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1 tissue fluorophores (flavins) and absorbers (haemoglobin).
2 P = 0.03] without significant differences in haemoglobin.
3 with a small but significant improvement in haemoglobin.
4 les, is common in biological systems such as haemoglobin.
5 ne, and reduced levels of random glucose and haemoglobin.
6 concentrations, and deferrals because of low haemoglobin.
7 f the T. congolense receptor in complex with haemoglobin.
8 sickle-cell disease that are based on fetal haemoglobin.
9 cription of HpuA's role in direct binding of haemoglobin.
10 de chains for packing against the surface of haemoglobin.
11 ly adapted to hypoxia and have high affinity haemoglobin.
12 12 years, no signs of critical illness, and haemoglobin 100 g/L or lower (if aged 3 months or younge
13 ent adverse events were anaemia or decreased haemoglobin (45 [22%] patients), and elevations in alani
15 f grade 3 or higher was anaemia or decreased haemoglobin (80 [22%] patients in the rucaparib group vs
16 orrectly spliced beta-globin mRNA and led to haemoglobin A synthesis, and consequently improved thala
18 ssays to elucidate the origins of vertebrate haemoglobin, a heterotetramer of paralogous alpha- and b
19 enrolment, and centrally confirmed glycated haemoglobin A1c (HbA(1c)) of 48-58 mmol/mol (6.5-7.5%) a
21 abetic patients, including disease duration, haemoglobin A1c (HbA1c) levels and urine albumin creatin
22 trol-specified as a decrease in glycosylated haemoglobin A1C (HbA1c) of >/=2% points over 3 months.
24 ng: achievement of all recommended levels of haemoglobin A1c (HbA1c), BP, and cholesterol; risky pres
25 ve at correcting hyperglycaemia and lowering haemoglobin A1c levels than Exendin-4, suggesting that G
26 ratory data including serum fasting glucose, haemoglobin A1c levels, creatinine levels, and the urina
27 t, fasting glucose, 2-h glucose and insulin, haemoglobin A1c, high-density lipoprotein or blood press
28 , lipid profile, glucose tolerance, glycated haemoglobin A1c, salivary cortisol, sitting height, and
29 S children than in HbAA children with normal haemoglobin (adjusted incidence rate ratio [aIRR] 0.66 [
30 sing the Fick equation, we model how altered haemoglobin affinity and the associated haemoglobin conc
31 cations, with regard to exercise, of altered haemoglobin affinity for oxygen are not fully understood
33 a and hypoxia to determine how their altered haemoglobin affinity impacts hypoxic exercise tolerance.
35 in BMC Gastroenterology evaluated the faecal haemoglobin, age and sex test (FAST) score in the assess
37 y, the presence of the NO scavenging protein haemoglobin alpha (Hbalpha) within nanometer proximity t
38 V4(EC) channels with eNOS and the absence of haemoglobin alpha favour TRPV4(EC) -eNOS signalling in p
39 ence of the nitric oxide-scavenging protein, haemoglobin alpha, limits TRPV4(EC) -eNOS signalling in
44 ed symptoms potentially related to donation, haemoglobin and ferritin concentrations, and deferrals b
45 tion, physical activity, cognitive function, haemoglobin and ferritin concentrations, and deferrals b
46 g men [for all listed symptoms]), lower mean haemoglobin and ferritin concentrations, and more deferr
48 xidative stress, agents that counteract free haemoglobin and haem, anti-inflammatory agents, anti-thr
50 567, combined P = 5.5 x 10 - 8 adjusted for haemoglobin and hydroxyurea) and validated it in indepen
51 ositive correlation between mean corpuscular haemoglobin and in vitro growth of BCG in whole blood fr
