ライフサイエンスコーパス: haemoglobin

1 tissue fluorophores (flavins) and absorbers (haemoglobin).

2 cription of HpuA's role in direct binding of haemoglobin.

3 de chains for packing against the surface of haemoglobin.

4 played no interference with the detection of haemoglobin.

5 les, is common in biological systems such as haemoglobin.

6 al constriction and desaturation of cortical haemoglobin.

7 ular imaging based on endogenous contrast of haemoglobin.

8 ne, and reduced levels of random glucose and haemoglobin.

9 concentrations, and deferrals because of low haemoglobin.

10 f the T. congolense receptor in complex with haemoglobin.

11 sickle-cell disease that are based on fetal haemoglobin.

12 .45), low albumin (0.10, 0.03-0.39), and low haemoglobin (0.72, 0.64-0.81) at baseline.

13 12 years, no signs of critical illness, and haemoglobin 100 g/L or lower (if aged 3 months or younge

14 ent adverse events were anaemia or decreased haemoglobin (45 [22%] patients), and elevations in alani

15 edema (9 [23%] of 40 patients) and decreased haemoglobin (6 [15%]).

16 tamine Hagedorn, NPH) while ANCOVAs compared haemoglobin A(1c) (HbA(1c)) and weight change.

17 0 years) with type 2 diabetes, high glycated haemoglobin A(1c) (HbA(1c)) concentrations (>7.5%; >58 m

18 The primary outcome was change in haemoglobin A(1c) (HbA(1c)) from baseline.

19 formin or sulfonylurea monotherapy with mean haemoglobin A(1c) (HbA(1c)) of 7.9% were randomly assign

20 e of less than 0.5 U/kg per day and glycated haemoglobin A(1c) (HbA(1C)) of less than 6.5% at 1 year.

21 y central randomisation to intensive (target haemoglobin A(1c) [HbA(1c)] of <6.0%) or standard (7.0-7

22 The mean haemoglobin A(1c) concentration (HbA(1c)) was 0.9% lower

23 mass index 30 kg/m(2) or higher, or glycated haemoglobin A(1c) greater than 6%.

24 primary outcome was change from baseline in haemoglobin A(1c)(HbA(1c)) at 24 weeks.

25 primary endpoint was improvement in glycated haemoglobin A(1c)(HbA(1c)) concentration and blood press

26 h exposures was prevented by the presence of haemoglobin (a NO scavenger), uric acid (a peroxynitrite

27 ded a small and non-significant increase for haemoglobin A1c (0.04% [-0.04 to 0.13]), p=0.290).

28 h established type 2 diabetes, mean glycated haemoglobin A1c (HbA1c) concentration of 67 mmol/mol (8.

29 The primary outcome was a change in glycated haemoglobin A1c (HbA1c) from baseline to week 26, with a

30 trol-specified as a decrease in glycosylated haemoglobin A1C (HbA1c) of >/=2% points over 3 months.

31 ears or older with type 2 diabetes, glycated haemoglobin A1c (HbA1c) of 7.0% or more, receiving metfo

32 8-80 years with type 2 diabetes and glycated haemoglobin A1c (HbA1c) of 7.0-9.5% on stable metformin

33 ive or inadequately controlled (glycosylated haemoglobin A1c [HbA1c] >/=7.0% to </=10.0%) patients wi

34 Mean glycated haemoglobin A1c concentrations were also higher in the f

35 ve at correcting hyperglycaemia and lowering haemoglobin A1c levels than Exendin-4, suggesting that G

36 e, total cholesterol, and glycaemic control (haemoglobin A1c) after 2 years.

37 t, fasting glucose, 2-h glucose and insulin, haemoglobin A1c, high-density lipoprotein or blood press

38 , lipid profile, glucose tolerance, glycated haemoglobin A1c, salivary cortisol, sitting height, and

39 bles including renal function, diabetes, and haemoglobin A1c.

40 .06-0.12), haemoglobin CC (0.27, 0.11-0.63), haemoglobin AC (0.83, 0.67-0.96), homozygous alpha-thala

41 44 reported data for haemoglobin AS, 19 for haemoglobin AC and CC, and 18 for alpha-thalassaemia.

