ライフサイエンスコーパス: Hb

1 incidence; 39 +/- 16 to 33 +/- 17 bursts.100 Hb(-1) ; P = 0.01) and diastolic operating pressure (82

2 Only 10-18% Hb was rinsed away in (i), and the effect of this rinsin

3 RBC populations to a resolution of 1 x 10(7) Hb molecules per cell (4 x 10(7) atoms of Fe per cell or

4 We demonstrate that this N9 NA has an active Hb site which binds to sialic acid, which enhances overa

5 ion and P(50) , an index of oxygen affinity [Hb = -0.3135(P(50) ) + 23.636].

6 e insufficient to provide protection against Hb-driven disease processes in conditions such as sickle

7 aseline resolution is achieved between alpha-Hb, beta-Hb, and glycated beta-Hb.

8 His mother has Sickle cell anaemia (Hb SS) and his father is a carrier of heterozygous alpha

9 maquine developed moderately severe anaemia (Hb < 8 g/dL).

10 and the interaction between ssDNA2-NH(2) and Hb with the ratio 1:1 was characterized by agarose gel.

11 sor towards acrylamide due to acrylamide and Hb adducts and change of reduction/oxidation process of

12 Bland-Altman plots for AbsCD4, CD4%, and Hb levels demonstrated close agreement between the BD FA

13 e 95% CI of the slopes for AbsCD4, CD4%, and Hb levels were 0.94-0.99, 0.99-1.01 and 0.86-0.93, respe

14 ar correlation between the AbsCD4, CD4%, and Hb values generated by the two platforms.

15 A comparison of the Hb-free and Hb-bound forms reveals that Hb binding alters the positi

16 evel, reticulocyte count, G6PD genotype, and Hb type.

17 d differences in interactions between Hp and Hb are not yet fully understood.

18 agnitude larger than the prefactor of Mb and Hb ( approximately 10(9) s(-1)).

19 factors associated with CO binding in Mb and Hb.

20 To estimate RBF, at least WBF and Hb are needed.

21 ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone-based ch

22 5% CI: 95,574-141,505), 91 (88%) had anemia (Hb < 10 g/dL) at presentation.

23 nt with a variable fraction below the anemic Hb concentration, the distribution around the mean has a

24 58.5%) of the children surveyed were anemic (Hb level: 9.75 g/dL [9.59-9.91]).

25 g ice-storage were studied: (i) rinsing away Hb with water or 0.9% NaCl with/without antioxidants (Du

26 Anemia was defined as baseline Hb (hemoglobin) <12 g/dL for men and <11 g/dL for women.

27 Besides Hb, iron is an obligate component of mitochondrial enzym

28 between alpha-Hb, beta-Hb, and glycated beta-Hb.

29 esolution is achieved between alpha-Hb, beta-Hb, and glycated beta-Hb.

30 her our data indicate an association between Hb/iron levels and BCG growth in vitro, which may in par

31 to recognizing the complex interplay between Hb (hemoglobin) and oxygen, carbon dioxide, and nitric o

32 he understanding of the relationship between Hb and magnetism has enabled the quantitative measuremen

33 Different Hp genotypes bind Hb with different affinities, with Hp 2-2 being the weak

34 the fraction of RBCs that are below the bulk Hb concentration that defines anemia varies not only fro

35 n HF can or cannot be generally inferred by [Hb] measurements and clinical correlates remains unclear

36 cking velocimetry system, and the calculated Hb concentration from these measurements was compared to

37 e (CD4%) and total hemoglobin concentration (Hb) in capillary and venous blood samples of HIV-negativ

38 metry (SpO2%), and hemoglobin concentration (Hb).

39 nosed according to hemoglobin concentration [Hb], hence may be the result of hemodilution or true red

40 rom apart trigger heme release by contacting Hb's F-helix.

41 ing SFOL, RBF, Hct, Hb, and mean corpuscular Hb content (MCHC) from prefortification (1988-1994) and

42 lly reduced graphene oxide-chitosan (ERGO-CS/Hb/FTO) based biocompatible coatings.

43 on reveal the successful grafting of ERGO-CS/Hb/FTO.

