ライフサイエンスコーパス: hemoglobin

1 n molecule-1) and 1 clinical variable (total hemoglobin).

2 ol or racial differences in the glycation of hemoglobin.

3 5-coordinate hemes present in myoglobin and hemoglobin.

4 ainly associated with mean serum corpuscular hemoglobin.

5 ng to racial differences in the glycation of hemoglobin.

6 nd optical absorption of biomolecules, i.e., hemoglobins.

7 group, including the mean relative change in hemoglobin (0.84 g/dl; 95% confidence interval, 0.58 to

8 estrictive (hemoglobin 7-8 g/dL) or liberal (hemoglobin 10-11 g/dL) transfusion strategy throughout h

9 rgoing delayed clamping had higher levels of hemoglobin (10.4 vs 10.2 g/dL; difference, 0.2 g/dL; 95%

10 fter aneurysmal subarachnoid hemorrhage with hemoglobin 7-13 g/dL.

11 block randomized patients to a restrictive (hemoglobin 7-8 g/dL) or liberal (hemoglobin 10-11 g/dL)

12 (IQR), 10 (5-9) y of T2D duration; glycated hemoglobin 7.0% +/- 0.8%; body mass index (in kg/m(2)) 2

13 - 261 vs 33 +/- 33 pg/mL, P = .04) but lower hemoglobin (8.4 +/- 0.3 vs 10.9 +/- 1.4 g/dL, P = .004)

14 a-glutamyl transferase, lower pretherapeutic hemoglobin, a higher Gleason score, a higher number of p

15 Baseline descriptive data, hemoglobin A1c (%) level, time since diagnosis of T1DM (

16 g glucose (>/=7.0 mmol/L [>/=126 mg/dL]) and hemoglobin A1c (>/=6.5%) in persons without diagnosed di

17 entral adiposity, stable adiposity, baseline hemoglobin A1c (HbA1c) > 5.05%, HbA1c < 4.92%] and assay

18 glucose >/=200 mg/dl (11.1 mmol/l), glycated hemoglobin A1c (HbA1c) >6.5%, self-reported physician-di

19 The primary end point was change in hemoglobin A1c (HbA1c) from baseline to week 26.

20 Hemoglobin A1C (HbA1c) levels are often obtained in pote

21 asma insulin levels, insulin resistance, and hemoglobin A1c (HbA1c) levels in first-episode antipsych

22 Debate exists as to whether the higher hemoglobin A1c (HbA1c) levels observed in black persons

23 ultiple daily injections of insulin, and had hemoglobin A1c (HbA1c) levels of 7.5% to 9.9% (mean, 8.5

24 ng multiple daily insulin injections and had hemoglobin A1c (HbA1c) levels of 7.5% to 9.9%.

25 ded 161 individuals with type 1 diabetes and hemoglobin A1c (HbA1c) of at least 7.5% (58 mmol/mol) tr

26 Whether preoperative hemoglobin A1c (HbA1c) or postoperative glucose levels a

27 Hemoglobin A1c (HbA1c) reflects past glucose concentrati

28 ssociation between baseline and time-varying hemoglobin A1c (HbA1c) values and development of communi

29 ne at week 100 by age, duration of diabetes, hemoglobin A1c (HbA1c), body mass index (BMI), best-corr

30 arkers [blood pressure, waist circumference, hemoglobin A1c (HbA1c), insulin resistance, triglyceride

31 Unfortunately, tests such as hemoglobin A1c (HbA1c)/fasting plasma glucose (FPG) alon

32 ith suboptimally controlled type 1 diabetes (hemoglobin A1c [HbA1c] >8.0%) were recruited from the Di

33 random glucose level of at least 200 mg/dL, hemoglobin A1c concentration of at least 6.5% of total h

34 sex, race/ethnicity, net worth, and glycated hemoglobin A1c fraction (HbA1c).

35 The mean (SD) hemoglobin A1c level was 7.8% (2.4%) (to convert to prop

36 ntation resulted in a remarkable decrease in hemoglobin A1c levels (7.4+/-1.9 pre-LVAD versus 6.0+/-1

37 Patients with higher hemoglobin A1c levels (OR, 1.19 per unit change; 95% CI,

38 litus and prediabetes was estimated based on hemoglobin A1c measurements.