42 S children than in HbAA children with normal haemoglobin (adjusted incidence rate ratio [aIRR] 0.66 [

43 sensitivity cardiac troponin T (cTnT-hs) and haemoglobin, age, and previous bleeding.

44 lobin were recorded in any individual in the haemoglobin analysis (n=70) during follow-up.

45 leading to a modest global increase in mean haemoglobin and a reduction in anaemia prevalence.

46 We obtained data about haemoglobin and anaemia for children aged 6-59 months an

47 protein cholesterol, triglycerides, glycated haemoglobin and C-reactive protein, participants were cl

48 atment groups for the stratification factors haemoglobin and corrected serum calcium.

49 However, many chromophores, such as haemoglobin and cytochromes, absorb but have undetectabl

50 tion, physical activity, cognitive function, haemoglobin and ferritin concentrations, and deferrals b

51 g men [for all listed symptoms]), lower mean haemoglobin and ferritin concentrations, and more deferr

52 Hydroxyurea increased haemoglobin and fetal haemoglobin, and decreased white b

53 Haemoglobin and haem fractionation assays suggest a mode

54 Treatment also increased haemoglobin and haematocrit, and decreased red blood cel

55 567, combined P = 5.5 x 10 - 8 adjusted for haemoglobin and hydroxyurea) and validated it in indepen

56 ress genes involved in capturing circulating haemoglobin and in iron regulation.

57 ositive correlation between mean corpuscular haemoglobin and in vitro growth of BCG in whole blood fr

58 e assembly of polypeptides and proteins like haemoglobin and its sickle cell mutation.

59 system, containing different combinations of haemoglobin and natural antioxidants (l-ascorbic acid an

60 nt in blood glucose, lipid profile, glycated haemoglobin and other parameters in streptozotocin-induc

61 ldren from those houses who were sampled for haemoglobin and parasitaemia.

62 gnificantly increased PTT and INR, decreased haemoglobin and platelet count).

63 al (ie, maternal and child anthropometry and haemoglobin and preterm birth) and socioenvironmental de

64 itation method, three proteins (tropomyosin, haemoglobin and the stress-shock protein ubiquitin) were

65 Hydroxyurea increased haemoglobin and fetal haemoglobin, and decreased white blood-cell count.

66 rate (ESR), C-reactive protein (CRP) values, haemoglobin, and leukocyte values.

67 n, mean corpuscular volume, mean corpuscular haemoglobin, and mean corpuscular haemoglobin concentrat

68 Cholesterols, fasting glucose, glycosylated haemoglobin, and proinflammatory markers in the blood as

69 score (age, biomarkers [GDF-15, cTnT-hs, and haemoglobin], and clinical history [previous bleeding])

70 re P. falciparum malaria in individuals with haemoglobin AS (OR 0.09, 95% CI 0.06-0.12), haemoglobin

71 o use as a transfusion trigger; the value of haemoglobin as a surrogate indicator for transfusion ben

72 However, ticks require dietary haemoglobin as an exogenous source of haem since, feedin

73 oea and endocarditis, and extracts haem from haemoglobin as an important iron source within the iron-

74 In meta-analysis of prospective trials only haemoglobin AS was consistently associated with protecti

75 62 identified studies, 44 reported data for haemoglobin AS, 19 for haemoglobin AC and CC, and 18 for

76 Haemoglobin AS, CC, and AC genotypes and homozygous and

77 gate the temporal switch from fetal to adult haemoglobin, as occurs in humans.

78 s revealed a well-defined reduction peak for haemoglobin at about -0.30 V (vs. Ag/AgCl) at the red bl

79 Mean glycated haemoglobin at baseline was 9% (75 mmol/mol) in both gro

80 primary endpoint was change in mean glycated haemoglobin between baseline and end of the randomised p

81 sify functional sequences and yet retain the haemoglobin binding function.