52 sis indicated a negative correlation between haemoglobin and mean MCAv (r = -0.589, regression coeffi
53 ging protein that binds and neutralises free haemoglobin and modulates inflammation and endothelial p
55 Within FEAST participants, we also compared haemoglobin and plasma biochemistry between bolus and no
56 al (ie, maternal and child anthropometry and haemoglobin and preterm birth) and socioenvironmental de
60 re admission, poor nutritional status, lower haemoglobin, and positive urine tests (TB-LAM and/or Xpe
61 Cholesterols, fasting glucose, glycosylated haemoglobin, and proinflammatory markers in the blood as
62 ow baseline clinical severity, high baseline haemoglobin, and week 4 clinical remission were associat
63 score (age, biomarkers [GDF-15, cTnT-hs, and haemoglobin], and clinical history [previous bleeding])
64 sses, including agents that reactivate fetal haemoglobin, anti-sickling agents, anti-adhesion agents,
66 oea and endocarditis, and extracts haem from haemoglobin as an important iron source within the iron-
69 ded regimen, the difference in the amount of haemoglobin at day 84 was -2.2 g/L (95% CI -4.6 to 0.1)
70 used a block design stratified by amount of haemoglobin at enrolment (above and below the median amo
72 lpha-thalassaemia, haemoglobin H disease and haemoglobin Bart's hydrops fetalis, are an important pub
73 racorporeal pulsatile-perfusion system and a haemoglobin-based, acellular, non-coagulative, echogenic
75 ein we report crystal structures of apo- and haemoglobin-bound HpuA, an essential component of this h
76 lood cell variants were haemoglobin S (HbS), haemoglobin C (HbC), alpha thalassaemia, ABO blood group
78 and regional databases up to Nov 14, 2014, "haemoglobin colour scale" in alternative spellings publi
80 nan assay, body-mass index <18.5 kg/m(2), or haemoglobin concentration <100 g/L) were recommended to
81 st common of which were anaemia or decreased haemoglobin concentration (70 [19%] vs one [1%]) and inc
82 metadata-only and combined models predicted haemoglobin concentration (in g dl(-1)) with mean absolu
83 fter CaO2 was reduced by 10% by lowering the haemoglobin concentration (isovolaemic haemodilution; Lo
86 logy Group (ECOG) performance status of 0-3, haemoglobin concentration 9 g/dL or higher, absolute neu
87 an 0.33 g/dL (95% CI 0.20-0.46) reduction in haemoglobin concentration after 8 h (p<0.0001), and at 2
88 This increase may be caused by the reduced haemoglobin concentration after long-duration spacefligh
89 nverse correlation (r = -0.82) between blood haemoglobin concentration and P(50) , an index of oxygen
91 ntrations (lower bound of the 95% CI for the haemoglobin concentration at which the OR of death equal
92 core by 0.26 (95% CI 0.09-0.43; p=0.003) and haemoglobin concentration by 2.9 g/L (95% CI 0.90-4.90;
93 ndpoint was the mean within-person change in haemoglobin concentration during 28 days of study follow
94 l below 80 g/L) or liberal (transfusion when haemoglobin concentration fell below 100 g/L) RBC transf
95 g) to either a restrictive (transfusion when haemoglobin concentration fell below 80 g/L) or liberal
96 ally appropriate and relatively safe minimum haemoglobin concentration for proceeding to surgery coul
97 l improvement-erythroid (HI-E), defined as a haemoglobin concentration increase of 1.5 g/dL or higher
98 ered haemoglobin affinity and the associated haemoglobin concentration influences oxygen consumption
100 simple, cheap quantitative method to assess haemoglobin concentration outside of the laboratory.
