ライフサイエンスコーパス: HbA1c

1 HbA1c (mean 8.1% [SD 0.9] for metformin and 8.0% [0.8] f

2 HbA1c and a short questionnaire on general health might

3 HbA1c concentrations were persistently lower in the sacu

4 HbA1c data at follow-up were available for 146 people in

5 HbA1c is considered one of the primarily factor to disce

6 HbA1c was measured at baseline then every 24 weeks and F

7 HbA1c was obtained every 3 mo; 1,5-anhydroglucitol was o

8 ater decrease in fasting insulin (P = 0.04), HbA1c (P = 0.0001), and HOMA-IR (P = 0.02), and a lesser

9 ty, baseline hemoglobin A1c (HbA1c) > 5.05%, HbA1c < 4.92%] and assayed using GC-MS, chromatograms we

10 mass index, 31.4 kg/m(2) [range, 18.2-60.1]; HbA1c level, 7.6%, [range, 5.2-11.0]).

11 ssociation studies (GWAS) have identified 18 HbA1c-associated genetic variants.

12 eline HbA1c was 8.05% (SD 0.85); at week 30, HbA1c significantly decreased by 1.45% (95% CI -1.65 to

13 ere: weight -3.77 kg (95% CI: -4.55; -2.99), HbA1c -0.21% (-0.29; -0.13), FBG -2.40 mg/dL (-3.59; -1.

14 , stable adiposity, baseline hemoglobin A1c (HbA1c) > 5.05%, HbA1c < 4.92%] and assayed using GC-MS,

15 g/dl (11.1 mmol/l), glycated hemoglobin A1c (HbA1c) >6.5%, self-reported physician-diagnosed diabetes

16 is to evaluate the value of hemoglobin A1c (HbA1c) as a screening tool for ketosis in T2DM patients.

17 rimary outcome was change in hemoglobin A1c (HbA1c) from baseline to 12-month follow-up, and equivale

18 mary end point was change in hemoglobin A1c (HbA1c) from baseline to week 26.

19 Hemoglobin A1C (HbA1c) levels are often obtained in potential pancreas g

20 els, insulin resistance, and hemoglobin A1c (HbA1c) levels in first-episode antipsychotic-naive indiv

21 sts as to whether the higher hemoglobin A1c (HbA1c) levels observed in black persons than in white pe

22 jections of insulin, and had hemoglobin A1c (HbA1c) levels of 7.5% to 9.9% (mean, 8.5%).

23 y insulin injections and had hemoglobin A1c (HbA1c) levels of 7.5% to 9.9%.

24 als with type 1 diabetes and hemoglobin A1c (HbA1c) of at least 7.5% (58 mmol/mol) treated with multi

25 Whether preoperative hemoglobin A1c (HbA1c) or postoperative glucose levels are more useful i

26 Hemoglobin A1c (HbA1c) reflects past glucose concentrations, but this re

27 en baseline and time-varying hemoglobin A1c (HbA1c) values and development of community antiinfective

28 y age, duration of diabetes, hemoglobin A1c (HbA1c), body mass index (BMI), best-corrected visual acu

29 essure, waist circumference, hemoglobin A1c (HbA1c), insulin resistance, triglycerides, HDL cholester

30 ated with acute decreases in hemoglobin A1c (HbA1c).

31 Unfortunately, tests such as hemoglobin A1c (HbA1c)/fasting plasma glucose (FPG) alone fail to diagno

32 controlled type 1 diabetes (hemoglobin A1c [HbA1c] >8.0%) were recruited from the Diabetes Center fo

33 [2-hCG] level, and glycated hemoglobin A1c [HbA1c] level) at enrollment, and cases were tested again

34 Proportions achieving HbA1c level less than 7% plus BP less than 130/80 mm Hg

35 ration clinical categories and 0.640 for ADA HbA1c clinical categories (difference -0.005, 95% CI -0.

36 ration clinical categories and 0.688 for ADA HbA1c clinical categories for all-cause mortality.

