ライフサイエンスコーパス: hemoglobin

1 - 1 acid glycoprotein as a sugar source with hemoglobin.

2 abundant alpha- and beta-globin chains from hemoglobin.

3 role in mediating the positive influence of hemoglobin.

4 owth and iron content when grown in THYB and hemoglobin.

5 traits such as fasting glucose and glycated hemoglobin.

6 red cell distribution width, hematocrit, or hemoglobin.

7 ormation increases with the concentration of hemoglobin.

8 a model to produce ROS and react with human hemoglobin.

9 g the proteolytic catabolism of erythrocytic hemoglobin.

10 d blood cells (RBCs) and recycling iron from hemoglobin.

11 independent antisickling properties of fetal hemoglobin.

12 ternative to established chemical assays for hemoglobin.

13 estimated quantitatively for adult and fetal hemoglobins.

14 -for-age z score (WAZ): +0.37, P = 0.04] and hemoglobin (+0.65 g/dL, P = 0.007) and a lower adjusted

15 gher maternal biomarker were significant for hemoglobin (1.9%), iron biomarkers (ranging from 0.4 to

16 0.5 (10(6)/muL) and 6.5 +/- 0.4 (10(6)/muL); Hemoglobin: 17.5 +/- 1.2 g/dL and 19.2 +/- 3.0 g/dL; and

17 Thirteen people with T2DM (glycated hemoglobin, 6.9+/-1.0%) and 12 age-matched healthy contr

18 Intact tetrameric hemoglobin (64 kDa) and trimeric reactive intermediate d

19 erritin (95% CI 103.1-125.3) and 5.7 g/L for hemoglobin (95% CI 4.3-7.2) with significantly higher va

20 le cell trait, low hemoglobin S and elevated hemoglobin A were associated with faster eGFR decline, b

21 D score was associated with a greater 1-year hemoglobin A(1c) reduction to sulfonylureas in the Genet

22 ke, inpatient admission), laboratory values (hemoglobin A(1c), blood urea nitrogen, serum creatinine)

23 by sex, history of ischemic stroke, glycated hemoglobin A(1c), body mass index, blood pressure, or es

24 the use of DM medication, a DM diagnosis, or hemoglobin A1c >= 6.5%.

25 - standard deviation was 14.0 +/- 1.5 years, hemoglobin A1C (HbA1C) level was 8.5 +/- 1.3%, and media

26 tion was collected using a questionnaire and hemoglobin A1c (HbA1c) levels were measured.

27 24 years with type 1 diabetes and screening hemoglobin A1c (HbA1c) of 7.5% to 10.9%.

28 re-9 score of at least 10 (range, 0-27); and hemoglobin A1c (HbA1c) of at least 8%, systolic blood pr

29 a meta-analysis for the glycemic outcome of hemoglobin A1c (HbA1c).

30 lycemia, hyperglycemia, and glucose control; hemoglobin A1c (HbA1c); and cognition and patient-report

31 %) had diabetes, 1268 (34%) had prediabetes (hemoglobin A1c [HbA1c] 5.7-6.4%), and 606 (16%) had norm

32 Among patients with hemoglobin A1c greater than or equal to 8.0% treated in

33 emia increased; however, among patients with hemoglobin A1c greater than or equal to 8.0%, the opposi

34 n 6.5% and 6.5-7.9% but not among those with hemoglobin A1c greater than or equal to 8.0%.

35 ed with higher mortality among patients with hemoglobin A1c less than 6.5% (p < 0.0001 for each).

36 ed with higher mortality among patients with hemoglobin A1c less than 6.5% and 6.5-7.9% but not among

37 Among patients with hemoglobin A1c less than 6.5%, mortality increased as me

38 ncreasing mortality only among patients with hemoglobin A1c less than 6.5%.