101 characteristics and the interference of high haemoglobin concentration released by erythrocyte lysis
102 low oxygen affinity haemoglobin and reduced haemoglobin concentration seen in vivo may be unable to
103 gs, heart rate, systolic blood pressure, and haemoglobin concentration strongly discriminated safe di
105 0.16 (95% CI 0.08-0.23) higher and the mean haemoglobin concentration was 2.03 g/L (1.28-2.79) highe
107 ed with improved survival when the admission haemoglobin concentration was up to 77 g/L (95% CI 65-11
108 orted diabetes, the combined model predicted haemoglobin concentration with a mean absolute error of
109 's r 0.918-0.957) and was less influenced by haemoglobin concentration, number of RBCs and number of
110 low-affinity haemoglobin, which predicts low haemoglobin concentration, oxygen consumption at rest ca
111 s were recruitment rate, protocol adherence, haemoglobin concentration, RBC exposure, selection bias,
112 ot significantly associated with harm at any haemoglobin concentration-ie, the OR of death comparing
117 iants (13, 26 and 39 mmHg) and corresponding haemoglobin concentrations (19.5, 15.5 and 11.4 g dL(-1)
118 for haemoglobin (FIT), which examine faecal haemoglobin concentrations (f-Hb), assist in deciding wh
119 LSPAC), we examined associations of maternal haemoglobin concentrations (g/dL) in pregnancy with hayf
120 versus not transfused was less than 1 at all haemoglobin concentrations (lower bound of the 95% CI fo
122 ion was associated with improved survival at haemoglobin concentrations above the currently recommend
125 comes were infant length-for-age Z score and haemoglobin concentrations at 18 months of age among chi
126 ant factor to consider preoperatively as low haemoglobin concentrations can have a negative effect on
127 To investigate the relation between maternal haemoglobin concentrations in pregnancy and childhood re
128 esting of anaemia, and methods of optimising haemoglobin concentrations in the context of paediatric
129 rdiovascular disease, and with postoperative haemoglobin concentrations lower than 100 g/L within 3 d
130 ion was associated with improved survival at haemoglobin concentrations up to 105 g/L (95% CI 71-115)
132 lly significant dose-dependent reductions in haemoglobin concentrations were the most common laborato
133 had recorded pre-delivery and post-delivery haemoglobin concentrations, and overall 1412 women deliv
134 sis symptoms, body-mass index, point-of-care haemoglobin concentrations, and urine lipoarabinomannan
137 prepared by the spontaneous self-assembly of haemoglobin-containing erythrocyte membrane fragments on
138 iogenesis, showed a significant reduction of haemoglobin content (54.2%) in sponges implanted into Sl
141 sociations were observed with lung function, haemoglobin, creatinine, glucose levels or resting blood
142 , history of bleeding, and three biomarkers (haemoglobin, cTn-hs, and GDF-15 or cystatin C/CKD-EPI) w
143 n volumes remained stable for 12 months (ie, haemoglobin decrease not more than 15 g/L, platelet coun
145 d for cluster design, the mean difference in haemoglobin decreases between groups was not significant
148 exogenous source of haem since, feeding with haemoglobin-depleted serum led to aborted embryogenesis.
152 d 1.10 [1.06-1.14] in women), and lower mean haemoglobin (difference per week shorter inter-donation
153 th amplification of plasmepsin 2-3, encoding haemoglobin-digesting proteases, regardless of the locat
154 th amplification of plasmepsin 2-3, encoding haemoglobin-digesting proteases, regardless of the locat
155 , blood meal concentration, novel methods of haemoglobin digestion, haem detoxification, vitellogenes
158 the co-inheritance of beta-thalassaemia with haemoglobin E resulting in haemoglobin E/beta-thalassaem
159 thalassaemia with haemoglobin E resulting in haemoglobin E/beta-thalassaemia, have been described.