37 l concentration categories and 0.672 for ADA HbA1c clinical categories for atherosclerotic cardiovasc

38 ration clinical categories and 0.722 for ADA HbA1c clinical categories for peripheral arterial diseas

39 entration cutoff 6.1-6.9 mmol/L), HbA1c (ADA HbA1c cutoff 5.7-6.4% [39-46 mmol/mol] and International

40 jor clinical outcomes, whereas using the ADA HbA1c cutoff (2027 [19%] of 10 884 people; 18.0-19.4) an

41 Prediabetes defined using the ADA HbA1c cutoff showed a significant overall improvement in

42 After demographic adjustment, HbA1c-based definitions of prediabetes had higher hazard

43 ox regression, with adjustment for sex, age, HbA1c, DN, diabetes duration, smoking, systolic blood pr

44 rejections were statistically similar among HbA1c strata.

45 ratios for community-treated infection at an HbA1c level of >/=10.50%, as compared with 5.50%-<6.49%,

46 hecks increased (4.92, 6.89, and 9.71 for an HbA1c <5.7%, 5.7%-6.4%, and >6.5%, respectively; P < .00

47 e 1 diabetes for at least 2 years and had an HbA1c level of 6.0% to 12.0%.

48 uded 3778 patients with known diabetes or an HbA1c >/=6.5% at screening out of 8399 patients with HFr

49 patients, 2-hCG level > 11 mmol/L, 6.8%; and HbA1c level > 6.5%, 9.3%), compared with controls (n = 4

50 ed effect of age, body-mass index (BMI), and HbA1c showed that the diabetes factor HbA1c contributes

51 es, low-density lipoprotein cholesterol, and HbA1c and lower high-density lipoprotein cholesterol (P

52 ith body mass index, waist circumstance, and HbA1c (all P < 0.05), but not with adiponectin and lepti

53 Fasting glucose concentration and HbA1c were measured at visit 2 and fasting glucose conce

54 (aged >/=18 years) with type 1 diabetes and HbA1c below 7.5% from Addenbrooke's Hospital (Cambridge,

55 r 4 weeks in adults with type 1 diabetes and HbA1c below 7.5% is safe and well tolerated, improves gl

56 01 concurrent measures of 2-hour glucose and HbA1c concentration for those with SCT (mean, 5.35%) vs

57 c was negatively correlated with glucose and HbA1c levels in DM2.

58 2 concurrent measures of fasting glucose and HbA1c levels.

59 All glucose and HbA1c results from LTx until study end were included, an

60 ists in the relationship of mean glucose and HbA1c.

61 Demographics, health history, and HbA1c levels were retrieved from medical charts.

62 with patients with no diabetes mellitus and HbA1c < 6.0%).

63 mg significantly improved blood pressure and HbA1c and was tolerated similarly to placebo.

64 hanges in seated systolic blood pressure and HbA1c measured in the full analysis set, which included

65 between plasma organophosphate residues and HbA1c but no association with acetylcholine esterase was

66 asma insulin levels, insulin resistance, and HbA1c levels were calculated.

67 To evaluate the association between SCT and HbA1c for given levels of fasting or 2-hour glucose leve

68 After adjusting for sex and HbA1c, AL progression was also statistically significant

69 und between the lens densitometry values and HbA1c levels (r = 0.743; P = .084).

70 ciation between right hippocampal volume and HbA1c was found in patients with the Hp 1-1 genotype, wi

71 o measure important health outcomes, such as HbA1c, at follow-up.

72 On average, HbA1c levels overestimate the mean glucose concentration

73 Baseline HbA1c and self-reported general health distinguished par

74 st 30 days before screening, with a baseline HbA1c of 7.0%-10.0% (53-86 mmol/mol).

75 thod of insulin administration, and baseline HbA1c.

76 Interaction between baseline HbA1c and ranolazine's effect on Seattle Angina Question

77 1.08 (95% CI: 1.02, 1.14) for early baseline HbA1c, 1.55 (95% CI: 1.42, 1.71) for updated mean HbA1c,

78 After adjusting for baseline HbA1c, significant changes were still observed for sever

79 48 years [SD, 13]; 44% women; mean baseline HbA1c level, 8.6% [SD, 0.6%]; and median diabetes durati

80 From a mean baseline HbA1c of 8.17% (SD 0.89), at week 30, 0.5 and 1.0 mg sem

81 Mean baseline HbA1c was 8.05% (SD 0.85); at week 30, HbA1c significant

82 Mean baseline HbA1c was 8.53% (70 mmol/mol; SD 0.67% [7.3 mmol/mol]).

83 rs [SD, 8.9]; women, 47 [48%]; mean baseline HbA1c, 6.7%), 93 participants completed the trial.

