ライフサイエンスコーパス: hemoglobin A

1 bunits of intact, tetrameric, cyanomet human hemoglobin A.

2 operties closely approximate those of normal hemoglobin A.

3 of betaC112G are essentially those of human hemoglobin A.

4 ucture and facilitate its incorporation into hemoglobin A.

5 t was found to specifically cross-link human hemoglobin A(0) in the beta-cleft chains under oxygenate

6 te seasonal variations in population monthly hemoglobin A(1c) (A1c) values over 2 years (from October

7 nsulin independence (primary), insulin dose, hemoglobin A(1c) (HbA(1c) ), and mixed meal tolerance te

8 mplications Trial) in participants with mean hemoglobin A(1c) (HbA(1c)) >=9.0% (n=83) and <=7.0% (n=8

9 is in younger children increased with higher hemoglobin A(1c) (HbA(1c)) (relative risk [RR], 1.68 per

10 highlighted racial differences in control of hemoglobin A(1c) (HbA(1c)) and low-density lipoprotein (

11 Drug treatment intensification and hemoglobin A(1c) (HbA(1c)) and low-density lipoprotein c

12 of participants with prediabetes found that hemoglobin A(1c) (HbA(1c)) levels differed between black

13 -term glycemic control by averaging multiple hemoglobin A(1c) (HbA(1c)) measurements taken in the yea

14 The possible effect of plasma hemoglobin A(1c) (HbA(1c)) on the development of transpl

15 sional organizations advise setting specific hemoglobin A(1c) (HbA(1c)) targets for patients, and ind

16 Perform a point-of-care (POC) hemoglobin A(1c) (HbA(1c)) test via fingerstick to deter

17 fferences between black and white persons in hemoglobin A(1c) (HbA(1c)) values are well established,

18 Plasma lipoprotein, glucose, hemoglobin A(1c) (HbA(1c)), alanine aminotransferase, an

19 ng drugs for their ability to lower glycated hemoglobin A(1c) (HbA(1c)).

20 ic angina to be associated with a decline in hemoglobin A(1c) (HbA(1c)).

21 Both mean hemoglobin A(1c) (odds ratio, 1.5 [95% confidence interv

22 sociations of diabetes and glycemic control (hemoglobin A(1C) [HbA(1C)] <7% vs >=7%) with progression

23 arterial pressure [MAP], triglycerides, and hemoglobin A(1c) [HbA(1c)]) mediated by gestational diab

24 vascular disease risk factors, elevated mean hemoglobin A(1c) and macroalbuminuria were significantly

25 Incretins lowered hemoglobin A(1c) compared with placebo (weighted mean di

26 When persons with known diabetes, hemoglobin A(1c) concentrations of 7% or greater, or a h

27 In placebo-controlled trials, hemoglobin A(1c) data are presented as the difference be

28 o or other diabetes medication, and reported hemoglobin A(1c) data in nonpregnant adults with type 2

29 After 24 weeks, mean hemoglobin A(1c) decreased by 0.79% to 0.96% with dapagl

30 justment for C-reactive protein and glycated hemoglobin A(1c) did not materially attenuate this assoc

31 l B limited to age, systolic blood pressure, hemoglobin A(1c) if diabetic, smoking, total and high-de

32 , 15.7% to 22.3%) had poor glycemic control (hemoglobin A(1c) level > 9.5%), and 65.7% (CI, 62.0% to

33 2.07; 95% CI, 1.39-3.10), as well as higher hemoglobin A(1c) level (OR, 1.45; 95% CI, 1.20-1.75), lo

34 Hemoglobin A(1c) level and systolic blood pressure, meas

35 nts with type 2 diabetes mellitus (such as a hemoglobin A(1c) level as low as 6.5% to 7.0%) to avoid

36 atient adherence to diabetes screening using hemoglobin A(1c) level at in-person vs telemedicine enco

37 Most medications decreased the hemoglobin A(1c) level by about 1 percentage point and m

38 Primary end point was change in hemoglobin A(1c) level from baseline to 12 weeks.

39 Hemoglobin A(1c) level less than 7% was achieved by 32%

40 Secondary outcomes included hemoglobin A(1c) level less than 8% and less than 7%, hy

41 nically significant respiratory disease, and hemoglobin A(1c) level of 8% to 11% who were receiving d

42 Reductions in hemoglobin A(1c) level were greater with inhaled insulin

43 Glycemic control (hemoglobin A(1c) level) obtained at baseline and monthly

44 therapy produced the greatest reductions in hemoglobin A(1c) level.