162 ctors that regulate the binding of oxygen to haemoglobin, explored the determinants of a human's accl
163 rly for reagents designed to increase foetal haemoglobin expression as we have additionally demonstra
166 Quantitative faecal immunochemical tests for haemoglobin (FIT), which examine faecal haemoglobin conc
167 ariants, we demonstrate that the affinity of haemoglobin for oxygen is highly correlated with haemogl
172 study was to determine whether high affinity haemoglobin (HAH) affects maximal and submaximal exercis
177 is that humans exhibit an acute reduction in haemoglobin (Hb) binding affinity for oxygen that facili
179 barachnoid haemorrhage (aSAH), extracellular haemoglobin (Hb) in the subarachnoid space is bound by h
181 gating vascular function in humans ABSTRACT: Haemoglobin (Hb) may impact the transduction of endothel
182 eased following the experimental addition of haemoglobin (Hb) or ferric iron, and reduced following a
185 arm: a negative intervention effect on mean haemoglobin (Hb) status (-2.6 g/l; 95% CI -4.5, -0.8; p
186 -upper arm circumference [MUAC], oedema) and haemoglobin (Hb) were measured in children aged 6-59 mon
187 ments for type 2 diabetes, lowering glycated haemoglobin (HbA(1c)) and weight, but are currently only
188 agnosed with type 2 diabetes with a glycated haemoglobin (HbA(1c)) concentration of 7.5% or higher (>
190 mmol/L, triglycerides <=1.7 mmol/L, glycated haemoglobin (HbA1c) <=53 mmol/mol (<=7.0%), systolic blo
191 d remission of diabetes, defined as glycated haemoglobin (HbA1c) of less than 6.5% (<48 mmol/mol) aft
194 ssociations between multimorbidity, glycated haemoglobin (HbA1c), and mortality in people with T2D ha
195 se and insulin measures, as well as glycated haemoglobin (HbA1c), are used to diagnose and monitor di
196 nsification: age, sex, deprivation, glycated haemoglobin (HbA1c), body mass index (BMI), smoking stat
197 age, waist-to-hip ratio (WHR), glycosylated haemoglobin (HbA1c), diabetes duration, retinopathy, nep
198 iated with improvements in glucose, glycated haemoglobin (HbA1c), weight, waist circumference, anxiet
205 ly occurring Hereditary Persistance of Fetal Haemoglobin (HPFH) -175T>C point mutation associated wit
206 day 84 and was measured as the difference in haemoglobin in each screen-and-treat group compared with
209 Patients with MDD had smaller changes in oxy-haemoglobin in the frontal and temporal cortices than HC
210 sing a 52-channel system, and changes in oxy-haemoglobin in the frontal and temporal regions were qua
211 th symptomatic recurrence after AL, the mean haemoglobin increased 0.13 g/dL (95% CI 0.01-0.26) for e
213 rterial hypotension, tachycardia, decreasing haemoglobin, increasing acute phase reactants tests, and
214 lassemia represents a heterogeneous group of haemoglobin inherited disorders, among the most common g
217 microscopy, anaemia (study defined values or haemoglobin less than age-adjusted and sex-adjusted valu
218 on during deep breathing was associated with haemoglobin level (regression coefficient = 0.022; p < 0
219 they received blood transfusion to maintain haemoglobin level at 100 g/L or higher, or restrictive t
221 n which they received blood transfusion when haemoglobin level was lower than 80 g/L or if they had s
222 e-induced AI in mice (indicated by increased haemoglobin level, serum iron, FPN expression and decrea
223 genetic variation associated with the fetal haemoglobin level, the mouse orthologue of which is nece
224 an 12 months, 11-15); patients with baseline haemoglobin levels 10 g/dL or greater (median 17 months,
226 phenotype, with sustained elevation of blood haemoglobin levels into the normal range, reduced reticu
227 ian 17 months, 14-NA) than for patients with haemoglobin levels less than 10 g/dL (median 10 months,
231 eing ART experienced, having severe anaemia (haemoglobin < 80 g/l), being unable to walk unaided, and
232 n the 8 weeks before treatment (and baseline haemoglobin <10 g/dL), or high transfusion burden, defin
235 actate dehydrogenase >upper limit of normal, haemoglobin <110 g/L for women or <120 g/L for men, and
236 .60-0.86; p=0.04) in anaemic pregnant women (haemoglobin <110g/L) as compared with non-anaemic pregna
237 per L; for patients with polycythaemia vera, haemoglobin <15.0 g/L without phlebotomy) with complete
