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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 , 15.7% to 22.3%) had poor glycemic control (hemoglobin A(1c) level > 9.5%), and 65.7% (CI, 62.0% to

27 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

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

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

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

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

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

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

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

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

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

37 [-27.9 mg/dL; CI, -34.3 to -21.5 mg/dL]) and hemoglobin A(1c) levels (mean difference, -0.39% [CI, -0

38 -37.4 mg/dL; CI, -61.0 to -13.7 mg/dL]), and hemoglobin A(1c) levels (mean difference, -0.49% [CI, -0

39 12-month change in hemoglobin A(1c) levels (primary outcome), hypoglycemic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 -50), 30 patients with diabetes eligible for hemoglobin A(1c) testing (IQR, 15-55), and 0 patients ho

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

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

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

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

71 0 subjects at the study's conclusion; and if hemoglobin A(1c) was reported.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 5% to 56.9%]) and were less likely to have a hemoglobin A(1c)level greater than or equal to 9.5%.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Hemoglobin A (HbA) is an allosterically regulated nitrit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 incorporation into less stable mixed valence Hemoglobin A tetramers.

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

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

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

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