39 to insulin was associated with a decrease in hemoglobin A1c of approximately 1.0%.

40 density or foveal avascular zone metrics and hemoglobin A1C or duration of diabetes.

41 Hemoglobin A1c stratified by the presence or absence of

42 shared decision making, glycemic biomarkers, hemoglobin A1c target ranges, individualized treatment p

43 xamination (OR = 1.49; CI, 1.28-1.74), prior hemoglobin A1c test (OR = 1.45; CI, 1.28-1.64), and havi

44 -adhered to, whereas guidelines for glycated hemoglobin A1c testing for type 2 diabetes mellitus coul

45 cators: disease monitoring (eye examination, hemoglobin A1c testing, and low-density lipoprotein chol

46 Preoperative hemoglobin A1c was not significantly associated with mor

47 type, NAS >/= 5, bilirubin, body mass index, hemoglobin A1C, and dyslipidemia.

48 mass index, diabetes duration, glycosylated hemoglobin A1c, and fasting C-peptide.

49 ciation was independent of diabetes control (hemoglobin A1c, blood pressure, and lipid levels), prese

50 i-diabetic medications, as well as levels of hemoglobin A1C, cholesterol, hemoglobin, creatinine, and

51 in (numeric rating scale), level of glycated hemoglobin A1c, level of C-reactive protein, body mass i

52 d outcomes included intermediate outcomes of hemoglobin A1c, weight, systolic blood pressure, and hea

53 ore and liver stiffness) and correlated with hemoglobin A1C.

54 Hemoglobin AC, which reduces severe malaria risk, reduce

55 Fetal hemoglobin achieved levels of 68.6 +/- 3.9% in the IGF2B

56 Coma Scale, base excess, platelet count and hemoglobin, adrenaline, and syndecan-1 were the only ind

57 cause and length of end-stage renal disease, hemoglobin, albumin, selected comorbidities, race and ty

58 % specificity, which was higher than that of hemoglobin alone (P < 0.001 and P = 0.003, respectively)

59 We report here a new hemoglobin alpha chain variant in a female patient with

60 es that probably include binding of degraded hemoglobin, among other things, that significantly reduc

61 p between the production of cell-free plasma hemoglobin and acute kidney injury in infants and childr

62 he dityrosine cross-linked residues in human hemoglobin and alpha-synuclein under oxidative condition

63 Secondary outcomes included hemoglobin and anemia levels at 12 months of age and fer

64 Lys) and selected proteins (bovine and human hemoglobin and beta-lactoglobulin-A) were characterized.

65 dence of an association between lowest daily hemoglobin and brain dysfunction (p = 0.69 for delirium)

66 There was no evidence of association between hemoglobin and brain or renal dysfunction, or ICU mortal

67 multaneously, changes in cortical oxygenated hemoglobin and deoxygenated hemoglobin inferring prefron

68 Follow-up included blood levels of hemoglobin and ferritin at 8 and 12 months of age.

69 d clamping, compared with early clamping, on hemoglobin and ferritin levels at 8 and 12 months of age

70 Mean hemoglobin and hematocrit increases after 90 d were grea

71 Circulating hemoglobin and heme represent erythrocytic danger-associ

72 terone acetate use associated with increased hemoglobin and immune activation (HBD, HBB, IL36G), and

73 Change in plasma hemoglobin and male gender were found to be risk factors

74 PMS/GTF2E2) associated with mean corpuscular hemoglobin and mean corpuscular volume.

75 Recent studies have shown that globins like hemoglobin and myoglobin can also oxidize H2S to thiosul

76 Hemoglobin and other proteins were washed off with 3 M N

77 ICU-admission hemoglobin and proteinemia were respectively median (int

78 emonstrated that MMB treatment can normalize hemoglobin and red blood cell numbers.

79 nd polysulfide formation, coordinates ferric hemoglobin and, in the presence of air, generated thiosu

80 ions in insulin, insulin C-peptide, glycated hemoglobin, and homeostasis model assessment of insulin

81 label-free simultaneous sensing of DNA/RNA, hemoglobins, and lipids.