84 ittee review of medical records, or baseline HbA1c of 6.5% (48 mmol/mol) or greater or fasting plasma

85 Patients with the poorest baseline HbA1c values (>/=9.0%) had the worst associated changes

86 na at 6 months was proportionate to baseline HbA1c, but the effect on angina dissipated by 12 months.

87 Participants with baseline HbA1c > 5.05% had 21-fold (95% CI: 19.84, 21.41) higher

88 rically greater among patients with baseline HbA1c >/=7.5% than those with HbA1c <7.5% (interaction p

89 CRT, BCVA, HbA1c, and prevalence of systemic arterial hypertension

90 t gain was associated with marginally better HbA1c outcomes only among patients with near normal HbA1

91 boronic acid (APBA), which selectively binds HbA1c via cis-diol interactions.

92 ticipants with HbA1c 6.8% or higher, or both HbA1c less than 6.8% and Short Form Health Survey (SF-36

93 in right hippocampal volume is explained by HbA1c levels among Hp 1-1 carriers and that 3.22% is exp

94 1-1 carriers and that 3.22% is explained by HbA1c levels among Hp 1-1 noncarriers.

95 tions, and glycemic control, as reflected by HbA1c reduction, results in decreased risk of microvascu

96 ponse and web-response system, stratified by HbA1c, BMI, region, and estimated glomerular filtration

97 ions based on fasting glucose concentration, HbA1c, and 2 h glucose concentration during over two dec

98 thout SCT data, those without any concurrent HbA1c and glucose measurements, and those with hemoglobi

99 2 diabetes and inadequate glycaemic control (HbA1c 8-12% [64-108 mmol/mol]) despite stable metformin

100 Long-term glycemic control (HbA1c <7%) was seen in 63% of patients (vs 31% at baseli

101 -matched subjects had good glycemic control (HbA1c <8%).

102 ed control versus uniform intensive control (HbA1c level <7%) for the U.S. population with type 2 dia

103 , team diabetes patients had less-controlled HbA1c (Odds ratio=0.83, 95% CI: 0.66, 0.99), increased h

104 ever, only AED group significantly decreased HbA1c (-4.4%, p = 0.01) compared with the NI group (-0.6

105 placebo, ranolazine significantly decreased HbA1c by 0.42 +/- 0.08% (adjusted mean difference +/- SE

106 er 2 inhibition with canagliflozin decreases HbA1c, body weight, BP, and albuminuria, implying that c

107 had inadequately controlled type 1 diabetes (HbA1c between >/=7.7% and </=11.0% [>/=61.0 mmol/mol and

108 th moderately or poorly controlled diabetes (HbA1c 6.8% or higher) and subjects with well controlled

109 and subjects with well controlled diabetes (HbA1c less than 6.8%) and good self-reported health (85%

110 Age, duration of diabetes, HbA1c, BMI, BCVA, and CST had no impact on the ability t

111 we researched the relationship between donor HbA1c levels and postoperative pancreas graft survival.

112 ough routinely measured, the impact of donor HbA1c levels on pancreas graft outcomes has not been rep

113 t organization use of HbA1c shows that donor HbA1c levels between 3.5 and 6.2 in otherwise transplant

114 ), and HbA1c showed that the diabetes factor HbA1c contributes significantly to the extent of chlorin

115 5% confidence interval (CI): 0.94, 1.00) for HbA1c measured at early baseline, 1.09 (95% CI: 1.03, 1.

116 In logistic regression models adjusting for HbA1c, postoperative glucose levels, postoperative insul

117 worth, and glycated hemoglobin A1c fraction (HbA1c).

118 Outcomes were grouped into: objective (e.g., HbA1c levels), subjective (e.g., self-efficacy), and hea

119 For a given HbA1c level, the mean glucose concentration was signific

120 with LDL cholesterol, fasting blood glucose, HbA1c, fasting insulin, bodyweight, waist-to-hip ratio,

121 d GEE analyses, for a given fasting glucose, HbA1c values were statistically significantly lower in t

122 .9, >/=6.0 % and not available, or 2 groups: HbA1c <5.7, >/=5.7%).