45 [-27.9 mg/dL; CI, -34.3 to -21.5 mg/dL]) and hemoglobin A(1c) levels (mean difference, -0.39% [CI, -0

46 -37.4 mg/dL; CI, -61.0 to -13.7 mg/dL]), and hemoglobin A(1c) levels (mean difference, -0.49% [CI, -0

47 12-month change in hemoglobin A(1c) levels (primary outcome), hypoglycemic

48 to examine the relationship between baseline hemoglobin A(1c) levels and the prevalence and the 3-yea

49 lacebo treatment, most of these agents lower hemoglobin A(1c) levels approximately 1% to 2%.

50 Those with hemoglobin A(1c) levels between 5.5 and 6.4% exhibited n

51 ly assigned patients, the 12-month change in hemoglobin A(1c) levels compared with usual care was -0.

52 py results in modest 12-month improvement in hemoglobin A(1c) levels compared with usual care, but mo

53 lycemic control compared with baseline: Mean hemoglobin A(1c) levels decreased by 0.0071 +/- 0.0072 (

54 to examine the association between maternal hemoglobin A(1c) levels during pregnancy and risk of aut

55 inopathy at 3 years compared with those with hemoglobin A(1c) levels of 5.0-5.4% (adjusted odds ratio

56 hold for the risk of incident retinopathy at hemoglobin A(1c) levels of 6.0-7.0%.

57 ression analysis found that individuals with hemoglobin A(1c) levels of 6.5-6.9% were at significantl

58 Mean hemoglobin A(1c) levels over the preceding 22 years were

59 Black-white differences in hemoglobin A(1c) levels were also smaller after age 65 y

60 Hemoglobin A(1c) levels were higher in black than in whi

61 Hemoglobin A(1c) levels were obtained for 293 patients a

62 nsulin in decreasing fasting glucose levels, hemoglobin A(1c) levels, and the incidence of hypoglycem

63 Most 2-drug combinations similarly reduce hemoglobin A(1c) levels, but some increased risk for hyp

64 ely (79.9%) explained by fasting insulin and hemoglobin A(1c) levels; after further adjustment of the

65 ectal cancer screening in eligible patients; hemoglobin A(1c) measurement and control in patients wit

66 d not change, the proportion of persons with hemoglobin A(1c) of 6% to 8% increased from 34.2% to 47.

67 ants with diabetes were defined by levels of hemoglobin A(1c) of 6.5% or greater, use of glucose-lowe

68 g gestational diabetes mellitus) or glycated hemoglobin A(1c) of 6.5% or greater.

69 To examine whether hemoglobin A(1c) of 6.5% or higher defines a threshold f

70 of C-reactive protein, fasting insulin, and hemoglobin A(1c) or exclusion of cases diagnosed during

71 nt) and stroke volume (-2.3 mL per unit mean hemoglobin A(1c) percent) and positively related to the

72 end-diastolic volume (-3.0 mL per unit mean hemoglobin A(1c) percent) and stroke volume (-2.3 mL per

73 ere 78.1% vs. 65.9% [P < 0.001] and adjusted hemoglobin A(1c) rates were 90.3% vs. 74.9% [P < 0.001])

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

75 lycemic control efforts should individualize hemoglobin A(1c) targets so that those targets and the a

76 -50), 30 patients with diabetes eligible for hemoglobin A(1c) testing (IQR, 15-55), and 0 patients ho

77 of mammography for women 66 to 69 years, and hemoglobin A(1c) testing for 66- to 75-year-olds with di

78 For ambulatory costs, mammography rate, and hemoglobin A(1c) testing rate, the percentage of primary

79 inal results support the validity of the new hemoglobin A(1c) threshold of 6.5% or higher for diagnos

80 The average hemoglobin A(1c) was 10.8 +/- 2.8% (95 +/- 7 mmol/mol) a

81 Mean hemoglobin A(1c) was 7% (SD, 1.9%) with 20% insulin inde

82 The new diagnostic threshold of hemoglobin A(1c) was made based on evidence from cross-s

83 Hemoglobin A(1c) was normal in control subjects and simi

84 0 subjects at the study's conclusion; and if hemoglobin A(1c) was reported.