82 phenotype, hereditary persistence of foetal haemoglobin, borderline HbA(2), and congenital dyserythr

83 ein we report crystal structures of apo- and haemoglobin-bound HpuA, an essential component of this h

84 de recommending optimisation of glycosylated haemoglobin, but no trial results have shown unequivocal

85 Haemoglobin C (HbC) is one of the commonest structural h

86 lood cell variants were haemoglobin S (HbS), haemoglobin C (HbC), alpha thalassaemia, ABO blood group

87 centration and not absolute red cell mass of haemoglobin can be identified; and disagreement about th

88 haemoglobin AS (OR 0.09, 95% CI 0.06-0.12), haemoglobin CC (0.27, 0.11-0.63), haemoglobin AC (0.83,

89 The WHO Haemoglobin Colour Scale (HCS) is a simple, cheap quanti

90 and regional databases up to Nov 14, 2014, "haemoglobin colour scale" in alternative spellings publi

91 quire haem through the uptake of haptoglobin-haemoglobin complexes.

92 ary endpoints included frequency of anaemia (haemoglobin concentration <80 g/L) and parasitaemia at t

93 st common of which were anaemia or decreased haemoglobin concentration (70 [19%] vs one [1%]) and inc

94 fter CaO2 was reduced by 10% by lowering the haemoglobin concentration (isovolaemic haemodilution; Lo

95 logy Group (ECOG) performance status of 0-3, haemoglobin concentration 9 g/dL or higher, absolute neu

96 We established baseline haemoglobin concentration and eligibility over a 4-week

97 We estimated trends in the distributions of haemoglobin concentration and in the prevalence of anaem

98 s shown to be associated with differences in haemoglobin concentration at high altitude.

99 was the prevalence of anaemia, defined as a haemoglobin concentration below 110 g/L.

100 ndpoint was the mean within-person change in haemoglobin concentration during 28 days of study follow

101 orpuscular haemoglobin, and mean corpuscular haemoglobin concentration existed between those animals

102 l below 80 g/L) or liberal (transfusion when haemoglobin concentration fell below 100 g/L) RBC transf

103 g) to either a restrictive (transfusion when haemoglobin concentration fell below 80 g/L) or liberal

104 y of the arithmetic mean maximum decrease in haemoglobin concentration from enrolment to day 28 of fo

105 l improvement-erythroid (HI-E), defined as a haemoglobin concentration increase of 1.5 g/dL or higher

106 The primary outcome was mean change in haemoglobin concentration measured during the third trim

107 simple, cheap quantitative method to assess haemoglobin concentration outside of the laboratory.

108 gs, heart rate, systolic blood pressure, and haemoglobin concentration strongly discriminated safe di

109 societies, including the specification of a haemoglobin concentration threshold to use as a transfus

110 Mean last recorded haemoglobin concentration was 116 (SD 24) g/L for patien

111 haemolysis, and the mean maximum decrease in haemoglobin concentration was not associated with the do

112 reduces transfusion requirements, stabilises haemoglobin concentration, and improves quality of life.

113 status, alkaline phosphatase concentration, haemoglobin concentration, and investigator site.

114 trimoxazole use were current CD4 cell count, haemoglobin concentration, BMI, and previous WHO stage 3

115 nal assessments included blood counts, fetal haemoglobin concentration, chemistry profiles, spleen fu

116 no statistically significant differences in haemoglobin concentration, mean corpuscular volume, mean

117 's r 0.918-0.957) and was less influenced by haemoglobin concentration, number of RBCs and number of

118 s were recruitment rate, protocol adherence, haemoglobin concentration, RBC exposure, selection bias,

119 EGLN1 and EPAS1 genes, associated with lower haemoglobin concentration.

120 LSPAC), we examined associations of maternal haemoglobin concentrations (g/dL) in pregnancy with hayf

121 Secondary outcomes were the changes in haemoglobin concentrations 24 h and 28 days after transf

122 Low haemoglobin concentrations and anaemia are important ris

123 To investigate the relation between maternal haemoglobin concentrations in pregnancy and childhood re

124 rdiovascular disease, and with postoperative haemoglobin concentrations lower than 100 g/L within 3 d

125 The mean change in haemoglobin concentrations was 3.5 g/L (SD 16.1) in the

126 lly significant dose-dependent reductions in haemoglobin concentrations were the most common laborato

127 had recorded pre-delivery and post-delivery haemoglobin concentrations, and overall 1412 women deliv

128 In terms of effects on haemoglobin concentrations, neither oxytocin nor misopro

129 ns, changes of dose, and close monitoring of haemoglobin concentrations.