82 Decompartmentalized hemoglobin, arginase 1, asymmetric dimethylarginine, and

83 y or Austria), body mass index, and glycated hemoglobin as covariates were used to account for releva

84 ceptors CD36 and integrin alpha5beta1, while hemoglobin AS did not modify IE adhesion to any receptor

85 thrombocytosis that correlates with glycated hemoglobin as well as increased plasma S100A8/A9 levels.

86 otential treatments for hemolysis and plasma hemoglobin-associated renal dysfunction.

87 ients who achieved a >/=1.0 g/dl increase in hemoglobin at any time during a 16-week randomized perio

88 hese color values to a concentration of free hemoglobin, based on a built-in calibration curve, and r

89 parasites with peptide corresponding to the hemoglobin binding domain in PfHDP resulted in food vacu

90 , we identified two heme binding sites and a hemoglobin binding site in PfHDP.

91 ound the modeled PfHDP structure in the heme/hemoglobin-binding pockets from Maybridge Screening Coll

92 sulfide is susceptible to oxidation in human hemoglobin but is stabilized against it in HbI, a specia

93 Hemoglobin S (HbS) and hemoglobin C (HbC) mutations are frequently encountered

94 e findings indicate that schoolchildren with hemoglobin C mutation might contribute disproportionatel

95 Hemoglobin C trait did not associate with prevalent CKD

96 f-reported blacks (739 with SCT and 243 with hemoglobin C trait).

97 with SCT, six of 243 (2.5%) individuals with hemoglobin C trait, and 234 of 8927 (2.6%) noncarriers.

98 Mutations in hemoglobin can cause a wide range of phenotypic outcomes

99 g 3 serum biomarker concentrations and serum hemoglobin, can identify infants with acute intracranial

100 on include sickle cell disease, thalassemia, hemoglobin CC, and hereditary spherocytosis, where cellu

101 luded complete resolution of IDA (defined as hemoglobin concentration >11 g/dL, mean corpuscular volu

102 We assessed relations between anemia (hemoglobin concentration <110 g/L) and severe anemia (he

103 ations and hematocrit percentages in anemic (hemoglobin concentration <12 g/dL) Indian women of repro

104 n concentration <110 g/L) and severe anemia (hemoglobin concentration <70 g/L) and individual-level (

105 Associations between high hemoglobin concentration and adverse birth outcomes are

106 Hemoglobin concentration and arterial-venous oxygen cont

107 effects of nonpulmonary factors (especially hemoglobin concentration and arterial-venous oxygen cont

108 ing PRBC transfusion using a liberal trigger hemoglobin concentration and fewer patients being "overt

109 de complex resulted in a greater increase in hemoglobin concentration at 12 weeks.

110 The oxy-hemoglobin concentration change and the beta band power

111 sulfate with iron polysaccharide complex on hemoglobin concentration in infants and children with nu

112 or without multiple micronutrients (MMNs) on hemoglobin concentration in nonpregnant Cambodian women

113 After transfusion of one unit of RBC, hemoglobin concentration increased from 8.5 g/dL (7.6-9.

114 sue phantoms yielded a mean error of 9.2% on hemoglobin concentration measurement, comparable to that

115 n of the protein reported here, we show that hemoglobin concentration observed in human red blood cel

116 confidence interval: 1.01-1.28) and a lower hemoglobin concentration of -0.84 g/L (95% confidence in

117 Perfusate was plasma-based with a hemoglobin concentration of 4 to 6 g/dL.

118 rtion of patients overtransfused to a target hemoglobin concentration of 9.0 g/dL (54.8% vs 43.9%, P

119 closed loop: 24 +/- 0.4 mm Hg; p < 0.05) and hemoglobin concentration were significantly decreased af

120 Patients were followed for 28 days to record hemoglobin concentration, adverse events, and gametocyte

121 ar infrared spectroscopy (FDNIRS) to measure hemoglobin concentration, oxygen saturation, and indices

122 trial, nonpregnant women (aged 18-45 y) with hemoglobin concentrations </=117 g/L (capillary blood) w

123 of an iron-supplement bar leads to increased hemoglobin concentrations and hematocrit percentages and

124 nsumption of iron-supplement bars in raising hemoglobin concentrations and hematocrit percentages in

125 outcomes were 90-d changes from baseline in hemoglobin concentrations and hematocrit percentages.

