ライフサイエンスコーパス: oxyhemoglobin

1 ff of resonance with the Soret transition of oxyhemoglobin.

2 micromol/L), as well as by the NO scavenger oxyhemoglobin.

3 ecular replacement phases derived from human oxyhemoglobin.

4 on of a linear transition between deoxy- and oxyhemoglobin.

5 tion by glucose treatment can be reversed by oxyhemoglobin.

6 d to an electronic structural formulation of oxyhemoglobin.

7 cted given the abundance of the NO-scavenger oxyhemoglobin.

8 idation of endogenous NO by cell-free plasma oxyhemoglobin.

9 s contrasted to the diamagnetic character of oxyhemoglobin.

10 nterbalanced by an equal initial decrease in oxyhemoglobin.

11 de slower than that by equal amounts of free oxyhemoglobin.

12 micromol/L), indomethacin (5 micromol/L), or oxyhemoglobin (10 micromol/L) inhibited the response to

13 Oxyhemoglobin (10(-6) mol/L) abolished acetylcholine-med

14 The CO scavenger oxyhemoglobin (20 muM) and the heme oxygenase inhibitor

15 rat isolated superior cervical ganglia with oxyhemoglobin (25-100 microm) completely blocked LTP.

16 Addition of oxyhemoglobin (a scavenger of extracellular NO) during t

17 Oxyhemoglobin, a .NO scavenger, completely attenuated de

18 minnesota on the rate of oxidation of native oxyhemoglobin A0 and hemoglobin cross-linked between the

19 o-L-arginine (an NO synthase inhibitor), and oxyhemoglobin (an NO scavenger).

20 The addition of oxyhemoglobin, an NO scavenger, stimulates cell aggregat

21 t inelastic X-ray scattering (RIXS) to study oxyhemoglobin and a related heme {FeO(2)}(8) model compo

22 de (NO), mediated by NO scavenging by plasma oxyhemoglobin and by arginine degradation by plasma argi

23 han CPN or its active subunit in hydrolyzing oxyhemoglobin and cleaved oxyhemoglobin twice as fast as

24 nhibit NO-sGC, also inhibited the effects of oxyhemoglobin and CPTIO, slowing down the deactivation o

25 llowing IR there was significant decrease in oxyhemoglobin and cytochrome oxidase and an increase in

26 In this model, spectral images, based upon oxyhemoglobin and deoxyhemoblobin signals in the 525-645

27 e spatial distribution of the percentages of oxyhemoglobin and deoxyhemoglobin in specific skin tissu

28 e when using relative concentrations of both oxyhemoglobin and deoxyhemoglobin, rather than either sp

29 fter injections of lysed blood, whole blood, oxyhemoglobin and saline into the cisterna magna.

30 trate during the reaction of hydroxyurea and oxyhemoglobin and the lack of nitrous oxide production i

31 ed blood cells (RBCs), RBC lysates, purified oxyhemoglobin, and a mouse model.

32 gen saturation, nitrite will also react with oxyhemoglobin, and although this complex autocatalytic r

33 tissue chromophores, including water, lipid, oxyhemoglobin, and deoxyhemoglobin.

34 owever, recent reports indicate that Mg-GTP, oxyhemoglobin, and reducing and oxidizing agents could d

35 The K-edge XAS and RIXS data of pfpO(2) and oxyhemoglobin are compared with the data for low-spin Fe

36 otoproducts from ligand photodissociation of oxyhemoglobin are measured in the Soret spectral region

37 nd ferric-Hb, thus revealing the fraction of oxyhemoglobin as well as any baseline drifts and protein

38 rogen bond in both alpha- and beta-chains of oxyhemoglobin, as revealed by heteronuclear NMR spectra

39 mplex releases nitric oxide as judged by the oxyhemoglobin assay and an NO specific EPR specific trap

40 and processed visualizing the percentage of oxyhemoglobin at each pixel detector and presented conti

41 e greater light absorption by hemoglobin and oxyhemoglobin at short wavelengths compared to longer wa

42 Oxyhemoglobin attenuated the effect of SNP but not of L-

43 Deoxyhemoglobin (deoxyHb), but not oxyhemoglobin, binds avidly and reversibly to band 3, th

44 Because deoxyhemoglobin, but not oxyhemoglobin, binds band 3 reversibly with high affinit

45 injections of lysed blood, whole blood, and oxyhemoglobin but not saline.