130 iogenesis, showed a significant reduction of haemoglobin content (54.2%) in sponges implanted into Sl

131 videnced by increased numbers of vessels and haemoglobin content in these implants.

132 in treatment one to three times per week for haemoglobin control in haemodialysis patients.

133 city of 55-90% of the predicted value, and a haemoglobin-corrected carbon monoxide diffusing capacity

134 Surprisingly, haemoglobin could be completely substituted by serum pro

135 sociations were observed with lung function, haemoglobin, creatinine, glucose levels or resting blood

136 , history of bleeding, and three biomarkers (haemoglobin, cTn-hs, and GDF-15 or cystatin C/CKD-EPI) w

137 n volumes remained stable for 12 months (ie, haemoglobin decrease not more than 15 g/L, platelet coun

138 d for cluster design, the mean difference in haemoglobin decreases between groups was not significant

139 rasite-encoded and its detoxification during haemoglobin degradation, critical to parasite survival,

140 th host haem, a product of parasite-mediated haemoglobin degradation.

141 In the second survey, haemoglobin density was measured and filter paper blood

142 exogenous source of haem since, feeding with haemoglobin-depleted serum led to aborted embryogenesis.

143 s female siblings fed either bovine blood or haemoglobin-depleted serum.

144 Haemoglobin-derived compounds, eumelanic pigments and pr

145 ticks do not acquire bioavailable iron from haemoglobin-derived haem.

146 ect current shift, arterial constriction and haemoglobin desaturation, lasting at least an hour.

147 th amplification of plasmepsin 2-3, encoding haemoglobin-digesting proteases, regardless of the locat

148 th amplification of plasmepsin 2-3, encoding haemoglobin-digesting proteases, regardless of the locat

149 , blood meal concentration, novel methods of haemoglobin digestion, haem detoxification, vitellogenes

150 of studying the electrochemical behaviour of haemoglobin directly from human blood, for various scien

151 Inherited haemoglobin disorders, including thalassaemia and sickle

152 esian hierarchical mixture model to estimate haemoglobin distributions and systematically addressed m

153 ntres have independently shown that heme and haemoglobin drive an atheroprotective macrophage subset.

154 EW: Several studies have recently shown that haemoglobin drives a novel macrophage subset that is pro

155 earance half-life were seen in patients with haemoglobin E (0.55 h; p=0.078), those of male sex (0.96

156 the co-inheritance of beta-thalassaemia with haemoglobin E resulting in haemoglobin E/beta-thalassaem

157 h 18 microsatellite markers and patients for haemoglobin E, alpha-thalassaemia, and a mutation of G6P

158 studies have investigated beta-thalassaemia, haemoglobin E, P. vivax malaria, or pregnancy-associated

159 thalassaemia with haemoglobin E resulting in haemoglobin E/beta-thalassaemia, have been described.

160 Haemoglobin electrophoresis by isoelectric focusing was

161 Patient underwent full blood count and haemoglobin electrophoresis to exclude thrombocytosis an

162 ctors that regulate the binding of oxygen to haemoglobin, explored the determinants of a human's accl

163 gh density lipoprotein cholesterol, glycated haemoglobin, fibrinogen, C-reactive protein and Framingh

164 The mean change from baseline haemoglobin for patients who had switched to intravenous

165 Supplementation of serum with haemoglobin fully restored egg fertility.

166 d were correlated with the level of glycated haemoglobin, glycaemic level, and time of disease onset.

167 in the RDT evaluation and 391 (children with haemoglobin >8.0 gm/dl) were followed-up to assess treat

168 At 6 months, mean glycated haemoglobin had decreased by 1.1% (SD 1.2; 12 mmol/mol,

169 macrophages, where it acts as a receptor for haemoglobin:haptoglobin complexes.

170 ation of NO signalling by demonstrating that haemoglobin (Hb) alpha (encoded by the HBA1 and HBA2 gen

171 Electrostatic interactions between haemoglobin (Hb) and muscle components of fish may be an

172 oietic response, resulting in near sea-level haemoglobin (Hb) concentration.