39 140 mg/dL or 110-160 mg/dL for patients with hemoglobin A1c less than 7% or greater than or equal to

40 ure level >90 mm Hg), uncontrolled diabetes (hemoglobin A1c level >8%), obesity (body mass index >30)

41 d oral glucose tolerance (P < 0.01), reduced hemoglobin A1c levels (P = 0.01), and improved insulin s

42 Although mean hemoglobin A1c levels between groups were equivalent, th

43 ly correlated with fasting blood glucose and hemoglobin A1c levels in men with T2DM, but not women wi

44 ical variables, including age, gender, race, hemoglobin A1C levels, blood pressure, cholesterol level

45 Preadmission glycemia, reflected by hemoglobin A1c obtained at the onset of ICU admission, h

46 HDL-, blood pressure-, fasting glucose- and hemoglobin A1C values.

47 age, sex, hypertension, hyperlipidemia, and hemoglobin A1c were collected.

48 w prehospital admission levels (estimated by hemoglobin A1C) but not to absolute hypoglycemia levels.

49 determined by assessment of HbA1c (glycated hemoglobin A1c) levels, which poorly reflects direct glu

50 Plasma lipids, hemoglobin A1C, body composition, the oral glucose toler

51 age, race, gender, laterality, insulin use, hemoglobin A1c, creatinine, blood urea nitrogen, and est

52 ntrolled for age, gender, race or ethnicity, hemoglobin A1c, duration of diabetes, high-density lipop

53 Patients were stratified by hemoglobin A1c: less than 6.5.(n = 4,406), 6.5-7.9% (n =

54 -related declines in four of these measures: hemoglobin, alkaline phosphatase, platelets, and lymphoc

55 Supplementation with hemoglobin allowed Spn to resume growth in an iron-deple

56 panied by an increase in red blood cells and hemoglobin and a decrease in reticulocyte counts.

57 g aging rate biomarkers, including declining hemoglobin and anemia, may be targeted to delay the effe

58 mers to generate free amino acids from human hemoglobin and are drug targets for the design of novel

59 CO causes toxicity by binding to hemoglobin and by inhibiting mitochondrial cytochrome c

60 xists a direct relationship between glycated hemoglobin and cardiovascular disease (CVD), clinical tr

61 evels, larger weight and body length, higher hemoglobin and cholesterol levels and a higher frequency

62 icipants were screened for DM using glycated hemoglobin and fasting plasma glucose at TB treatment an

63 es to prevent the toxic effects of cell-free hemoglobin and heme.

64 ression initiating ART, baseline low BMI and hemoglobin and high CRP and D-dimer levels may be clinic

65 We determined total hemoglobin and methemoglobin (MetHb) concentrations, cyt

66 associated with the respiratory function in hemoglobin and myoglobins.

67 NIRS was used to measure cerebral hemoglobin and oxygen saturation.

68 s have observed an unexpected improvement in hemoglobin and RBC transfusion-independence in patients

69 rity of our plasma sample by quantitation of hemoglobin and report hemolysis as either minimal (<=5%)

70 nvades red blood cells, where it catabolizes hemoglobin and sequesters the released toxic heme as inn

71 dose was negatively associated with achieved hemoglobin and vanadium while positively associated with

72 ecognizing the complex interplay between Hb (hemoglobin) and oxygen, carbon dioxide, and nitric oxide

73 ival rates, mean arterial pressure, lactate, hemoglobin, and estimated intravascular volume changes.

74 alt oxide (LCO), on the growth, development, hemoglobin, and heme synthesis gene expression in the la

75 se fetuses had reduced liver iron stores and hemoglobin, and markedly increased FPN in the liver, but

76 re admission, poor nutritional status, lower hemoglobin, and positive urine tests (TB-LAM and/or Xper

77 nd changes in the levels of lipids, glycated hemoglobin, and prolactin were similar in the trial grou

78 pancellular hereditary persistence of fetal hemoglobin are both relatively benign conditions.

79 Thus, methods to detect and quantify hemoglobin are important for clinical laboratories, bloo

80 History of ascites, albumin and hemoglobin are major determinants of the development of

81 Concentrations of hemoglobin as low as 6.45 x 10(-3) mg mL(-1) in solution

82 and also insights into the factors governing hemoglobin assembly during erythropoiesis.

83 al presence of pathogen, we sought to assess hemoglobin-based oxygen carrier (HBOC-201) in oxygen del

84 Administration of hemoglobin-based oxygen carriers (HBOCs) into the system

85 antage of our technique as compared to other hemoglobin-based POC diagnostic techniques.