46 Oxyhemoglobin concentration (HbO) was correlated with th

47 primary outcome measures were the changes in oxyhemoglobin concentration (NadirHbO, i.e., lowest oxyh

48 globin concentration (NadirHbO, i.e., lowest oxyhemoglobin concentration and PeakHbO, i.e., peak chan

49 Moreover, the oxyhemoglobin concentration changes elicited by a syllab

50 basal subarachnoid cisterns where blood and oxyhemoglobin concentrations were likely highest.

51 tion of these N-hydroxyurea derivatives with oxyhemoglobin correlates well with that compound's oxida

52 During arterial occlusion, a decrease in oxyhemoglobin corresponds to an increase in NADH fluores

53 imaging (DOSI) to measure concentrations of oxyhemoglobin (ctO(2)Hb), deoxy-hemoglobin (ctHHb), tota

54 sis allows the determination of fractions of oxyhemoglobin, deoxyhemoglobin, and high-spin and low-sp

55 as used to determine tissue concentration of oxyhemoglobin, deoxyhemoglobin, total hemoglobin, tissue

56 s used to measure absolute concentrations of oxyhemoglobin, deoxyhemoglobin, water, and lipid in tumo

57 tive association between hypersomnolence and oxyhemoglobin desaturation (DeltaSaO2) was observed with

58 arrowing disrupting ventilation, and causing oxyhemoglobin desaturation and poor sleep quality.

59 ) supplementation in subjects who experience oxyhemoglobin desaturation during physical activity but

60 n OAD and SAH and (2) identify predictors of oxyhemoglobin desaturation during sleep in persons havin

61 ea and hypopnea and the duration of arterial oxyhemoglobin desaturation during sleep.

62 INVOS 3100A to detect rapid tissue vascular oxyhemoglobin desaturation in the brain during circulato

63 Nocturnal oxyhemoglobin desaturation indices and pulse event indic

64 Using a protocol in which oxyhemoglobin desaturation was prevented or reversed by

65 Sleep disruption and arterial oxyhemoglobin desaturation were significantly more sever

66 nights; p < 0.001) that were associated with oxyhemoglobin desaturation, arousals from sleep, and alt

67 ctive sleep apnea syndrome without prolonged oxyhemoglobin desaturation, early adenotonsillectomy, as

68 pnea result in sleep disruption and arterial oxyhemoglobin desaturation.

69 Patients exhibiting oxyhemoglobin desaturations at night showed higher plasm

70 In the same ganglia, prolonged washout of oxyhemoglobin did not uncover any potentiation of the co

71 In initial validation studies, the oxyhemoglobin dissociation curve for mouse blood was acc

72 To assess the position of these patients' oxyhemoglobin dissociation curves, we plotted arterial a

73 We found right-shifted oxyhemoglobin dissociation curves, with pH-corrected p50

74 yoglobin-facilitated diffusion and nonlinear oxyhemoglobin dissociation in the RBCs and plasma.

75 Cone-shaped tissue geometry and nonlinear oxyhemoglobin dissociation were assumed.

76 ltaneously drawn arterial saturation (SaO2 = oxyhemoglobin divided by oxyhemoglobin plus reduced hemo

77 ect on H/R-induced stasis, though unmodified oxyhemoglobin exacerbated stasis.

