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 o the atmospheric partial pressure of O(2) ( pO2 )(17-19).

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

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

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

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

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

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

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

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

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

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

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

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

21 ime microscopy, and calcium, blood flow, and pO2 measurements, we characterized this initial dip in p

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

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

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

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

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

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

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

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

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

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

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

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

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

35 AT pO2 was negatively associated with AT gene expression of

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

37 AT pO2 was positively associated with the expression of gen

38 tion with an inverse relationship between AT pO2 and plasma BCAA concentrations.

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

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

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

42 = -0.79, P < 0.05), suggesting that lower AT pO2 could drive AT inflammation in obesity.

43 erythrocytes were added to the perfusate at pO2 of 500 mmHg.

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

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

46 group and was negatively correlated with AT pO2, whereas the plasma concentrations of other cytokine

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

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

49 Average pO2 is important for determining if a transplant site an

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

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

52 MRI platform is used to map changes in blood pO2 (BOLD), volume (CBV), and velocity (CBFv).

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

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

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

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

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

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

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

60 arison of PET tracer uptake to corresponding pO2 values.

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

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

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

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

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

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

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

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

69 EPR pO2 image voxel distributions in these approximately 0.5

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

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

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

73 characterized by generally low, fluctuating pO2 between an O(2)-free state before 2.4 billion years

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

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

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

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

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

79 mical emulsions combined with breathing high pO2 gases.

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

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

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

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

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

85 %, whereas SP release during severe hypoxia (pO2, 11+/-6 mmHg) was 2-fold higher than the normoxic co

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

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

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

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

90 compared dose escalation (boost) in hypoxic (pO2 <= 10 torr) and non-hypoxic tumor subvolumes.

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

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

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

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

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

96 ements, we characterized this initial dip in pO2 in mice chronically implanted with a glass cranial w

97 In awake mice, the dip in pO2 was absent in capillaries as well as, surprisingly,

98 st and efficient to reveal an initial dip in pO2.

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

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

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

102 argue this was primarily driven by increased pO2.

103 tissue hypoxia markers, suggesting increased pO2.

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

105 se isotopic couplings reflect the increasing pO2 , which may have driven episodic ocean oxygenation t

106 ce was paralleled by an increase of lesional pO2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 9L had more low pO2 measurements < or =2.5 mm Hg than did FSA, whereas b

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

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

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

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

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

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

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

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

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

131 .5% pO2, but will respond at higher or lower pO2 values.

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

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

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

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

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

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

138 Median pO2 was inversely related to radial distance from microv

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

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

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

142 >10 mm Hg but only 35% for those with median pO2 values of <10 mm Hg (P=0.01).

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

144 fore 2.4 billion years ago (Ga) and a modern pO2 state after 0.41 Ga, with relatively elevated levels

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

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

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

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

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

150 measurements of the partial pressure of O2 (pO2) in cortical tissue by means of 2-photon phosphoresc

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

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

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

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

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

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

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

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

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

160 icant increase in frequency and magnitude of pO2 fluctuations.

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

162 tein levels remained constant, regardless of pO2.

163 fluorescence intensity in response to pH or pO2 changes.

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

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

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

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

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

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

170 or measuring the partial pressure of oxygen (pO2) in alginate microcapsules implanted intraperitoneal

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

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

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

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

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

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

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

178 ition of oxygen carriers, arterial perfusate pO2 was maintained at 500 mmHg.

179 Peritoneal pO2 levels were measured on days 0 and 7 using fluorine-

180 The peritoneal pO2 of normal NHPs is relatively low and we predict woul

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

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

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

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

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

186 tabolic rate of O2 (CMRO2) based on 2-photon pO2 measurements around diving arterioles and applied th

187 eduction in tissue perfusion, and two-photon pO2 microscopy revealed a drop in venous pO2 during the

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

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

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

191 e containing perfusate at more physiological pO2 of 200 mmHg.

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

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

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

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

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

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

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

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

200 ted subcutaneous AT oxygen partial pressure (pO2); liver and whole-body insulin sensitivity; AT expre

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

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

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

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

205 These high-resolution pO2 measurements demonstrate that in awake mice recovere

206 ET, and it was poorly influenced by resting pO2.

207 ally unhealthy obese (MUO; n = 20).RESULTSAT pO2 progressively declined from the MHL to the MHO to th

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

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

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

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

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

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

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

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

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

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

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

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

220 Temporal pO2 instability was observed in all experiments during a

221 Temporal pO2 instability was observed in all experiments.

222 Temporal pO2 records were evaluated for their potential radiobiol

223 d-sulfur species, while triggering temporary pO2 drawdowns as negative feedback(15).

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

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

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

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

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

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

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

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

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

233 concentrated near the infusion site, and the pO2 measurement using magnetic resonance relaxometry was

234 persed throughout the peritoneal cavity, the pO2 level was 61 +/- 11 mm Hg.

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

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

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

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

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

240 These pO2 values change markedly after radiation and chemother

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

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

243 litates oxygen release, and increases tissue pO2.

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

245 a needle oxygen electrode to measure tissue pO2.

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

247 ed O2 consumption, and elevated renal tissue pO2.

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

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

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

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

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

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

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

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

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

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

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

259 rrelating Cu-ATSM uptake with measured tumor pO2.

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

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

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

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

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

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

266 esthetized mice, a transient dip in vascular pO2 was detected in this glomerulus when functional hype

267 This vascular pO2 dip was not observed in other glomeruli responding n

268 ton pO2 microscopy revealed a drop in venous pO2 during the intracranial pressure spikes suggesting i

269 vitrectomy substantially increases vitreous pO2.

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

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

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

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