86 low fixed ESA dose versus dosing based on a hemoglobin-based, titration-dose algorithm in such patie

87 4 weeks) versus administered according to a hemoglobin-based, titration-dose algorithm, for up to 2

88 absence of epiretinal membrane, and glycated hemoglobin below 9 as predictive of DR ultra-response.

89 L (95% CI: 0.04, 0.48; P = 0.02) increase in hemoglobin but no effect on anthropometry or iron or vit

90 lated to the history of ascites, albumin and hemoglobin but not to tumour load or to response to ther

91 with other protective polymorphisms, such as hemoglobin C.

92 vailability due to the presence of cell-free hemoglobin (CFH) increases vascular tone in severe malar

93 We also observed that levels of hemoglobin chains, possibly related to defects in iron m

94 Mean hemoglobin change was significantly higher among LNG-IUS

95 erential, 2) quantitative red blood cell and hemoglobin characterization, 3) clear identification of

96 uration of the delay period to intracellular hemoglobin composition also explains why sickle trait, t

97 nt (AbsCD4), CD4 percentage (CD4%) and total hemoglobin concentration (Hb) in capillary and venous bl

98 monstrated by osmotically induced changes to hemoglobin concentration (i.e., diffusive tortuosity) an

99 ignificantly increased cerebral deoxygenated hemoglobin concentration (P < 0.01, d = 0.86), and signi

100 frequency band (0.08-0.15 Hz) for oxygenated hemoglobin concentration (P = 0.02, d = 0.99) and total

101 Patterns of tumor total hemoglobin concentration (THb) and oxygen saturation (sO

102 0.93, compared with an AUC of 0.67 for fecal hemoglobin concentration alone.

103 s with AAs or CRC more accurately than fecal hemoglobin concentration alone.

104 study groups on the primary study outcomes (hemoglobin concentration and prevalence of ZPP >= 80 umo

105 rmation about tissue oxygenation, perfusion, hemoglobin concentration and water concentration, hence

106 timodal multiphoton approach for quantifying hemoglobin concentration at single RBC resolution.

107 assembly pathway inside red cells, where the hemoglobin concentration is very high.

108 re found to have hypoxia, increased cerebral hemoglobin concentration, and altered cerebrovascular ac

109 had no observable impact on mean corpuscular hemoglobin concentration, red cell distribution width, h

110 Consequently, changes in RBC shape and hemoglobin concentration, which are common manifestation

111 hat have demonstrated reductions in glycated hemoglobin concentration.

112 ), but a significant effect was detected for hemoglobin concentrations (adjusted effect: 3.08 g/L; 95

113 fortified cassava improved serum retinol and hemoglobin concentrations modestly in Nigerian preschool

114 ncreased disease severity (lower glucose and hemoglobin concentrations, malaria retinopathy, acute ki

115 bricated OriCols inflated to 30 cc minimized hemoglobin contamination (<4.68 ng/ml) compared with col

116 The hemoglobin content of blood is an important health indic

117 anemia, alterations secondary to the primary hemoglobin defect have a potential impact on HSC-niche c

118 s an undegradable crystalline product of the hemoglobin degradation pathway in the parasite and posse

119 ns are strikingly multifaceted, ranging from hemoglobin degradation to secretory organelle protein pr

120 ny hemorrhagic injuries due to hemolysis and hemoglobin degradation, which not only mediates local ce

121 antial activity against schistosomes-another hemoglobin-degrading pathogen.

122 NETs (~90 nm diameter) were fabricated from hemoglobin-depleted mice erythrocyte-ghosts and doped wi

123 Subacute decrease of hemoglobin deposition was also observed.

124 ic basis common to ticks, including heme and hemoglobin digestion, iron metabolism, and reactive oxyg

125 homeostasis, we selected beta-thalassemia, a hemoglobin disorder, as a paradigm.

126 ), mechanical ventilation (2 points), lowest hemoglobin during hospitalization greater than or equal

127 sex included HIV research domain and type of hemoglobin eligibility criterion, but individual associa

128 e device did not interfere with IgG, IgA, or hemoglobin ELISA.

129 tall natural mutations that upregulate fetal hemoglobin expression in the BCL11A enhancer or in the t

130 hy mice suppressed erythropoiesis, decreased hemoglobin expression, and caused anemia.