173 Furthermore, leakage of haemoglobin (Hb) inside the RBCs at high melittin concen

174 eased following the experimental addition of haemoglobin (Hb) or ferric iron, and reduced following a

175 e sphingonisne kinase 1 (Sphk1) activity and haemoglobin (Hb) oxygen (O2) release capacity.

176 ters for ferric hydroxamates and haemin (Hn)/haemoglobin (Hb) respectively.

177 arm: a negative intervention effect on mean haemoglobin (Hb) status (-2.6 g/l; 95% CI -4.5, -0.8; p

178 mince (pH 6), with added myoglobin (Mb) and haemoglobin (Hb), from bighead carp (Hypophthalmichthys

179 cts allosterically with the abnormal form of haemoglobin (Hb), HbS, in red blood cells (RBCs) from pa

180 en changes in IHL with those in glycosylated haemoglobin (HbA(1)c), body weight, and volume of abdomi

181 cacy endpoint was the change in glycosylated haemoglobin (HbA(1c)) concentration from baseline to the

182 combined cohorts, compared with the glycated haemoglobin (HbA(1c)) decile with the lowest hazard (med

183 The primary endpoint was change in glycated haemoglobin (HbA(1c)) from baseline to week 26.

184 t was a comparison of change in glycosylated haemoglobin (HbA(1c)) from baseline to week 52 between t

185 with type 2 diabetes mellitus and a glycated haemoglobin (HbA(1c)) of 7.0-10.0% after 3 months or mor

186 ormin, and at baseline had mean glycosylated haemoglobin (HbA(1c)) of 8.5% (SD 1.1), fasting plasma g

187 random capillary blood glucose and glycated haemoglobin (HbA(1c)) tests, a fasting capillary blood g

188 e primary outcome was change in glycosylated haemoglobin (HbA(1c)).

189 ome was change in proportion of glycosylated haemoglobin (HbA(1c)).

190 >/=18 years) with type 1 diabetes (glycated haemoglobin [HbA(1c)] </=10% [86 mmol/mol]), who had bee

191 d inadequate glycaemic control (glycosylated haemoglobin [HbA(1c)] 7.5-10.0%) on metformin (>or=1500

192 lerance test below 11.1 mmol/L, and glycated haemoglobin (HbA1c) <6%.

193 /day), aged 18 years or older, with glycated haemoglobin (HbA1c) 7.0% or greater (>/=53 mmol/mol) and

194 Anthropometry, glycated haemoglobin (HbA1c) and IgA tissue transglutaminase (tTg

195 d remission of diabetes, defined as glycated haemoglobin (HbA1c) of less than 6.5% (<48 mmol/mol) aft

196 se and insulin measures, as well as glycated haemoglobin (HbA1c), are used to diagnose and monitor di

197 MATERIAL/METHODS: Glycated haemoglobin (HbA1c), total cholesterol (TCH), high- and

198 iated with improvements in glucose, glycated haemoglobin (HbA1c), weight, waist circumference, anxiet

199 blood lipids, insulin, glucose, and glycated haemoglobin (HbA1c).

200 surement of serum uric acid and glycosylated haemoglobin (HbA1C).

201 y (pump or injections) and baseline glycated haemoglobin (HbA1c).

202 racellular vesicles (STBEVs) and free foetal haemoglobin (HbF) into the maternal circulation.

203 Sickle haemoglobin (HbS) is the most common and clinically sign

204 n 100 years since the first report of sickle haemoglobin (HbS).

205 ly occurring Hereditary Persistance of Fetal Haemoglobin (HPFH) -175T>C point mutation associated wit

206 ucei HpHbR in complex with human haptoglobin-haemoglobin (HpHb), revealing an elongated ligand-bindin

207 Global mean haemoglobin improved slightly between 1995 and 2011, fro

208 Herein, the detection of haemoglobin in human red blood cells on glassy carbon el

209 In addition, we could not consider haemoglobin in our analysis.

210 Lower maternal haemoglobin in pregnancy may be a risk factor for allerg

211 c and diastolic blood pressures and glycated haemoglobin in the 1958 British Birth Cohort (1958BC, up

212 Haemoglobin increased by a median of 26 g/L (IQR 21-31)

213 llosteric proteins, originally developed for haemoglobin, is an excellent model for acetylcholine rec

214 ct in the synthesis of beta-globin chains of haemoglobin, leading to the accumulation of free alpha-g

215 ing ribavirin required dose modification for haemoglobin less than 100 g/L or anaemia.