78 Oxyhemoglobin exposed to a continuous flux of H(2)O(2) u

79 Oxyhemoglobin flare on day 1 was adequate to discriminat

80 Oxyhemoglobin had no significant effect on the maintenan

81 ly Fe(II) with 6-8% Fe(III) character, while oxyhemoglobin has a very mixed wave function that has 50

82 The electronic structure of oxyhemoglobin has been controversial since the discovery

83 n reported that the rate of NO reaction with oxyhemoglobin (Hb) within RBCs is nearly three orders of

84 see text] can be computed from the ratio of oxyhemoglobin HbO[Formula: see text] and deoxyhemoglobin

85 The delta value of oxyhemoglobin ( -HbO) determined by functional near-infr

86 ing the percentage of hemoglobin existing as oxyhemoglobin (HbO(2)) as an index of skin tissue perfus

87 ng activity of ubiquinone 0 (UQ(0)) to human oxyhemoglobin (HbO(2)) using electron spin resonance (ES

88 or "initial dip" reports local conversion of oxyhemoglobin (HbO) to HbR, i.e., oxygen consumption cau

89 The distributions of oxyhemoglobin (HbO), deoxyhemoglobin (Hb), and total hem

90 Simultaneously, changes in cortical oxyhemoglobin (HbO), deoxyhemoglobin (HHb), and total he

91 g intrinsic optical absorption contrast from oxyhemoglobin (HbO2) and deoxyhemoglobin (HbR), FOG allo

92 lar to the LFOs of deoxyhemoglobin (HbR) and oxyhemoglobin (HbO2) in both large blood vessels and cap

93 rared spectroscopy (NIRS) can measure tissue oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), and cytochro

94 re important functional parameters including oxyhemoglobin (HbO2), deoxyhemoglobin (HbR), oxygen satu

95 /xanthine oxidase or the potent NO scavenger oxyhemoglobin impaired EDR.

96 ely due to the oxidative reaction of NO with oxyhemoglobin in arterioles and surrounding tissue.

97 red spectroscopy was used to measure percent oxyhemoglobin in capillaries and laser Doppler flowmetry

98 Chicken Hb D differs most from human oxyhemoglobin in the AB and GH corners of the alpha subu

99 ral, parenchymal response to the presence of oxyhemoglobin in the subarachnoid space and not as a str

100 Lysed blood, whole blood and oxyhemoglobin induced HO-1 in all of the cortex, hippoca

101 oxidation of nitric oxide (NO) to nitrate by oxyhemoglobin is a fundamental reaction that shapes our

102 he chemical nature of the dioxygen moiety of oxyhemoglobin is crucial for elucidation of its physiolo

103 show that the difference between pfpO(2) and oxyhemoglobin is due to a distal histidine H bond to O(2

104 brane-associated ferric iron and cytoplasmic oxyhemoglobin is promotive of hemoglobin oxidation and d

105 how that pfpO(2) is similar to Fe(II), while oxyhemoglobin is qualitatively similar to Fe(III), but w

106 The oxyhemoglobin L-edge XAS data further show that the O(2)

107 nchanged regional tissue perfusion and ileal oxyhemoglobin levels compared with controls.

108 images using deoxyhemoglobin (mean, 0.0782), oxyhemoglobin (mean, 0.0833), and total hemoglobin (mean

109 -1 DNA-binding activity was not blocked with oxyhemoglobin, nor was it related to the rate of NO evol

110 ing exercise would affect the rate of muscle oxyhemoglobin (O2Hb) desaturation when performing work a

111 equency similar to that of oxymyoglobins and oxyhemoglobins of vertebrates (571 cm(-1)).

112 showed no flare and a subsequent decrease in oxyhemoglobin on day 1.

113 iation, as was evident from the inability of oxyhemoglobin or CPTIO to deactivate NO-sGC.

114 eaction was observed only in the presence of oxyhemoglobin or superoxide anion (generated by xanthine

115 eine were not affected by local injection of oxyhemoglobin or the nitric oxide synthase inhibitor L-n

116 wing injections of lysed blood, whole blood, oxyhemoglobin, or saline.