131 iated with faster eGFR decline, but elevated hemoglobins F and A(2) were renoprotective.

132 , we extract melanin [Formula: see text] and hemoglobin [Formula: see text] concentrations from video

133 nt in the digest as the reference peptide in hemoglobin from 18 oral cancer patients and 15 healthy c

134 d method utilized a lysis approach to remove hemoglobin from the suspension of infected and uninfecte

135 Only two hemoglobin functions are well established in nodules: Lb

136 Hemoglobin functions as a tetrameric oxygen transport pr

137 on with older age, sex, anemia, obesity, low hemoglobin, gastroduodenal ulcers, rehospitalization, cr

138 nishes CHD4 levels and derepresses the fetal hemoglobin genes.

139 ncentrations of albumin, immunoglobulin, and hemoglobin, giving a prediction error of the spiked conc

140 ratio increment; p < 0.001) and glycosylated hemoglobin greater than or equal to 6.5% (48 mmol/mol) (

141 5% confidence interval, 1.06-1.80; P = .02), hemoglobin (>=12 vs <12 g/dL) (2.32; 1.71-3.14; P < .01)

142 ength) and by comparing wild-type cells with hemoglobin H (HbH) thalassemia (shorter pathlength and r

143 evels of CD163, a scavenger receptor for the hemoglobin-haptoglobin complex.

144 be survivable once the nonpolymerizing fetal hemoglobin has been replaced by adult hemoglobin S at ab

145 ost-translational oxidative modifications of hemoglobin have been used as a surrogate biomarker for m

146 ects primarily by increasing the affinity of hemoglobin (Hb) for oxygen (O(2)).

147 l bioelectrode based on redox active protein hemoglobin (Hb) has been offered here for the determinat

148 ia focuses on measuring the concentration of hemoglobin (Hb) in blood.

149 Hemolysis and accumulation of cell-free hemoglobin (Hb) in the circulation or in confined tissue

150 SFOL and/or Hct are sometimes unavailable; hemoglobin (Hb) is generally available in surveys.

151 ow PLA2 inhibits lipid oxidation promoted by hemoglobin (Hb) is important for its applications in mus

152 The oxygen transport function of hemoglobin (HB) is thought to have arisen ~500 million y

153 rum haptoglobin protein (Hp) scavenges toxic hemoglobin (Hb) leaked into the bloodstream from erythro

154 Sickle cell disease (SCD) results from a hemoglobin (Hb) mutation betaGlu6 -> betaVal6 that chang

155 aureus obtains iron by extracting heme from hemoglobin (Hb) using the closely related IsdB and IsdH

156 onents enable S. aureus to extract heme from hemoglobin (Hb), transport it into the bacterial cytopla

157 Oxygen (O2) delivery facilitated by hemoglobin (Hb)-based O2 carriers (HBOCs) is a promising

158 needed based on their high susceptibility to hemoglobin (Hb)-mediated lipid oxidation.

159 e randomly assigned to either a restrictive (hemoglobin [Hb] threshold < 70 g/L) or liberal (Hb thres

160 controlling for age, sex, baseline glycated hemoglobin (HbA(1c)), baseline CMT, baseline VA, laser h

161 sis, serum fasting glucose (FG) and glycated hemoglobin (HbA(1c)), were estimated to be 51-62%.

162 beta6 Glu -> Val) on the beta-chain of adult hemoglobin (HbA) that results in sickled hemoglobin (HbS

163 decreased C-peptide, and increased glycated hemoglobin (HbA1c) compared with sham-operated controls.

164 al domain OCT (SD-OCT) tests, and 2 glycated hemoglobin (HbA1c) measures over time with a minimum fol

165 ence was estimated using laboratory glycated hemoglobin (HbA1c) or fasting plasma glucose in TB patie

166 igh- compared with low-fat dairy on glycated hemoglobin (HbA1c), body weight, and cardiovascular dise

167 lycerol (TG), fasting glucose (FG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric a

168 essure (BP), fasting blood glucose, glycated hemoglobin (HbA1c), triglyceride levels, triglycerides a

169 Fetal hemoglobin (HbF) can blunt the pathophysiology, temper t

170 A high level of erythrocyte fetal hemoglobin (HbF) comprising alpha- and gamma-globins may

171 Fetal hemoglobin (HbF) induction in erythroid progeny after ba

172 stress and oxidative modification of sickle hemoglobin (HbS) play a role in sickle cell disease (SCD

173 interest given the HbF inhibition of sickle hemoglobin (HbS) polymerization.