216 they received blood transfusion to maintain haemoglobin level at 100 g/L or higher, or restrictive t

217 n which they received blood transfusion when haemoglobin level was lower than 80 g/L or if they had s

218 e-induced AI in mice (indicated by increased haemoglobin level, serum iron, FPN expression and decrea

219 genetic variation associated with the fetal haemoglobin level, the mouse orthologue of which is nece

220 an 12 months, 11-15); patients with baseline haemoglobin levels 10 g/dL or greater (median 17 months,

221 ed inflammatory cytokine concentrations, low haemoglobin levels and high parasite density, suggesting

222 Lower haemoglobin levels and higher parasite densities were as

223 phenotype, with sustained elevation of blood haemoglobin levels into the normal range, reduced reticu

224 ian 17 months, 14-NA) than for patients with haemoglobin levels less than 10 g/dL (median 10 months,

225 n the 8 weeks before treatment (and baseline haemoglobin <10 g/dL), or high transfusion burden, defin

226 Anaemia (haemoglobin <11 g/dL) in late pregnancy was negatively a

227 pper arm circumference <23.5 cm) or anaemic (haemoglobin <110 g/L) at enrolment had a reduction in ea

228 .60-0.86; p=0.04) in anaemic pregnant women (haemoglobin <110g/L) as compared with non-anaemic pregna

229 per L; for patients with polycythaemia vera, haemoglobin <15.0 g/L without phlebotomy) with complete

230 V(O2peak), peak cardiac output (Q(peak)), haemoglobin mass (Hb(mass)) and blood volumes were asses

231 termination of the trial and the omission of haemoglobin measurement after day 42, resulting in an in

232 However, the first haemoglobin measurement in pregnancy (<18 weeks' gestati

233 The last haemoglobin measurement was also negatively associated w

234 The effect of natural antioxidants towards haemoglobin-mediated lipid oxidation during enzymatic hy

235 oactive metabolites rather than free NO from haemoglobin-mediated reduction of nitrite.

236 o SNAP, damage was only partially blocked by haemoglobin, melatonin, cyclosporin A and DPQ, but was n

237 nd severity of anaemia (total lymphocyte and haemoglobin model), because CD4 cell count is not routin

238 6% (48.2-71.4) with the total lymphocyte and haemoglobin model.

239 the amount of O(2) bound to the erythrocyte haemoglobin molecules, rather than the amount of O(2) in

240 d to quantify the relation between different haemoglobin mutations and malaria protection to strength

241 Baseline median haemoglobin of 10.3 g/dL (IQR 9.3-11.7) increased to 11.

242 nd in those with anaemia, as any increase in haemoglobin of 20 g/L or higher observed in at least two

243 er the run-in period, patients with glycated haemoglobin of 8.0-12.0% (64-108 mmol/mol) were randomly

244 monthly transfusions to maintain 30% sickle haemoglobin or lower, while those assigned to the altern

245 o creatinine, thyrotropin, calcium, glycated haemoglobin, or lithium measurements between Oct 1, 1982

246 es of using a biologically relevant process (haemoglobin oxidation), and not requiring the addition o

247 Similar trends were observed for serum and haemoglobin oxidation.

248 ctrum, thereby allowing facile assessment of haemoglobin oxygen levels, providing contrast from readi

249 n concentrations, and more deferrals for low haemoglobin (p<0.0001 for each) than those observed in t

250 Haemoglobin polymerisation, leading to erythrocyte rigid

251 undertaken blood tests (albumin, creatinine, haemoglobin, potassium, sodium, urea, and white blood ce

252 ex blood tests results (albumin, creatinine, haemoglobin, potassium, sodium, urea, white cell count a

253 ine plasma powder; seven peptides for bovine haemoglobin powder, including six peptides for bovine bl

254 mproved knowledge of the regulation of fetal haemoglobin production in human beings and the developme

255 Induction of fetal haemoglobin production is a promising strategy for the t

256 The electrochemical behavior of iron ion in haemoglobin provides insight to the chemical activity in

257 The haptoglobin-haemoglobin receptor (HpHbR) of African trypanosomes all

258 The haptoglobin-haemoglobin receptor of the African trypanosome species,

259 f trypanosome lytic factor 1 via haptoglobin-haemoglobin receptor.