126 Reevaluation of cutoffs for hemoglobin concentrations and indicators of iron status

127 k with adverse outcomes is more evident when hemoglobin concentrations are measured in early pregnanc

128 generally became weaker or nonexistent when hemoglobin concentrations are measured in the second or

129 There was no significant difference in mean hemoglobin concentrations between the iron-ingot group (

130 risk of adverse birth outcomes and maternal hemoglobin concentrations during pregnancy; however, it

131 diagnosis of ID anemia (IDA) by screening of hemoglobin concentrations followed by iron treatment.

132 tered iron homeostasis and elevated maternal hemoglobin concentrations have also been associated with

133 determine whether there was a difference in hemoglobin concentrations in rural Cambodian anemic wome

134 he iron ingot nor iron supplements increased hemoglobin concentrations in this population at 6 or 12

135 ociation between birth outcomes and maternal hemoglobin concentrations or iron status.

136 um ferritin, serum transferrin receptor, and hemoglobin concentrations were measured.

137 For low hemoglobin concentrations, the link with adverse outcome

138 ciated with increased anemia risks and lower hemoglobin concentrations, while early introduction of m

139 identify independent determinants of anemia (hemoglobin concertation <120 g/L).Anemia prevalence was

140 re, we report the crystal structure of human hemoglobin containing low spin ferric sulfide, the first

141 ficant differences (p < 0.001) in quantified hemoglobin content and oxygenation between the unequivoc

142 ficantly increased red blood cell counts and hemoglobin content in the blood, improved erythroid diff

143 ll as levels of hemoglobin A1C, cholesterol, hemoglobin, creatinine, and alkaline phosphatase.

144 e limitations with the original longitudinal hemoglobin data used to inform the current CDC reference

145 d, for example, fasting glucose and glycated hemoglobin decreased from 6.1 to 5.4 mmol/mol and 41.8%

146 en during a period coincident with extensive hemoglobin degradation by the parasite.

147 Hemoglobin degradation/hemozoin formation, essential ste

148 Hemoglobin diffusion has since a long time been recogniz

149 We show that hemoglobin diffusion in solution can be described as Bro

150 n up to physiological concentration and that hemoglobin diffusion in the red blood cells and in solut

151 ed abundance of PfKelch13 protein, decreased hemoglobin digestion, and enhanced glutathione productio

152 alence of iron deficiency is low and genetic hemoglobin disorders are high.

153 ed the Hbb(th3/+) beta-thalassemia mouse and hemoglobin E (HbE)/beta-thalassemia patients to investig

154 Hemoglobin electrophoresis was used to detect structural

155 mean corpuscular volume >70 fL, reticulocyte hemoglobin equivalent >25 pg, serum ferritin level >15 n

156 nism for chronoregulation of fetal and adult hemoglobin expression in humans.

157 The reprogramming of hemoglobin expression was achieved at the transcriptiona

158 Furthermore, fetal hemoglobin expression was inhibited during erythropoiesi

159 e investigated the association between fecal hemoglobin (fHb) concentrations below the FIT cut-off va

160 resulted in reduced heme synthesis, reduced hemoglobin formation, and perturbation of erythroid regu

161 st it in HbI, a specialized sulfide-carrying hemoglobin from a mollusk adapted to life in a sulfide-r

162 Free hemoglobin from ongoing hemolysis scavenges nitric oxide

163 regulatory sequences of the embryonic betaH1 hemoglobin gene expressed specifically in primitive eryt

164 UHb) overexpressing the barley non-symbiotic hemoglobin gene HvHb1 that oxidizes NO to NO3(-).

165 ection-related phenotypes depend on the host hemoglobin genotype, we followed 500 Malian individuals

166 ture positivity, CSF white blood cell count, hemoglobin, Glasgow Coma Scale, and pulse rate), and wer

167 multivessel CAD, diabetes with glycosylated hemoglobin >7%, and persistent angina were all associate

168 atients who achieved a sustained increase in hemoglobin (>/=0.75 g/dl over any 4-week period during t

169 es baseline body mass index and glycosylated hemoglobin have missing values.

170 using the two model systems tetrameric human hemoglobin (Hb) and human IgG4.

171 ety of fecal immunochemical tests (FITs) for hemoglobin (Hb) are used in colorectal cancer screening.