174 ult hemoglobin (HbA) that results in sickled hemoglobin (HbS).

175 een-group differences were found in glycated hemoglobin, HDL-cholesterol, or triglyceride concentrati

176 Index score (4 studies, n = 318; P < .001), hemoglobin, hematocrit, and albumin may predict colectom

177 A mutant in the hemoglobin/heme-binding protein Spbhp-37 was impaired fo

178 Blood hemoglobin (HGB) levels were lower throughout the lifesp

179 ted tumors, we performed a polymerized human hemoglobin (hHb) (PolyhHb) enhanced oxygenation simulati

180 n of oxygenated (HbO) and deoxygenated (HbR) hemoglobin, holds promise to study functional activity f

181 ly occurring hereditary persistence of fetal hemoglobin (HPFH) mutations, editing of transcriptional

182 ion of fecal level of MIR421, MIR27a-3p, and hemoglobin identified patients with CRC with an area und

183 (e.g., horseradish peroxidase (HRP), bovine hemoglobin, immunoglobulin G, and glucose oxidase (GOx))

184 eiving >=3 mo of SQ-LNS, their LAZ, WAZ, and hemoglobin improved.

185 d electrolytes, blood gases, and plasma-free hemoglobin in arterial blood, as well as blood entering

186 ng protective effect against the toxicity of hemoglobin in cell experiments.

187 represses gamma-globin expression and fetal hemoglobin in erythroid cells.

188 found that increased levels of 2 miRNAs and hemoglobin in feces can identify patients with AAs or CR

189 Total hemoglobin in full blood is also accurately determined.

190 , and the presence of microscopic amounts of hemoglobin in places where it normally does not occur, e

191 Additionally, oxygenated hemoglobin in the MT group tended to be lower than in th

192 amics could be enhanced by elevation of free hemoglobin in the plasma, which occurs in diseases such

193 ralized linear models (non-ART group pVL and hemoglobin) in as-treated analyses.

194 near infrared perfusion indices (NIR), organ hemoglobin indices (OHI) and tissue water indices (TWI)

195 Remarkably, hemoglobin induced a sizable transcriptome remodeling, e

196 Spbhp-37 was impaired for growth on heme and hemoglobin iron.

197 Hemoglobin, iron, ferritin, folate and vitamin B(12), in

198 Alternatively, when acellular hemoglobin is diluted into blood plasma after red cell l

199 In summary, the data show that hemoglobin is highly beneficial for Spn cultivation in v

200 However, the rate of NO degradation in hemoglobin is orders of magnitude higher than in brain t

201 density lipoprotein cholesterol and glycated hemoglobin, led to a greater degree of attenuation.

202 with mortality in patients with glycosylated hemoglobin less than 6.5% (odds ratio = 1.08 per 0.1 str

203 Primary outcome was incident anemia (hemoglobin level <130 g/L in men or <120 g/L in women).

204 years and older with iron-deficiency anemia (hemoglobin level <=11 g/dL; serum ferritin level <=100 n

205 esence of HIV infection, body mass index, or hemoglobin level (P > 0.05).

206 primary end point was the change in glycated hemoglobin level from baseline to week 26.

207 el of 9.0 g or more per deciliter or a fetal hemoglobin level of 20% or more after 24 months.

208 The primary outcome was a hemoglobin level of 9.0 g or more per deciliter or a fet

209 obin level score [calculated as the glycated hemoglobin level plus 4 times the insulin dose] of <=9)

210 defined as an insulin dose-adjusted glycated hemoglobin level score [calculated as the glycated hemog

211 ed mean change from baseline in the glycated hemoglobin level was -1.33 percentage points in the icod

212 n the two groups; the mean baseline glycated hemoglobin level was 8.09% in the icodec group and 7.96%

213 ars (range, 2-36 years), and median glycated hemoglobin level was 8.8% (IQR, 7.4%-10%).

