ライフサイエンスコーパス: oxyhemoglobin

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

2 ecular replacement phases derived from human oxyhemoglobin.

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

4 tion by glucose treatment can be reversed by oxyhemoglobin.

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

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

7 s contrasted to the diamagnetic character of oxyhemoglobin.

8 nterbalanced by an equal initial decrease in oxyhemoglobin.

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

10 d to an electronic structural formulation of oxyhemoglobin.

11 ff of resonance with the Soret transition of 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 de (NO), mediated by NO scavenging by plasma oxyhemoglobin and by arginine degradation by plasma argi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 Oxyhemoglobin concentration (HbO) was correlated with th

44 Moreover, the oxyhemoglobin concentration changes elicited by a syllab

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Sleep disruption and arterial oxyhemoglobin desaturation were significantly more sever

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

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

61 pnea result in sleep disruption and arterial oxyhemoglobin desaturation.

62 Patients exhibiting oxyhemoglobin desaturations at night showed higher plasm

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

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

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

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

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

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

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

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

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

72 Oxyhemoglobin flare on day 1 was adequate to discriminat

73 Oxyhemoglobin had no significant effect on the maintenan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 -1 DNA-binding activity was not blocked with oxyhemoglobin, nor was it related to the rate of NO evol

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 ripped sickle or normal ghost membranes with oxyhemoglobin S.

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

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

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

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

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

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

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

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

127 Oxyhemoglobin saturation in the superior vena cava, righ

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

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

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

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

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

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

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

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

136 the tissue oxygen tension and the capillary oxyhemoglobin saturation.

137 obin formation was inversely proportional to oxyhemoglobin saturation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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