=20 mG) results in high sensitivity to pO2 due to oxygen-induced line broadening (DeltaLW/Delta

221 Cys residues subject to pO2-coupled oxidation are distributed widely within the

222 dues) to identify 13 Cys residues subject to pO2-coupled S-oxidation in SR vesicles.

223 d by collection of approximately 1,300 tumor pO2 image voxels, including the fraction of tumor voxels

224 rcent O2 breathing had no effect on 9L tumor pO2, and it decreased the magnitude of pO2 fluctuations

225 imals caused a decrease in the average tumor pO2 from 28.61 +/- 8.74 mm Hg to 20.81 +/- 7.54 mm Hg in

226 als breathing 100% oxygen, the average tumor pO2 increased to 45.88 +/-15.9 mm Hg, and the tumor upta

227 , precise, and sensitive to changes in tumor pO2 in highly vascular 786-0 renal cancer xenografts.

228 rrelating Cu-ATSM uptake with measured tumor pO2.

229 The tumor pO2 also substantially increased when the tumor-bearing

230 rbogen breathing further increased the tumor pO2 and increased radiation cytotoxicity as assessed by

231 c tumours with an average increase in tumour pO2 of 6.5mmHg in the period 10-30min following administ

232 so observed to significantly increase tumour pO2 levels (p<0.05) in mice bearing ectopic human xenogr

233 e was measured in tumor tissue under various pO2 levels.

234 Vascular pO2 was less sensitive to changes in RCF in well-vascula

235 vitrectomy substantially increases vitreous pO2.

236 diffusion distance limit (140 microm) where pO2 fluctuations were <2 mm Hg and median pO2 was <5 mm

237 ce were placed in a hypoxic environment with pO2 < 40 Torr.

238 wed a significant negative relationship with pO2 measurements in FaDu tumors.

239 including the fraction of tumor voxels with pO2 less than 10 mm Hg (HF10).