214 Mean baseline hemoglobin level was 9.3 g/dL, but 27% had hemoglobin <8

215 anges in kidney function, rejection rate, or hemoglobin level were reported.

216 ents with type 2 diabetes mellitus (glycated hemoglobin level, >=7%), chronic kidney disease (estimat

217 aboratory investigations showed mild anemia (hemoglobin level, 10 g/dL; normal range, 12-15 g/dL), a

218 abetes was inadequately controlled (glycated hemoglobin level, 7.0 to 9.5%) while taking metformin wi

219 n allow clinicians to manage it and optimize hemoglobin level, making patients better prepared for th

220 nd points included insulin use, the glycated hemoglobin level, the number of hypoglycemic events, the

221 nt difference between the groups in glycated hemoglobin level.

222 or removal of a single Tfr2 allele increased hemoglobin levels and RBCs.

223 llele deletion produced significantly higher hemoglobin levels and reduced splenomegaly.

224 p and 23 to the control group); the glycated hemoglobin levels at baseline ranged from 5.7 to 10.1%.

225 baseline anemia, canakinumab increased mean hemoglobin levels by 11.3 g/L (P < 0.001) compared with

226 multiple IRS rounds on malaria incidence and hemoglobin levels in a cohort of children in rural south

227 reduces the incidence of anemia and improves hemoglobin levels in patients with anemia.

228 placebo resulted in increase of ferritin and hemoglobin levels in repeat blood donors with low iron s

229 re likely to continue IUC use and had higher hemoglobin levels over time.

230 The mean hemoglobin levels significantly increased from 11.01 (pr

231 (19 g per liter) in the pretransfusion mean hemoglobin levels throughout the treatment period.

232 Confirmed malaria infections and hemoglobin levels were recorded over time for each parti

233 each of 4 rounds of IRS, malaria incidence, hemoglobin levels, and parasite density were evaluated a

234 h human platelet number but not leukocyte or hemoglobin levels.

235 ent a pharmacologic target for raising fetal hemoglobin levels.

236 D included BP >140/90 mm Hg, higher glycated hemoglobin, lower baseline eGFR, and higher baseline uri

237 e hemoglobin level was 9.3 g/dL, but 27% had hemoglobin <8 g/dL.

238 Decision-tree analysis identified hemoglobin <8.5 g/dL as predictive of IRIS and C-reactiv

239 nia (platelet count <=50 x 10(9)/L), anemia (hemoglobin <=10 g/dL), and bleeding (WHO grade >=2).

240 Referral Hospital with acute episodes of SA (hemoglobin <=5.0 g/dL) were followed up for 6 months aft

241 Baseline hemoglobin (<11 g/dl) (odds ratio [OR]: 1.97; p = 0.003)

242 ion on the ability of PLA2 to inhibit trout hemoglobin-mediated lipid oxidation were investigated in

243 This advanced oxidative modification in hemoglobin might be a potential biomarker to assess oxid

244 or Spn cultivation in vitro and suggest that hemoglobin might drive the pathogen adaptation in vivo.

245 uencing (RNA-Seq) techniques, high levels of hemoglobin mRNAs (hgbRNA) present in blood can occupy va

246 type 2 diabetes mellitus, with glycosylated hemoglobin of less than 12%, central area thickness of m

247 This prediction suggests why misassembled hemoglobins often get trapped as hemichromes that accumu

248 There was a 50% increase in deoxygenated hemoglobin on R0 and R8.

249 Low preoperative hemoglobin (OR 5.40, P < 0.001), contamination of the op

250 outcome was the total duration of hypoxemia (hemoglobin oxygen saturation [Spo2] <90%) per hour, with

251 ssociated with a higher increase in glycated hemoglobin (P = 0.027).

252 we examined how the HBOC, polymerized human hemoglobin (PolyhHb), in the relaxed (R) or tense (T) qu

253 te these manifestations by mitigating sickle hemoglobin polymerization and erythrocyte sickling.