44 The CSF Hb concentration after high-volume and low-volume aSAH w

45 om 9.1 to 10.3 g/dL; P < .001) and decreased Hb S (from 39.7% to 24.3%; P < .001).

46 Early preclinical data have described Hb as a brain nucleus activated in anticipation of avers

47 n contacts primarily function to destabilize Hb-heme interactions, thereby lowering DeltaH(*), while

48 XT-4000i hematology analyzer for determining Hb levels.

49 domains, which correlated with differential Hb-bound loci in each neuroblast.

50 d genetically confirmed sickle cell disease (Hb SS) or sickle beta thalassemia (Hb Sbeta), and underw

51 omains in the receptor to transiently engage Hb to remove its heme.

52 ve adapted to high altitude through enhanced Hb binding affinity for oxygen.

53 ng HbYX, RYX, or RHbX C-terminal extensions (Hb, hydrophobic moiety; R, arginine; Y, tyrosine; X, any

54 to actively extract heme from extracellular Hb.

55 restricts the availability of extracellular Hb-bound iron to invading pathogens.

56 examine faecal haemoglobin concentrations (f-Hb), assist in deciding who would benefit from colonosco

57 n one NHS Board in Scotland were examined: f-Hb was estimated using one HM-JACKarc FIT system (Kyowa

58 n group A, 252 of 296 (85.1%) with SBD had f-Hb > 10 mug Hb/g faeces, as did 528 of 1151 (45.8%) with

59 o returned a specimen for FIT analysis had f-Hb >=10 mug Hb/g faeces.

60 In group B, although 95.2% had f-Hb < 10 mug Hb/g faeces, 1371 (53.7%) had FAST score >=

61 ore did not seem to enhance the utility of f-Hb alone.

62 We investigated if the published f-Hb, age and sex test score (FAST score) added value.

63 , 1447 had colonoscopy data as well as the f-Hb result (group A): 2521 patients, also with f-Hb, were

64 result (group A): 2521 patients, also with f-Hb, were not immediately referred (group B).

65 ted with authentic NO to form nitrosyl(FeII)-Hb, the proposed precursor of SNO-Hb.

66 the globin chains: from paramagnetic ferrous Hb to diamagnetic ferrous oxyhemoglobin (oxyHb) with rev

67 S betaF41Y and betaF41Y/K82D enhanced ferryl Hb reduction by providing a pathway for electrons to red

68 IsdH(N2) accounted for the high affinity for Hb-Hp complexes.

69 and Sysmex XT-4000i hematology analyzer for Hb concentrations in resource-limited settings thus, imp

70 their assemblies influence Hp's capacity for Hb binding.

71 es in patients have established evidence for Hb involvement in major depression, addiction, and schiz

72 resis-mass spectrometry screening method for Hb proteoforms including sequence variants and modified

73 bin therapeutics to target 'toxic' cell-free Hb exposures.

74 , leaving IsdH unable to wrest the heme from Hb.

75 tract the oxidized form of heme (hemin) from Hb, IsdH and IsdB.

76 form a bridge through which heme moves from Hb to the receptor.

77 chanisms that may promote hemin release from Hb by altering the position of its F helix.

78 Thus, IsdH triggers heme release from Hb via a flexible, low-affinity interface that forms fle

79 SNO-Hb itself, whereby SNO is released from Hb and RBCs during deoxygenation, in proportion to the d

80 propose a model for IsdB heme transfer from Hb that involves unfolding of Hb and heme iron ligand ex

81 lds of 6.6 U/g Hb (70% activity) and 2.8 U/g Hb (30% activity).

82 normal (G6PDn) control samples was 10.0 U/g Hb (6.3-14.0) for the Trinity assay and 8.3 U/g Hb (6.8-

83 (6.3-14.0) for the Trinity assay and 8.3 U/g Hb (6.8-15.6) for the Randox assay.

84 b, yielding diagnostic thresholds of 6.6 U/g Hb (70% activity) and 2.8 U/g Hb (30% activity).

85 % G6PD activity) varied from 5.7 to 12.6 U/g Hb (p < 0.001).