260 occurs in the tsetse fly, where it acts as a haemoglobin receptor.

261 11A erythroid enhancer as a target for fetal haemoglobin reinduction.

262 ed cytotoxicity against eukaryotic cells and haemoglobin release from erythrocytes.

263 To address specific adaptations to the haemoglobin-rich diet, we compared the midgut transcript

264 Red blood cell variants were haemoglobin S (HbS), haemoglobin C (HbC), alpha thalassa

265 ), heart rate variability (HRV) and arterial haemoglobin saturation (S(aO(2))) were no different in 5

266 At task failure in normoxia (haemoglobin saturation (SpO2) approximately 94%, 656 +/-

267 ncrease in end-tidal P(CO(2)) and a 3% lower haemoglobin saturation.

268 le participants had haemoglobin SS (HbSS) or haemoglobin Sbeta(0)thalassaemia, were aged 9-18 months

269 tified age, smoking status, body mass index, haemoglobin, serum uric acid, serum albumin, albuminuria

270 contacts haptoglobin and the beta-subunit of haemoglobin, showing how the receptor selectively binds

271 decades has seen red blood cells (RBCs) and haemoglobin specifically emerge as prominent effectors i

272 Eligible participants had haemoglobin SS (HbSS) or haemoglobin Sbeta(0)thalassaemi

273 ible patients were aged at least 1 year, had haemoglobin SS or Sbeta(0)thalassaemia sickle-cell-disea

274 65 (97%) of 67 patients had the haemoglobin SS subtype and 54 (81%) were scheduled to un

275 erefore, be beneficial for patients with the haemoglobin SS subtype who are scheduled to undergo low-

276 Children's and women's haemoglobin statuses improved in some regions where conc

277 s the most common and clinically significant haemoglobin structural variant, but no contemporary esti

278 on channels to oxygen uptake and delivery by haemoglobin, structural changes are critical.

279 Using a database of sickle haemoglobin surveys, we created a contemporary global ma

280 derstanding of erythropoiesis in general and haemoglobin switching in particular.

281 Disorders of haemoglobin synthesis (thalassaemia) and structure (eg,

282 The loss of Atpif1 impairs haemoglobin synthesis in zebrafish, mouse and human haem

283 d type 2 diabetes do not meet their glycated haemoglobin targets and randomised controlled studies co

284 ival, haematological improvement measured by haemoglobin, time to next treatment, and patient-reporte

285 act in delaying the time required to oxidise haemoglobin to methaemoglobin.

286 int mutation in the beta-globin chain causes haemoglobin to polymerise within erythrocytes during deo

287 logy that have brought reactivation of fetal haemoglobin to the forefront of sickle-cell disease rese

288 e plasmepsins are involved in the parasite's haemoglobin-to-haemozoin conversion pathway, targeted by

289 ngly, the Sherpa and Tibetans share adaptive haemoglobin traits.

290 levels and might involve inhibition of host haemoglobin uptake into intra-erythrocytic parasites.

291 right coronary artery Z scores, age-adjusted haemoglobin values, duration of hospital stay, or any ot

292 n C (HbC) is one of the commonest structural haemoglobin variants in human populations.

293 Low haemoglobin was associated with higher ECP.

294 Maternal haemoglobin was not associated with offspring hayfever,

295 However, maternal haemoglobin was not associated with risk of childhood as

296 In 2011, concentrations of mean haemoglobin were lowest and anaemia prevalence was highe

297 ingful or statistically significant drops in haemoglobin were recorded in any individual in the haemo

298 haemolysis and anaemia by increasing foetal haemoglobin, which leads to lower hypoxic transcriptiona

299 ECISE-DAPT score (age, creatinine clearance, haemoglobin, white-blood-cell count, and previous sponta

300 Ferritin, haemoglobin with erythrocyte indices and serum iron were