117 is during the autoinactivation of eNOS using oxyhemoglobin oxidation assay for NO formation at room t

118 one-iron complex was found to be crucial for oxyhemoglobin oxidation.

119 n methemoglobin levels and a 40% decrease in oxyhemoglobin (oxygen-carrying form) levels compared to

120 a was about 8 muM; the hemoglobin was mainly oxyhemoglobin (oxyHb) (96%), which was converted to meth

121 Oxyhemoglobin (oxyhb) has been implicated in SAH-induced

122 However, the reaction of nitrite with oxyhemoglobin (oxyHb) is well established and generates

123 phate-buffered saline (PBS) with either free oxyhemoglobin (oxyHb) or red blood cells (RBCs).

124 ramagnetic ferrous Hb to diamagnetic ferrous oxyhemoglobin (oxyHb) with reversibly bound O2, or param

125 n between deoxyhemoglobin (deoxyHb), but not oxyhemoglobin (oxyHb), and other proteins for band 3.

126 radical and cysteine residue in two systems, oxyhemoglobin (oxyHb)/peroxynitrite/5,5-dimethyl-1-pyrro

127 ns may be based on the value of mixed venous oxyhemoglobin, oxyhemoglobin saturation is only reliably

128 Pulse oximetry slightly overestimated oxyhemoglobin percentage (by an average of 3.4 percentag

129 saturation (SaO2 = oxyhemoglobin divided by oxyhemoglobin plus reduced hemoglobin) measured by co-ox

130 ation requires free *NO, because addition of oxyhemoglobin prevents formation from either *NO donor o

131 imiting oxidative inactivation of nitrite by oxyhemoglobin, promoting nitrite reduction to NO by deox

132 s of storage, remains in the reduced ferrous oxyhemoglobin redox state and stoichiometrically reacts

133 deactivation was caused by scavengers of NO: oxyhemoglobin reduced the half-life of NO-sGC from 106 m

134 In addition, the oxyhemoglobin restored the rickettsia-mediated, rapid ki

135 ripped sickle or normal ghost membranes with oxyhemoglobin S.

136 hypoxemia index (percent of sleep time with oxyhemoglobin saturation < 90%) were used to quantify SD

137 e COVID-19 (confirmed or suspected), with an oxyhemoglobin saturation <94% or respiratory rate >24 br

138 et, number of sleep stage shifts, and lowest oxyhemoglobin saturation (SaO(2)) during sleep] and all

139 pnea hypopnea index (AHI), overnight average oxyhemoglobin saturation (SaO2) and percentage time SaO2

140 in Pao2 between 70 and 100 mm Hg or arterial oxyhemoglobin saturation (Spo2) between 94% and 98% (con

141 erial oxygen tension (PaO2, 55-86 mm Hg) and oxyhemoglobin saturation (SpO2, 92-95%).

142 r with cerebral oxygenation (regional tissue oxyhemoglobin saturation [rSO2]).

143 ble COPD with moderate resting desaturation (oxyhemoglobin saturation as measured by pulse oximetry [

144 al sleep time, sleep efficiency, and minimum oxyhemoglobin saturation compared with the healthy subje

145 With acute altitude, PaO2 and oxyhemoglobin saturation decreased and pulmonary artery

146 In situ magnetic resonance imaging and oxyhemoglobin saturation detection visualize the treatme

147 erebral extraction of oxygen (arteriojugular oxyhemoglobin saturation difference) was measured in eac

148 Average arterial oxyhemoglobin saturation during sleep (AvSpO(2)S) is a c

149 Oxyhemoglobin saturation in the superior vena cava, righ

150 on the value of mixed venous oxyhemoglobin, oxyhemoglobin saturation is only reliably measured in sa

151 re for cumulative sleep time percentage with oxyhemoglobin saturation less than 90% (CT90), and great