86 of 100% G6PD activity was defined as 9.4 U/g Hb, yielding diagnostic thresholds of 6.6 U/g Hb (70% ac

87 in control measurements (from 0.1 to 1.5 U/g Hb; p < 0.001) and study-wise mean coefficient of variat

88 Quantification of glycated Hb was in good correlation with the results obtained in

89 In clinical routine analysis of glycated Hb, sequence variants or other Hb proteoforms can cause

90 The habenula (Hb) is a central structure connecting forebrain to midbr

91 ar function in humans ABSTRACT: Haemoglobin (Hb) may impact the transduction of endothelium-dependent

92 photometry result in U/gHb, and haemoglobin (Hb) reading.

93 rcumference [MUAC], oedema) and haemoglobin (Hb) were measured in children aged 6-59 months following

94 emorrhage (aSAH), extracellular haemoglobin (Hb) in the subarachnoid space is bound by haptoglobin, n

95 s exhibit an acute reduction in haemoglobin (Hb) binding affinity for oxygen that facilitates adaptat

96 Lower haemoglobin (Hb) and high WBC counts were also significantly differen

97 ive intervention effect on mean haemoglobin (Hb) status (-2.6 g/l; 95% CI -4.5, -0.8; p = 0.005).

98 Furthermore, leakage of haemoglobin (Hb) inside the RBCs at high melittin concentration was a

99 ng the experimental addition of haemoglobin (Hb) or ferric iron, and reduced following addition of th

100 ecdysteroid glycosyltransferase, Hba_07292 (Hb-ugt-1), which was previously identified in the hemoly

101 e Hct (population median); #4) estimate Hct (Hb/MCHC); #5) assume SFOL = 0 and estimate Hct; and #6)

102 Using SFOL, RBF, Hct, Hb, and mean corpuscular Hb content (MCHC) from preforti

103 acid binding site, termed the hemadsorption (Hb) site, which is discrete from the enzymatically activ

104 tion was measured using the portable HemoCue Hb 201+ (HemoCue AB, Angelholm, Sweden) and a capillary

105 Hemoglobin (Hb) Bart's hydrops fetalis syndrome (BHFS) resulting fro

106 Hemoglobin (Hb) constitutes an important protein in clinical diagnos

107 Hemoglobin (Hb) data are limited in Southeast Asian glucose-6-phosph

108 Hemoglobin (Hb) multiplicity is common in fish, yet despite its ubiq

109 Hemoglobin (Hb) represents a model protein to study molecular adapta

110 ell disease (SCD) results from a hemoglobin (Hb) mutation betaGlu6 -> betaVal6 that changes normal Hb

111 od cells as the raw material and hemoglobin (Hb) embedded with ultrasmall hydroxyapatite (HAP, Ca(10)

112 stems such as myoglobin (Mb) and hemoglobin (Hb).

113 bits lipid oxidation promoted by hemoglobin (Hb) is important for its applications in muscle foods.

114 gen (O2) delivery facilitated by hemoglobin (Hb)-based O2 carriers (HBOCs) is a promising strategy to

115 sing double stranded DNA (dsDNA)/Hemoglobin (Hb)-modified screen printed gold electrode (SPGE) was de

116 immunochemical tests (FITs) for hemoglobin (Hb) are used in colorectal cancer screening.

117 is and accumulation of cell-free hemoglobin (Hb) in the circulation or in confined tissue compartment

118 s aureus that extracts heme from hemoglobin (Hb) to enable growth on Hb as a sole iron source.

119 ins iron by extracting heme from hemoglobin (Hb) using the closely related IsdB and IsdH surface rece

120 e S. aureus to extract heme from hemoglobin (Hb), transport it into the bacterial cytoplasm, and ulti

121 o model systems tetrameric human hemoglobin (Hb) and human IgG4.

122 Using human hemoglobin (Hb), we demonstrate the ability of the chip to perform h

123 ctions, acquires iron from human hemoglobin (Hb).

124 mance despite minimal changes in hemoglobin (Hb).

125 Transfusions increased hemoglobin (Hb; from 9.1 to 10.3 g/dL; P < .001) and decreased Hb S

126 The magnetic characteristics of hemoglobin (Hb) changes with the binding of dioxygen (O2) to the hem

127 ly by increasing the affinity of hemoglobin (Hb) for oxygen (O(2)).