238 V(O2peak), peak cardiac output (Q(peak)), haemoglobin mass (Hb(mass)) and blood volumes were asses
240 termination of the trial and the omission of haemoglobin measurement after day 42, resulting in an in
243 onsequently from pathophysiologic process of haemoglobin metabolism and its products, causing chronic
244 ger duration of diabetes and higher glycated haemoglobin, non-HDL cholesterol, and waist-to-height ra
245 reduced O(2crit)), associated with increased haemoglobin-O(2) affinity (~32% fall in P(50)) of red bl
246 also assessed blood acid-base chemistry and haemoglobin-O(2) binding affinity of sea bass in hypoxic
247 donation resulted in more deferrals for low haemoglobin (odds ratio per week shorter inter-donation
249 6 x 10(9) per L or higher (1.88, 1.27-2.79), haemoglobin of 11 g/dL or lower (1.71, 1.13-2.57), a pla
250 nd in those with anaemia, as any increase in haemoglobin of 20 g/L or higher observed in at least two
251 to 12 years with severe anaemia, defined as haemoglobin of less than 6 g/dL, at admission to hospita
252 tional cardiovascular risk factors, glycated haemoglobin of up to 9.5% (80 mmol/mol) on a maximum of
253 olment (above and below the median amount of haemoglobin on every enrolment day) and stage of gestati
254 monthly transfusions to maintain 30% sickle haemoglobin or lower, while those assigned to the altern
255 o creatinine, thyrotropin, calcium, glycated haemoglobin, or lithium measurements between Oct 1, 1982
257 y using photoacoustic imaging to measure the haemoglobin oxygen change (that is, the oxygen consumpti
259 n concentrations, and more deferrals for low haemoglobin (p<0.0001 for each) than those observed in t
261 ine plasma powder; seven peptides for bovine haemoglobin powder, including six peptides for bovine bl
262 mproved knowledge of the regulation of fetal haemoglobin production in human beings and the developme
264 tantly, unlike iPSCs, the line maintains the haemoglobin profile of the patient's red blood cells.
265 program a spatially coupled glucose oxidase/haemoglobin reaction cascade, which in the presence of g
270 (RBCs), the parasite replicates and consumes haemoglobin resulting in the release of free heme which
273 e growing understanding of the mechanisms of haemoglobin S polymerization and its effects on red bloo
274 tution in the beta-globin gene that produces haemoglobin S, which leads to the systemic manifestation
275 e blood Collectively, our data point towards haemoglobin scavenging of nitric oxide as a key regulato
276 ough alterations in shear stress stimuli and haemoglobin scavenging of nitric oxide; these two regula
277 Collectively, these findings indicate that haemoglobin scavenging of NO appears to be an important
279 tified age, smoking status, body mass index, haemoglobin, serum uric acid, serum albumin, albuminuria
282 ival, haematological improvement measured by haemoglobin, time to next treatment, and patient-reporte
283 int mutation in the beta-globin chain causes haemoglobin to polymerise within erythrocytes during deo
284 suggest there is no benefit of high affinity haemoglobin to preserve maximal oxygen uptake in acute h
285 logy that have brought reactivation of fetal haemoglobin to the forefront of sickle-cell disease rese
286 e plasmepsins are involved in the parasite's haemoglobin-to-haemozoin conversion pathway, targeted by
287 xploratory objective was to estimate optimal haemoglobin transfusion thresholds using generalised add
288 levels and might involve inhibition of host haemoglobin uptake into intra-erythrocytic parasites.
289 ues for high, normal and low oxygen-affinity haemoglobin variants (13, 26 and 39 mmHg) and correspond
290 o Clinic Laboratories database of rare human haemoglobin variants reveal a strong inverse correlation
295 phic candidate genes, however only one, beta haemoglobin, was differentially expressed in both the fo
296 ntage of the intrinsic optical properties of haemoglobin, we show that raster-scanning optoacoustic m
297 Changes in fasting glucose and glycated haemoglobin were not different between groups at 12 mont
298 ingful or statistically significant drops in haemoglobin were recorded in any individual in the haemo
299 haemolysis and anaemia by increasing foetal haemoglobin, which leads to lower hypoxic transcriptiona
301 ECISE-DAPT score (age, creatinine clearance, haemoglobin, white-blood-cell count, and previous sponta