152 of total sleep time spent below an arterial oxyhemoglobin saturation of 90% (19 +/- 32 vs. 6 +/- 13%

153 The room air oxyhemoglobin saturation was > or = 0.98 in all patients

154 Each standard deviation higher than <90% oxyhemoglobin saturation was associated with an adjusted

155 f total sleep time during which the arterial oxyhemoglobin saturation was less than 90 percent (6 +/-

156 OSA and <90% oxyhemoglobin saturation were not associated with uncont

157 which are accompanied by a > or = 4% drop in oxyhemoglobin saturation) [corrected], obtained by unatt

158 ypoxemia index (percent sleep time below 90% oxyhemoglobin saturation).

159 adjusting for demographic factors and awake oxyhemoglobin saturation, an FEV1/FVC value less than 65

160 s, arterial and mixed venous oxygen content, oxyhemoglobin saturation, and arterial blood lactate wer

161 the tissue oxygen tension and the capillary oxyhemoglobin saturation.

162 s quantified as percent sleep time with <90% oxyhemoglobin saturation.

163 obin formation was inversely proportional to oxyhemoglobin saturation.

164 Oxyhemoglobin saturations also fell (p < 0.05), coincidi

165 er, when superior vena cava and right atrial oxyhemoglobin saturations and SvO2 were compared, the ra

166 errors if superior vena cava or right atrial oxyhemoglobin saturations were substituted for true mixe

167 troscopy (XAS) in the 3s->2p fluorescence on oxyhemoglobin solutions, measured using a transition-edg

168 areas in both the T (deoxyhemoglobin) and R (oxyhemoglobin) structures; (2) the alpha1alpha2 subunit

169 N-hydroxyureas react 25-80-fold faster with oxyhemoglobin than with N-hydroxyurea, suggesting other

170 In the presence of oxyhemoglobin, the half-life was further reduced to 2.9

171 a that contain an N-hydroxy group react with oxyhemoglobin to form methemoglobin and variable amounts

172 Exposure of frozen solutions of oxyhemoglobin to gamma-irradiation at 77 K yields EPR- a

173 themoglobin (metHb) and that autoxidation of oxyhemoglobin to metHb must occur prior to extraction.

174 of inhaled NO gas oxidized 85-90% of plasma oxyhemoglobin to methemoglobin, thereby inhibiting endog

175 neuron-microglia cocultures were exposed to oxyhemoglobin to mimic SAH in vitro.

176 rtial pressure is calculated as the ratio of oxyhemoglobin to oxy- plus deoxyhemoglobin.

177 of light and could measure only the ratio of oxyhemoglobin to total hemoglobin, displayed as SpO2.

178 Levels of deoxyhemoglobin, oxyhemoglobin, total hemoglobin, and microvascular oxyge

179 nit in hydrolyzing oxyhemoglobin and cleaved oxyhemoglobin twice as fast as deoxyhemoglobin.

180 istically significant increase, or flare, in oxyhemoglobin was observed in partial responding (n = 11

181 edox active and promote oxidation of soluble oxyhemoglobin, we incubated native versus iron-stripped

182 ustic signal (n = 9, P = 0.01) and increased oxyhemoglobin-weighted photoacoustic signal (n = 9, P <

183 obin (HbNO) in contrast to the reaction with oxyhemoglobin, which produces methemoglobin and nitrate

184 stimulation was prevented by the presence of oxyhemoglobin, which quenches nitric oxide, and by an in

185 omonas, 1133 cm(-1) for Synechocystis) in an oxyhemoglobin with an iron-porphyrin, this study also re

186 accelerated dioxygenation reaction of plasma oxyhemoglobin with endothelium-derived NO to form bioina

187 thionite), or transiently, by rapidly mixing oxyhemoglobin with nitrite and dithionite simultaneously

188 e data indicate that the reaction of NO with oxyhemoglobin within RBCs is limited by the diffusion of