128 CD by modulating the affinity of hemoglobin (Hb) for oxygen, thus inhibiting HbS polymerization and d

129 n measuring the concentration of hemoglobin (Hb) in blood.

130 de based on redox active protein hemoglobin (Hb) has been offered here for the determination of methy

131 beta93C) to form S-nitroso (SNO) hemoglobin (Hb) is claimed to be essential for export of nitric oxid

132 ein was detected relative to the hemoglobin (Hb) fraction.

133 on their high susceptibility to hemoglobin (Hb)-mediated lipid oxidation.

134 bin protein (Hp) scavenges toxic hemoglobin (Hb) leaked into the bloodstream from erythrocytes.

135 r Hct are sometimes unavailable; hemoglobin (Hb) is generally available in surveys.

136 ssigned to either a restrictive (hemoglobin [Hb] threshold < 70 g/L) or liberal (Hb threshold < 90 g/

137 G6PD deficiency (P = <.001), higher Hb concentration at baseline (P = <.001), higher parasit

138 CMS subjects had lower SpO2, higher Hb, higher brain blood density, lower mean cerebral bloo

139 Furthermore, we noted that the Hp-Hb binding appears to trap IsdH in an initial state befo

140 here we measured heme extraction from the Hp-Hb complex by UV-visible spectroscopy and determined the

141 d determined the crystal structure of the Hp-Hb-IsdH complex at 2.9 angstrom resolution.

142 Human Hb research is still nascent but develops rapidly, along

143 V-Vis spectroscopy studies of adducted human Hb that revealed loss of alpha-helical content and deoxy

144 crystal structure of a complex between human Hb and IsdB.

145 y reported adduction of beta(93)Cys of human Hb, two novel sites of adduction were found; alpha(104)C

146 se phenotypes, we examined recombinant human Hb (rHb) Kirklareli containing the alpha H58L replacemen

147 th Hb concentration, highlighting that human Hb variants can serve as 'experiments of nature' to addr

148 sic temporal transcription factor Hunchback (Hb) specifically in the NB7-1 stem cell, which produces

149 of reduction/oxidation process of Hb-Fe(III)/Hb-Fe(II) was determined by square wave voltammetry (SWV

150 oelectrode has been designed by immobilizing Hb on electrochemically reduced graphene oxide-chitosan

151 f allosteric regulation of oxygen binding in Hb in the stereochemical model of Perutz, to blood flow

152 The primary end point was the change in Hb at day 7.

153 was associated with the greatest decrease in Hb level and 1 blood transfusion, followed by clinically

154 P = .027) influenced the initial decrease in Hb level, calculated as the nadir level minus the baseli

155 wed by clinically insignificant decreases in Hb levels.

156 y (CTV), we are able to detect difference in Hb concentration in two RBC populations to a resolution

157 This difference in Hb concentration was the result of routine RBC storage;

158 In G6PD-deficient patients the drop in Hb was 0.63 g/dL (95% CI 0.03, 1.24) greater in those wh

159 olinergic signaling and cell excitability in Hb-IP circuits, a key pathway involved in nicotine depen

160 However, the fall in Hb concentration at day 7 was greater in G6PD-deficient

161 n of this system through genetic mutation in Hb or through disease is a common factor in oxygenation

162 a subunits (F41Y), a substitution present in Hb Mequon; the second contained the Asp (K82D) found in

163 The mean reduction in Hb at day 7 was similar in each group, a difference in t

164 In G6PD-normal patients, the reduction in Hb was 0.22 g/dL (95% CI -0.08, 0.52) less in those who

165 We hypothesized that an acute reduction in [Hb] and haematocrit (Hct) would increase brachial artery

166 hematologic improvements including increased Hb and reduction in hemolysis and percentage of sickled

167 tic aldehydes, with the intent of increasing Hb affinity for O(2) with subsequent prevention of RBC s

168 components of the habenulo-interpeduncular (Hb-IP) circuit is unknown.

169 oxidative changes occurring in intracellular Hb obtained from RBCs and RBC-derived microparticles (MP

170 of S. aureus, and a ternary complex of IsdB.Hb.Hp was observed.