85 n, D-dimer, C-reactive protein, insulin, and hemoglobin A(1c) were assayed in blood samples acquired

86 Decreases in HOMA-IR and hemoglobin A(1c) were observed even with modest weight r

87 s, high-density lipoprotein cholesterol, and hemoglobin A(1c) were similar between the sexes.

88 mportantly, to control for initial values of hemoglobin A(1c), a retrospective case-control study was

89 e intercellular adhesion molecule-1, leptin, hemoglobin A(1c), and fasting insulin (adjusted odds rat

90 els of high-density lipoprotein cholesterol, hemoglobin A(1c), and fibrinogen attenuated 75% of the a

91 plasma lipid, lipoprotein, glucose, glycated hemoglobin A(1c), and fructosamine concentrations; insul

92 cardiovascular function (C-reactive protein, hemoglobin A(1c), and high density lipoprotein cholester

93 Older age, higher hemoglobin A(1c), and history of diabetes mellitus were

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

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

96 ar baseline values for DBP, SBP, AER AER and hemoglobin A(1c), but who did not progress to clinical d

97 ls adjusted for traditional risk factors and hemoglobin A(1c), detectable high-sensitivity cardiac tr

98 notype, the ZDF animals showed higher plasma hemoglobin A(1c), insulin, glucose, and free fatty acid

99 Process measures included frequency of hemoglobin A(1c), lipid, and urine protein testing; bloo

100 moking, alcohol consumption, fasting status, hemoglobin A(1c), physical activity, total energy intake

101 tors with age, sex, severity of retinopathy, hemoglobin A(1C), total cholesterol, creatinine, duratio

102 observed for levels of total adiponectin and hemoglobin A(1c), with a better metabolic profile among

103 gression to diabetes among older adults with hemoglobin A(1c)-defined prediabetes in clinical setting

104 nsity lipoprotein and total cholesterol, and hemoglobin A(1c).

105 nt (CI, -0.70 to -0.61 percentage point) for hemoglobin A(1c).

106 lcohol with HDL cholesterol, fibrinogen, and hemoglobin A(1c).

107 e associations of glycemic markers (HbA(1C) [hemoglobin A(1C)], fasting plasma glucose, and insulin r

108 5% to 56.9%]) and were less likely to have a hemoglobin A(1c)level greater than or equal to 9.5%.

109 Plasma glucose, insulin, hemoglobin A(1C,) free fatty acid, and apo B concentrati

110 , diastolic blood pressure, fasting glucose, hemoglobin A(1c,) smoking, albuminuria, hypertension, pr

111 ovides a maturation advantage for homozygous hemoglobin A (AA) or heterozygous hemoglobin S/hemoglobi

112 at hemoglobin S and normal adult hemoglobin, hemoglobin A, aggregate in high concentration phosphate

113 ion crowding by substitution of cross-linked hemoglobin A, amounting to 50% of the total hemoglobin.

114 nking hemoglobin A, hybrid formation between hemoglobin A and hemoglobin S was prevented, thus simpli

115 erentiated from these ES cells produced both hemoglobin A and hemoglobin S.

116 The reactions of oxygen with hemoglobin A and the effect of pH upon them may be repre

117 otein (AHSP) is believed to facilitate adult Hemoglobin A assembly and protect against toxic free alp

118 e (NO) with human serum albumin (HSA), human hemoglobin A, bovine myoglobin, and bovine cytochrome c

119 d protein that facilitates the production of Hemoglobin A by stabilizing free alpha-globin.

120 ften requires prandial intervention to reach hemoglobin A(c) (HbA(c)) targets.

121 eotide indicated that the levels of mRNA and hemoglobin A correlate well with the nuclear localizatio

122 Because the mouse does not have a true fetal hemoglobin, a delayed switching human gamma to beta(0) g

123 X-ray crystal structures of dehaloperoxidase-hemoglobin A (DHP A) from Amphitrite ornata soaked with

124 its level of expression diminishes and adult hemoglobin A formation begins; a causal relationship is

125 brids of a series of variants of human adult hemoglobin A have been measured at pH 7 in the presence

126 /cell) complexed with its zinc cofactor, and hemoglobin A (Hb-tetramer at approximately 450 amol/cell

127 With this method, we studied healthy hemoglobin A (HbA) and homozygous sickle hemoglobin (HbS

128 that binds monomeric alpha-subunits of human hemoglobin A (HbA) and modulates heme iron oxidation and

129 lar to those in the beta-chain of oxyferrous hemoglobin A (HbA) and oxyferrous myoglobin, respectivel