172 The magnetic characteristics of hemoglobin (Hb) changes with the binding of dioxygen (O2

173 weight protein was detected relative to the hemoglobin (Hb) fraction.

174 Hemoglobin (Hb) multiplicity is common in fish, yet desp

175 d O2-bound (oxy) hemes in myoglobin (MB) and hemoglobin (HB) solutions and in porphyrin compounds at

176 taphylococcus aureus that extracts heme from hemoglobin (Hb) to enable growth on Hb as a sole iron so

177 ther heme systems such as myoglobin (Mb) and hemoglobin (Hb).

178 Transfusions increased hemoglobin (Hb; from 9.1 to 10.3 g/dL; P < .001) and dec

179 A=1.71 pM; 95% CI: 0.72, 2.71), and glycated hemoglobin (HbA1c) (betaPFOS=0.03%; 95% CI: 0.002, 0.07;

180 ars = 2.07, OR15+years = 3.99), glycosylated hemoglobin (HbA1c) (OR6.5-6.9% = 1.33, OR7-7.9% = 1.86,

181 of ranolazine versus placebo on glycosylated hemoglobin (HbA1c) at 6- and 12-month follow-up.

182 The level of Glycated hemoglobin (HbA1c) is accordingly examined for checking

183 Glycated hemoglobin (HbA1c) is used to diagnose type 2 diabetes (

184 of periodontal status on changes of glycated hemoglobin (HbA1c) levels of patients with type 2 DM (DM

185 The duration of DM and the glycosylated hemoglobin (HbA1c) levels of the patients in the DM grou

186 in the 120 days after the index glycosylated hemoglobin (HbA1C) measurement.

187 Glycated proteins, such as glycated hemoglobin (HbA1c) or glycated albumin (GA) in the blood

188 s and glycemic control (assessed by glycated hemoglobin (HbA1c) values) in patients from the Kaiser P

189 (diabetes status, fasting glucose, glycated hemoglobin (HbA1c), fructosamine, glycated albumin), and

190 s (RCTs) that assessed the outcomes glycated hemoglobin (HbA1c), weight, body mass index (BMI; in kg/

191 had poor glycemic control (average glycated hemoglobin [HbA1c] >/=8% during the year) while the othe

192 ], fasting blood glucose [FBG], and glycated hemoglobin [HbA1c]) and survival in all lung transplant

193 of several endogenous peptides derived from hemoglobin (HBalpha and HBbeta) in the artemisinin-resis

194 Fetal hemoglobin (HbF) interferes with this polymerization, bu

195 ng of intracellular polymerization of sickle hemoglobin (HbS) and subsequent interaction with the mem

196 paper-based test capable of detecting sickle hemoglobin (HbS) in newborn blood samples with a limit o

197 hemolytic-endothelial dysfunction" and "high hemoglobin-hyperviscous" subphenotypes of sickle cell di

198 itric oxide (NO) is inactivated by cell-free hemoglobin in a dioxygenation reaction that also oxidize

199 k suggests that elevated levels of free cell hemoglobin in blood plasma can, as early as the first tr

200 rkers in stool that outperform or complement hemoglobin in detecting CRC and advanced adenomas.

201 Several protein combinations outperformed hemoglobin in discriminating CRC or advanced adenoma fro

202 ily iron supplementation for 12 wk increased hemoglobin in nonpregnant Cambodian women; however, MMNs

203 low HDL concentrations and elevated glycated hemoglobin in obese and diabetic patients.CCK responsive

204 n spin echo spectroscopy of the diffusion of hemoglobin in solutions with increasing protein concentr

205 cal test (FIT), as a direct measure of human hemoglobin in stool has a number of advantages relative

206 Total hemoglobin increased by 1.2-1.9 g/dL (P = 0.01) as retic

207 From baseline to 12 weeks, mean hemoglobin increased from 7.9 to 11.9 g/dL (ferrous sulf

208 tical oxygenated hemoglobin and deoxygenated hemoglobin inferring prefrontal activation were recorded

209 ty to biofouling (no protein matrix effects, hemoglobin interferences, and minimized turbidity), low

210 samples for hematologic and renal toxicity (hemoglobin, leukocytes, platelets, creatinine), and immu

211 mping also reduced the prevalence of anemia (hemoglobin level <11.0 g/dL) at 8 months in 197 (73.0%)

212 jaundice (254/318 [80%]) and severe anemia (hemoglobin level <5 g/dL) (238/310 [77%]).