171 oglobin [Hb] threshold < 70 g/L) or liberal (Hb threshold < 90 g/L) RBC transfusion strategy between

172 evious studies have indicated that RBCs lose Hb during ex vivo storage; however, it is not known if t

173 and reduced O(2) saturation, along with low Hb and leukocytosis, were important predictors for the d

174 PaO2 was no different between CON and Low [Hb], although CaO2 was 10.4%, 9.2% and 9.8% lower at 18%

175 dies including HF patients with anemia (low [Hb]) (7 studies, n=127), whereas only 2 of 10 studies in

176 ng body size-related adaptation of mammalian Hb.

177 We found that mammalian Hb cooperativity values all reside on a ridge of maximum

178 A 3:1 ratio of Mb:Hb promoted lipid oxidation similarly compared to adding

179 milarly compared to adding a 1:1 ratio of Mb:Hb to washed muscle.

180 Mean Hb concentrations at baseline (ie, day 0) were similar b

181 hotometry, the standard method for measuring Hb in clinical laboratories.

182 nfers benefits in chronic HF despite minimal Hb changes.

183 showed enhanced effects on Hb modification, Hb-O(2) affinity, and sickling inhibition, with sustaine

184 th 2 consecutive fHb concentrations of 0 mug Hb/g (P < .001).

185 nufacturers' thresholds (range, 2.0-17.0 mug Hb/g feces), at a uniform threshold (15 mug Hb/g feces),

186 baseline (below the cut-off value of 10 mug Hb/ g feces).

187 In group B, although 95.2% had f-Hb < 10 mug Hb/g faeces, 1371 (53.7%) had FAST score >= 2.12: clinic

188 52 of 296 (85.1%) with SBD had f-Hb > 10 mug Hb/g faeces, as did 528 of 1151 (45.8%) without SBD.

189 apan) with a cut-off for positivity >=10 mug Hb/g faeces.

190 specimen for FIT analysis had f-Hb >=10 mug Hb/g faeces.

191 T result (hemoglobin concentration of 10 mug Hb/g feces) were invited for consultation and scheduled

192 Hb/g feces), at a uniform threshold (15 mug Hb/g feces), and at adjusted thresholds yielding defined

193 est at 2 predefined cutoffs (10.2 and 17-mug Hb/g stool) for detecting advanced neoplasms (colorectal

194 I, -5.7% to 17.5%, P = .32) at cutoff 17-mug Hb/g stool.

195 -3.1% to 22.2%, P = .14) at cutoff 10.2-mug Hb/g stool and 28.6% in the aspirin and 22.5% in the pla

196 e FIT result was increased from 15 to 47 mug Hb/g feces halfway through 2014.

197 th 2 consecutive fHb concentrations of 8 mug Hb/g had a 14-fold increase in risk of AN compared with

198 NMR studies of the 220 kDa IsdH(N2N3):Hb complex reveal that it is dynamic, with persistent in

199 ging the crystal structure of the IsdH(N2N3):Hb complex, we have probed the mechanism of heme capture

200 % for every g/dL drop in postoperative nadir Hb [95% confidence interval (95% CI): 41-45].

201 particularly evident at postoperative nadir Hb values below 10 gm/dL.

202 ated intra-RBC concentrations of the natural Hb effector, 2,3-diphosphoglycerate.

203 space is bound by haptoglobin, neutralising Hb toxicity and helping its clearance.

204 ion betaGlu6 -> betaVal6 that changes normal Hb (HbA) into sickle Hb (HbS).

205 -2.0; 95% CI, -3.7 to -0.3; P=0.04), but not Hb (2.4 g/L; 95% CI, -3.5 to 8.4; P=0.41).

206 Reducing the activity of Hb-IP nAChRs, either volitionally during smoking cessati

207 hought to determine molecular adaptations of Hb.

208 human plasma and an efficient antagonist of Hb toxicity resulting from physiological red blood cell

209 ed the Asp (K82D) found in the beta cleft of Hb Providence; and the third had both of these beta subs

210 Here, we discuss key concepts of Hb toxicity and provide a perspective on the use of hapt

211 y of SNO formation at the beta93 cysteine of Hb.

212 eoxygenation, in proportion to the degree of Hb deoxygenation, to regulate vessels directly.