254 Although hemoglobin processing remains unaffected, PV5-deficient

255 The hemoglobin receptor, Spbhp-37, plays a role in mediating

256 IsdB and IsdH act as hemoglobin receptors and are known to actively extract h

257 estimate the parameters such as hematocrit, hemoglobin, red blood cell (RBC), white blood cell (WBC)

258 Reactivation of fetal hemoglobin remains a critical goal in the treatment of p

259 se involvement declined from 60% to 20%, and hemoglobin rose from 10.3 to 14.2 g/dL (P < .001 for all

260 In sickle cell trait, low hemoglobin S and elevated hemoglobin A were associated w

261 suggesting an epistatic relationship between hemoglobin S and PIEZO1 E756del.

262 fetal hemoglobin has been replaced by adult hemoglobin S at about 1 y after birth.

263 is caused by polymerization of the abnormal hemoglobin S upon deoxygenation in the tissues to form f

264 Low hemoglobin S was associated with faster eGFR decline in

265 , and the compound heterozygous condition of hemoglobin S with pancellular hereditary persistence of

266 We found accumulation of hemoglobin-scavenging cluster of differentiation 163 (CD

267 pid, high-density lipid, HbA1c (glycosylated hemoglobin), serum creatinine, eosinophils, lymphocyte,

268 treme altitude is not linked to elevation of hemoglobin, since CMS(+) and CMS(-) individuals had simi

269 ification of erythrocytes that are devoid of hemoglobin, so-called erythrocyte ghosts.

270 platelets, aspartate aminotransferase (AST), hemoglobin, sodium, patient age, and number of years sin

271 Red blood cell-based solutions, artificial hemoglobin solutions, and acellular solutions have all b

272 lower than previously estimated in acellular hemoglobin solutions, indicating the presence of diffusi

273 etry was used to measure MetHb (%) and other hemoglobin species.

274 ally higher percentage of female, older, and hemoglobin SS participants compared to the ACS group.

275 ith SCD-VOE (13.6 +/- 3 years; 67% male; 75% hemoglobin-SS) were randomized to 1 of 3 arginine doses:

276 yonic/fetal globin gene expression, impeding hemoglobin switching during erythroid differentiation.

277 pressor ETO2 during early erythropoiesis and hemoglobin switching is unclear.

278 sly unappreciated mechanism underlying human hemoglobin switching that illuminates new therapeutic op

279 s the genes encoding HbF and regulates human hemoglobin switching through variation in its expression

280 Legume nodules have two types of hemoglobins: symbiotic or leghemoglobins (Lbs) and nonsy

281 While most established hemoglobin tests involve the use of highly toxic reagent

282 ansitions of the quaternary structure of the hemoglobin tetramer (human) in aqueous solution (150 mM

283 s the host from oxidative damage by clearing hemoglobin that has leaked from red blood cells and also

284 in bone marrow and blood, increases in fetal hemoglobin that were distributed pancellularly, transfus

285 ly associated with their unique pH-sensitive hemoglobins that allow O(2) to be delivered to the retin

286 concentration (P = 0.02, d = 0.99) and total hemoglobin (tHb) concentration (P = 0.02, d = 0.50), ind

287 We examined the impact of hemoglobin, the largest iron reservoir in the body, on p

288 extremely-low-birth-weight infants, a higher hemoglobin threshold for red-cell transfusion did not im

289 Limited data suggest that higher hemoglobin thresholds for red-cell transfusions may redu

290 ding reduction in the percentage of glycated-hemoglobin to levels similar to lean, healthy mice.

291 se (CVD), clinical trials targeting glycated hemoglobin to near-normal levels using intensive therapy

292 maging uses the intrinsic characteristics of hemoglobin, to acquire tumor hemodynamic information, wh

293 cerebral oximetry index (COx and wCOx), and hemoglobin volume index (HVx and wHVx).

294 Hemoglobin was negatively associated with ESA dose and c

295 Pneumococcal growth with hemoglobin was unusually robust, exhibiting a prolonged

296 Glycosylated hemoglobin was used to estimate average glucose concentr

297 Tortuosity imposed by hemoglobin was verified by demonstrating restricted diff

298 acellular processes including endocytosis of hemoglobin, which is required for parasite growth and ar

299 9.0, -2.7 mm Hg) diets, and reduced glycated hemoglobin with the Mediterranean diet (-0.8 mmol/mol; -

300 e water with stimulated Raman scattering and hemoglobin with transient absorption.