213 There was an association between plasma hemoglobin level and change in creatinine that varied by

214 on independently of macrocirculation and the hemoglobin level in hemorrhagic shock patients.

215 The primary end point was a glycated hemoglobin level lower than 7.0% at week 24, with no epi

216 oportion of patients who achieved a glycated hemoglobin level lower than 7.0% with no severe hypoglyc

217 s, delayed cord clamping still resulted in a hemoglobin level of 0.3 (95% CI, 0.04-0.5) g/dL higher t

218 over 3 years among patients with a glycated hemoglobin level of 10%.

219 ealth Evaluation II score of 25 (19-31), and hemoglobin level of 10.0 (9.0-11.1) g/dL.

220 e of 58 mm/h (reference range, 3-23 mm/h), a hemoglobin level of 14.1 g/dL (reference range, 13.8-17.

221 over 5 years among patients with a glycated hemoglobin level of 6%, as compared with 4.3% over 3 yea

222 The primary outcome was a glycated hemoglobin level of 6.0% or less with or without the use

223 rcentage reduction from baseline in glycated hemoglobin level than did patients who received medical

224 The mean (SD) glycated hemoglobin level was 7.4% (0.5%).

225 At 24 months, the mean glycated hemoglobin level was 7.5+/-1.2% in each group, whereas t

226 as 16.4 years, and the mean (+/-SD) glycated hemoglobin level was 8.4+/-1.7%; 83.9% of the patients w

227 /-8 years, 66% were women, the mean glycated hemoglobin level was 9.2+/-1.5%, and the mean BMI was 37

228 age, sex, country, and SCD phenotype, a low hemoglobin level was significantly associated with TRV a

229 ssion Glasgow Coma Scale, glucose level, and hemoglobin level) and used in univariate, and multivaria

230 ncluded the change from baseline in glycated hemoglobin level, weight, systolic blood pressure, and m

231 e no longer significant after adjustment for hemoglobin level.

232 Hemoglobin levels and international normalized ratio val

233 phenomenon of a discrepancy between glycated hemoglobin levels and other indicators of average glycem

234 To determine the association between hemoglobin levels and the daily risk of individual organ

235 Hemoglobin levels increased by a median of 4.4 g/dL in t

236 ents with hemoglobinopathies, change in mean hemoglobin levels was similar in those receiving EBR/GZR

237 Glycated hemoglobin levels were lower with pump therapy than with

238 count, history of acute chest syndrome, and hemoglobin levels, demonstrated a higher hazard ratio fo

239 ge, higher frequency of bulky disease, lower hemoglobin levels, higher leukocyte counts, and similar

240 had significantly lower CD4 cell counts and hemoglobin levels, more advanced WHO stage, and higher H

241 active protein, lipoprotein(a), and glycated hemoglobin levels.

242 ted in the CVRF-free group with glycosylated hemoglobin levels.

243 with red-blood-cell traits, including fetal hemoglobin levels.

244 ollowing as significant risk factors for OS: hemoglobin < 100 g/L, leukocytes > 25 x 10(9)/L, platele

245 Hg, fasting glucose <100 mg/dl, glycosylated hemoglobin <5.7%, and total cholesterol <200 mg/dl.

246 ntent correlated with mean serum corpuscular hemoglobin, male sex, and age.

247 ctrometer and demonstrated the capability of hemoglobin measurement.

248 d diagnosis for ID is often limited to proxy hemoglobin measurements alone.

249 8% (2.4%) (to convert to proportion of total hemoglobin, multiply by 0.01), and the mean (SD) duratio

250 f sickle cell disease is polymerization of a hemoglobin mutant, hydroxyurea is the only drug approved

251 Associations between the lowest hemoglobin on a given day and organ dysfunctions the fol

252 The lowest hemoglobin on a given day was significantly associated w

253 Primary outcome was change in hemoglobin over 12 weeks.

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

255 laser wavelengths, the spatially distributed hemoglobin oxygenation reflecting the hypoxia in inflamm

256 ncreased mean signal intensity of oxygenated hemoglobin (P = 0.0002) and the development of punctate

257 rease in mean signal intensity of oxygenated hemoglobin (P = 0.004) by MSOT 2 d after inoculation.