213 This has prompted the development of Hb modifiers, such as aromatic aldehydes, with the inten

214 s further elucidation of the distribution of Hb concentration within RBCs from a donor sample to be d

215 n if this variability in the distribution of Hb content is a function of the age of the RBCs in a don

216 Expression of Hb genes correlated positively with mycobacterial growth

217 We find that prolonged expression of Hb leads to transient specification of U MN identity, an

218 The HDX of Hb at 0.14-1.1 s, resolved to peptide segments, correlat

219 On-chip HDX of Hb at time points ranging from 0.14-1.1 s demonstrates t

220 e method of blood sampling and the method of Hb measurement.

221 rstanding that centers on S-nitrosylation of Hb (ie, S-nitrosohemoglobin; SNO-Hb) as a purveyor of ox

222 When multiplied over the number of Hb molecules in a red blood cell (RBC), the effect is de

223 it lipid oxidation and suppress oxidation of Hb to form methemoglobin and ferryl hemoglobin were pH-d

224 tionale: Intraerythrocytic polymerization of Hb S promotes hemolysis and vasoocclusive events in the

225 and change of reduction/oxidation process of Hb-Fe(III)/Hb-Fe(II) was determined by square wave volta

226 d post-translational modifications (PTMs) of Hb and red blood cell (RBC) membrane proteins of transge

227 We also observe that atypical residues of Hb, His(58) and His(89) of alphaHb, coordinate to the he

228 ning protein regions in the alpha subunit of Hb, revealing new protected Hb regions that were not obs

229 In this complex, the alpha subunits of Hb are refolded with the heme displaced to the interface

230 oxidation of betaCys93 and ubiquitination of Hb betaLys145 (and betaLys96).

231 transfer from Hb that involves unfolding of Hb and heme iron ligand exchange.

232 These compounds showed enhanced effects on Hb modification, Hb-O(2) affinity, and sickling inhibiti

233 ically important both for in vitro growth on Hb and in infection models and is also highly up-regulat

234 eme from hemoglobin (Hb) to enable growth on Hb as a sole iron source.

235 Haptoglobin binds to a distinct site on Hb to inhibit heme transfer to IsdB and growth of S. aur

236 atus mainly concurs with diagnosis based on [Hb] and presents negative relationships with age, female

237 s of glycated Hb, sequence variants or other Hb proteoforms can cause interference, resulting in wron

238 concentration of oxygenated hemoglobin ([oxy-Hb]) in the cerebral cortex.

239 Notably, [oxy-Hb] change in the left dorsolateral prefrontal cortex du

240 Our results suggest that [oxy-Hb] change in the prefrontal cortex during the sustained

241 The [oxy-Hb] change during the sustained attention task (SAT) was

242 We found that the [oxy-Hb] change during the verbal fluency task (VFT) was redu

243 ors: the former with an aromatic penultimate Hb residue and the latter with the HbYX motif.

244 s the translational potential of preclinical Hb research.

245 alpha subunit of Hb, revealing new protected Hb regions that were not observed with pepsin.

246 Purified Hb auto-oxidized to metHb more rapidly than Hb in the he

247 Purified Hb promoted lipid oxidation in washed muscle slightly bu

248 rosocysteine or with hemolysates or purified Hb treated with authentic NO to form nitrosyl(FeII)-Hb,

249 f catalase and peroxiredoxin in the purified Hb.

250 x expression and reduced pupation rates in r Hb-ugt-1-injected larvae.

251 Injection of recombinant Hb-ugt-1 (rHb-ugt-1) into Drosophila melanogaster flies

252 lococcus aureus, which utilizes the released Hb as an iron source.

253 me (BV) and intravascular oxygen saturation (Hb(sat)) acquired concurrently using a wide-field multic

254 Mean (SD) Hb level was 133.7 (9.89) g/L and 130.00 (10.48) g/L amo

255 Nonetheless, our data show Hb acts as a potent regulator of neuromuscular wiring de

256 erythrocyte S1P binds to deoxygenated sickle Hb (deoxyHbS), facilitates deoxyHbS anchoring to the mem

257 al6 that changes normal Hb (HbA) into sickle Hb (HbS).