123 s according to their HbA1c levels (5 groups: HbA1c < 5.0, 5.0-5.4, 5.5-5.9, >/=6.0 % and not availabl

124 ents included in the HbA1c analysis, 46% had HbA1c <7.0%, 36% between 7.0% and 8.9%, and 19% >/=9.0%

125 icipants were receiving insulin, and 60% had HbA1c <7%.

126 ol) or in women with type 1 diabetes who had HbA1c lower than 8.8% (<73 mmol/mol).

127 as noted in men with type 1 diabetes who had HbA1c lower than 9.7% (<83 mmol/mol) or in women with ty

128 f diabetes, defined as glycated haemoglobin (HbA1c) of less than 6.5% (<48 mmol/mol) after at least 2

129 n measures, as well as glycated haemoglobin (HbA1c), are used to diagnose and monitor diabetes.

130 jections) and baseline glycated haemoglobin (HbA1c).

131 ith type 2 diabetes and glycated hemoglobin (HbA1c) >58 mmol/mol.

132 ecruited: subjects with glycated hemoglobin (HbA1c) </=7% and subjects with HbA1c >/=8%.

133 5% CI: 0.72, 2.71), and glycated hemoglobin (HbA1c) (betaPFOS=0.03%; 95% CI: 0.002, 0.07; betaPFOA=0.

134 The level of Glycated hemoglobin (HbA1c) is accordingly examined for checking diabetes mel

135 Glycated hemoglobin (HbA1c) is used to diagnose type 2 diabetes (T2D) and ass

136 ce, fat percentage, and glycated hemoglobin (HbA1c) level were recorded chairside.

137 al status on changes of glycated hemoglobin (HbA1c) levels of patients with type 2 DM (DMt2).

138 cated proteins, such as glycated hemoglobin (HbA1c) or glycated albumin (GA) in the blood, are essent

139 ic control (assessed by glycated hemoglobin (HbA1c) values) in patients from the Kaiser Permanente No

140 ugars and its effect on glycated hemoglobin (HbA1c), fasting blood glucose, insulin, and triglyceride

141 tatus, fasting glucose, glycated hemoglobin (HbA1c), fructosamine, glycated albumin), and a latent va

142 t assessed the outcomes glycated hemoglobin (HbA1c), weight, body mass index (BMI; in kg/m(2)), and L

143 for the recognition of glycated hemoglobin (HbA1c).

144 OR15+years = 3.99), glycosylated hemoglobin (HbA1c) (OR6.5-6.9% = 1.33, OR7-7.9% = 1.86, OR8%+ = 3.22

145 e versus placebo on glycosylated hemoglobin (HbA1c) at 6- and 12-month follow-up.

146 ation of DM and the glycosylated hemoglobin (HbA1c) levels of the patients in the DM group were recor

147 ycemic control (average glycated hemoglobin [HbA1c] >/=8% during the year) while the other 27 age- an

148 rol in type 2 diabetes (glycated hemoglobin [HbA1c] level <7%) is an established, cost-effective stan

149 lood glucose [FBG], and glycated hemoglobin [HbA1c]) and survival in all lung transplant (LTx) recipi

150 However, HbA1c levels (Hedges g = -0.08; CI, -0.34 to 0.18; P = .

151 7 [19%] of 10 884 people; 18.0-19.4) and IEC HbA1c cutoff (970 [9%] of 10 844 people; 8.4-9.5), and t

152 ol] and International Expert Committee [IEC] HbA1c cutoff 6.0-6.4% [42-46 mmol/mol]), and 2 h glucose

153 RETATION: Semaglutide significantly improved HbA1c and bodyweight in patients with type 2 diabetes co

154 cacy outcome was the change from baseline in HbA1c after 24 weeks of treatment in the full analysis s

155 The primary outcome was change in HbA1c from randomisation to 34 weeks' gestation in pregn

156 Mean change in HbA1c level from baseline to week 26 decreased with oral

157 treatment-group difference in mean change in HbA1c level from baseline was -0.6% (95% CI, -0.8% to -0

158 The primary outcome was change in HbA1c levels at 3 months.

159 dherence to glucose monitoring and change in HbA1c levels at 6 months.