258 dy and included concentration of melanin and hemoglobin, patient satisfaction questionnaires, clinica

259 No changes in hemoglobin, platelets, or leukocytes were observed in th

260 blood pressure, base excess, platelet count, hemoglobin, prehospital plasma, and prehospital fluids (

261 this signaling pathway result in a block in hemoglobin production and concomitant intracellular accu

262 thesis with the amount of heme available for hemoglobin production.

263 tin receptor (reduction of 43%) and glycated hemoglobin (reduction of 28%).

264 dicted proportions (95% CIs) of women with a hemoglobin response (>/=10 g/L at 12 wk) were 19% (14%,

265 s, increased intestinal iron absorption, and hemoglobin response to SF) among noninflamed, outpatient

266 Hemoglobin S (HbS) and hemoglobin C (HbC) mutations are

267 sickle cell disease is the polymerization of hemoglobin S (HbS) to form fibers that make red cells le

268 While adults heterozygous for hemoglobin S mutation were less often parasitemic compar

269 Common red blood cell polymorphisms (ie, hemoglobin S, glucose-6-phosphate dehydrogenase, and alp

270 ta-globin gene that causes polymerization of hemoglobin S.

271 , persistent inhibition of polymerization of hemoglobin S.

272 A1c concentration of at least 6.5% of total hemoglobin, self-reported use of diabetic medication, or

273 Blood was analyzed for hemoglobin, serum ferritin, and serum transferrin recept

274 in iron status over time, measured by sFer, hemoglobin, soluble transferrin receptor (sTfR), and est

275 kle cell genotypes included 27 patients with hemoglobin SS (58.7%), 14 SC (30.4%), 4 beta-thalassemia

276 ese phenotypes can provide new insights into hemoglobin structure and function as well as identify ne

277 ow progenitors generate red blood cells, how hemoglobin synthesis is regulated, and the molecular und

278 of celiac disease had a lower mean level of hemoglobin than persons without celiac disease.

279 methemoglobin, a non-oxygen-binding form of hemoglobin that readily loses heme.

280 d, < 9 g/dL) or to the restrictive strategy (hemoglobin threshold, < 7 g/dL) of RBC transfusion durin

281 Patients were randomized to the liberal (hemoglobin threshold, < 9 g/dL) or to the restrictive st

282 a dioxygenation reaction that also oxidizes hemoglobin to methemoglobin, a non-oxygen-binding form o

283 However, the association between these hemoglobin traits and ESRD remains unknown.

284 ptors, and examined the effects of host age, hemoglobin type, blood group and severe malaria on level

285 score the following day; for each increasing hemoglobin unit, the odds of worsened respiratory Sequen

286 ency of HbF-enriched erythropoiesis elevated hemoglobin using fewer reticulocytes.

287 yed cerebral ischemia across a wide range of hemoglobin values and suggests that restrictive transfus

288 ata used to inform the current CDC reference hemoglobin values, and presents additional normative dat

289 rable brain regions, across a broad range of hemoglobin values.

290 Hemoglobin variants C and S protect against severe malar

291 A1c and glucose measurements, and those with hemoglobin variants HbSS, HbCC, or HbAC were excluded.

292 lectrophoresis was used to detect structural hemoglobin variants.Anemia prevalence was 44% with the u

293 In this study in ICU patients, lower hemoglobin was associated with a higher probability of w

294 t atrial/pulmonary capillary wedge pressure, hemoglobin) was created.

295 , chronic obstructive pulmonary disease, and hemoglobin, was a powerful predictor of mortality.

296 sment of insulin resistance and glycosylated hemoglobin were measured from a fasting blood sample, an

297 lanine aminotransferase, total bilirubin, or hemoglobin were observed.

298 C and BSA) as well as of protein complexes (hemoglobin), which are not the result of an averaging pr

299 gand entry/exit site in the alpha-subunit of hemoglobin, which, to the best of our knowledge, represe

300 e cell and other genetic diseases related to hemoglobin, while in Oxford, the group of Dorothy Hodgki