130 ckle trait, the heterozygous state of normal hemoglobin A (HbA) and sickle hemoglobin S (HbS), confer

131 tifying the cross-linking sites in human oxy hemoglobin A (HbA) cross-linked with either bis(3,5-dibr

132 population of ligand-bound adult deoxy human hemoglobin A (HbA) generated by introducing CO into a sa

133 Hemoglobin A (HbA) is an allosterically regulated nitrit

134 The average HbF/hemoglobin A (HbA) ratio was 30.9% +/- 18.7% in cultures

135 in mice harboring the SCT mutation in human hemoglobin A (HbA) than in control mice harboring wild-t

136 comparison to COHbS, COHbA, or deoxygenated Hemoglobin A (HbA), none of which have the capacity to f

137 eins, which assemble with each other to form hemoglobin A (HbA), the major blood oxygen carrier.

138 Hemoglobin A (HbA), the oxygen delivery system in humans

139 by transfusing normal blood units containing hemoglobin A (HbA).

140 ed that HbF is digested only half as well as hemoglobin A (HbA).

141 compared with control mice expressing human hemoglobin A (HbA-BERK), indicating deep/musculoskeletal

142 um glucose, insulin, C-peptide, glycosylated hemoglobin A (HbA1c), and Homeostasis Model Assessment (

143 HbSS and control Townes mice homozygous for hemoglobin A (HbAA) mice after cold exposure at 10 degre

144 ubunit is labeled at a time, to carbonmonoxy-hemoglobin A (HbCO A).

145 F cells measure the presence of fetal hemoglobin, a heritable quantitative trait in adults tha

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

147 By cross-linking hemoglobin A, hybrid formation between hemoglobin A and

148 To study allosteric mechanism in hemoglobin, a hydrogen-exchange method was used to measu

149 ng agent in SCD, as well as a substitute for hemoglobin A in beta-thalassemia.

150 levels of correct human beta-globin mRNA and hemoglobin A in patients' erythroid cells were 77 and 54

151 hemin reduction and incorporation into adult Hemoglobin A is physiologically more important than AHSP

152 eciated, i.e. about 70 times less than adult hemoglobin A (Kd = 0.01 microM and 0.68 microM, for HbF

153 n low levels of chimerism resulted in robust hemoglobin-A levels.

154 lated strongly with serum levels of glycated hemoglobin, a measure of glycemic control.

155 When azide is bound in hemoglobin, a more complex evolution of the protein stru

156 This effect was abolished by hemoglobin, a NO scavenger.

157 a guanylate cyclase inhibitor, or 10 microM hemoglobin, a NO scavenger; and under 100% oxygen (hyper

158 ction oxidize the heme iron of iron-nitrosyl-hemoglobin, a product of the deoxy-reaction, which relea

159 However, these mutations could also affect hemoglobin A production through AHSP-independent effects

160 SCs can be gene corrected ex vivo and stable hemoglobin-A production can be achieved in vivo from HBB

161 ach to elucidating the solution structure of hemoglobin, a protein with molecular weight 64.5 kDa.

162 ons, can be used to study fibers of mutants, hemoglobin A/S, and mixtures and hybrids of hemoglobin S

163 moglobin A (AA) or heterozygous hemoglobin S/hemoglobin A (SA) donor erythroid precursor cells that r

164 th unknown functions, including nonsymbiotic hemoglobin, a senescence-associated protein, and two met

165 rison of the structures with that of natural hemoglobin A shows the absence of detectable changes in

166 mans, we estimated the influence of glycated hemoglobin (a surrogate of long-term glycemic control) o

167 The RPLC adsorption of hemoglobin (a system with diffusion-limited retention) w

168 Red blood cells express high levels of hemoglobin A tetramer (alpha2beta2) to facilitate oxygen

169 ontogeny, humans produce different forms of hemoglobin, a tetramer of alpha- and beta-like hemoglobi

170 incorporation into less stable mixed valence Hemoglobin A tetramers.

171 this feature of HbF could be transferred to hemoglobin A, the single amino acid difference in their

172 ls of correctly spliced beta-globin mRNA and hemoglobin A were approximately 25-fold over background.

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

174 le hemoglobin is substituted by cross-linked hemoglobin A, which does not polymerize, and which subst

175 enzyme(s) cleave SNO to NO whereas bacterial hemoglobin, a widely distributed flavohemoglobin of poor