258 S-nitrosothiol (SNO)-replete RBCs and by SNO-Hb itself, whereby SNO is released from Hb and RBCs duri

259 for nitrite () and S-nitrosohemoglobin (SNO-Hb) widely contested given their ability to transduce ni

260 sylation of Hb (ie, S-nitrosohemoglobin; SNO-Hb) as a purveyor of oxygen-dependent vasodilatory activ

261 osyl(FeII)-Hb, the proposed precursor of SNO-Hb.

262 bserve any gradients consistent with RBC SNO-Hb consumption and corresponding delivery of plasma S-ni

263 ditional conformation changes to the T-state Hb.

264 Not surprisingly, Hb dysfunction has been associated with psychiatric diso

265 ;) energetic marker), iron status, symptoms, Hb, exercise capacity, and safety.

266 disease (Hb SS) or sickle beta thalassemia (Hb Sbeta), and underwent allogeneic haematopoietic cell

267 Hb auto-oxidized to metHb more rapidly than Hb in the hemolysate (P<0.05).

268 ase activity, these results demonstrate that Hb-ugt-1 is an immunosuppressive factor and that its act

269 data provide support for the hypothesis that Hb isoform switching can provide a physiological benefit

270 Here we explore the hypothesis that Hb multiplicity plays a role in hypoxia tolerance using

271 Recently, we reported that Hb-dependent oxidative stress induced post-translational

272 H(N1), IsdH(N2), and IsdH(N3), revealed that Hb binding of IsdH(N1) and IsdH(N2) accounted for the hi

273 the Hb-free and Hb-bound forms reveals that Hb binding alters the positioning of the N2 domain.

274 extend the current knowledge by showing that Hb binding does not just depend on the donor's genotype,

275 Here, we suggest that Hb affinity and cooperativity reflect evolutionary and p

276 Haptoglobin and the Hb clearance pathway are therapeutic targets after aSAH.

277 nteraction between -OH groups in HAP and the Hb in RBCs.

278 roartemisinin/piperaquine and determined the Hb level, reticulocyte count, G6PD genotype, and Hb type

279 ox-dependent heme extraction, when Hb in the Hb-Hp complex was in the oxidized met form but not in th

280 ensitization of cholinergic circuitry in the Hb-IP system.

281 Haptoglobin is the Hb binding and clearance protein in human plasma and an

282 enabled the quantitative measurement of the Hb content in a single red blood cell, RBC, based on mag

283 t Hp binding prevents local unfolding of the Hb heme pocket, leaving IsdH unable to wrest the heme fr

284 ral features of the crystal structure of the Hb tetramer, with helices exhibiting no or minor HDX and

285 A comparison of the Hb-free and Hb-bound forms reveals that Hb binding alter

286 an literature on anatomy and function of the Hb.

287 ing activity despite moderate effects on the Hb-O(2) affinity, which we attribute to an O(2)-independ

288 was, respectively, higher and lower than the Hb-binding capacity of CSF haptoglobin.

289 vidence has now accumulated to show that the Hb encodes both rewarding and aversive aspects of extern

290 led that RBCs lose, on average, 17% of their Hb after 42 days of storage, the maximum FDA-approved le

291 miological data exist on the impact of these Hb variants on PAM.

292 inity and cooperativity of oxygen binding to Hb affect tissue oxygen delivery, only the former was th

293 at 23, a compound that specifically binds to Hb with nanomolar affinity and displays strong partition

294 In this study, cNIC-mediated changes to Hb-IP nAChR function were examined in mouse (male and fe

295 Lipid oxidation products due to Hb-mediated lipid oxidation were elevated 60-fold at pH

296 After HCT, mean pre-transfusion Hb levels were 70.9 g/L in the restrictive-strategy grou

297 SNO-RBCs or NO-treated Hb induced vasorelaxation, with no differences between b

298 ibited redox-dependent heme extraction, when Hb in the Hb-Hp complex was in the oxidized met form but

299 me transfer yet formed a stable complex with Hb (Kd = 6 +/- 2 mum) in solution with spectroscopic fea

300 alterations in P(50) associate directly with Hb concentration, highlighting that human Hb variants ca

301 alyses, RBCV was positively associated with [Hb] (B=6.10, SE=1.44) and negatively associated with age