160 The change in HbA1c levels from baseline did not differ significantly

161 nce (gain, loss, or no change) and change in HbA1c value, adjusting for individual- and area-level at

162 Following SVR, mean change in HbA1c was -0.022 +/- 0.53%; however, total and low-densi

163 Changes in HbA1c and glucose were minimal and did not differ by sus

164 We assessed changes in HbA1c, triglycerides, HDL cholesterol and BMI in a mixed

165 usual care resulted in a greater decrease in HbA1c level during 24 weeks.

166 he CPAP group achieved a greater decrease in HbA1c levels compared with the control group.

167 was associated with an absolute decrease in HbA1c of 0.81%-units (95% CI 0.66-0.96) per allele in he

168 Difference in HbA1c between weeks 26 and 69 for the 2 treatments.

169 We found a small difference in HbA1c in pregnant women using CGM (mean difference -0.19

170 % CI: 0.36%, 0.53%) lower mean difference in HbA1c, a 0.55 (95% CI: 0.02, 1.1) lower BMI, a 2.1-kg (9

171 There were no significant differences in HbA1c concentrations between randomised groups at screen

172 kept a focus on interancestry differences in HbA1c genetics performance that might influence race-anc

173 right hippocampal volume per 14% increase in HbA1c (P = 0.0007) versus a 0.009-mL decrease in Hp 1-1

174 progression was associated with increase in HbA1c in patients with DMt2.

175 Increase in HbA1c over time was statistically significant when sever

176 For every 1-point increase in HbA1c, the hazard for DR increased by 20% (HR = 1.20; 95

177 rgin of 0.3% to establish non-inferiority in HbA1c reduction.

178 taCTX in the SPI group with the reduction in HbA1c (r(2) = 0.42; p = 0.04) and HOMA-IR (r(2) = 0.54;

179 lsartan had a greater long-term reduction in HbA1c than those receiving enalapril.

180 emaglutide resulted in greater reductions in HbA1c and weight, with fewer hypoglycaemic episodes, and

181 g, or canagliflozin 300 mg had reductions in HbA1c of 0.81%, 0.82%, and 0.93%, respectively, at 1 yea

182 data indicate that the impact of increasing HbA1c and SBP on DR probability is incrementally the sam

183 lucose measurements, or genetically-informed HbA1c diagnostic thresholds in people with G6PD deficien

184 erides, LDL- and total cholesterol, insulin, HbA1c and HOMA-IR (p < 0.005, 0.01, < 0.001, < 0.005, 0.

185 se regression and HOMA-IR, glucose, insulin, HbA1c, leptin, and high-sensitivity C-reactive protein l

186 lucose concentration cutoff 6.1-6.9 mmol/L), HbA1c (ADA HbA1c cutoff 5.7-6.4% [39-46 mmol/mol] and In

187 -0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (95% CI: -12.90, -7.10 g/L; impaired gluc

188 s fasting triglycerides, blood lipoproteins, HbA1c, and body weight.We included 14 comparison arms fr

189 sk (such as metformin) are required, a lower HbA1c target may be appropriate.

190 nal treatment for 26 weeks resulted in lower HbA1c.

191 hritol compared with participants with lower HbA1c (P < 0.001, FDR = 0.00016).

192 variant of TMPRSS6 was associated with lower HbA1c levels (P = 8.66 x 10-10).

193 Mean HbA1c change from baseline to 28 weeks was 0.3% (SD 0.9;

194 Mean HbA1c levels decreased to 7.7% in the CGM group and 8.0%

195 Mean HbA1c reduction from baseline was 1.1% at 12 weeks and 1

196 Mean HbA1c was 7.92% (63 mmol/mol) during continuous glucose

197 s those without SCT (mean, 5.65%) for a mean HbA1c difference of -0.30% (95% CI, -0.39% to -0.21%).

198 e was 43.7 years, 45.3% were women, and mean HbA1c was 8.6% (70 mmol/mol).

199 raftment but with significant different mean HbA1c levels of 5.5 +/- 0.4% for SPK and 8.3 +/- 1.5% fo

200 ce of -0.90% (95% CI -1.22 to -0.58) in mean HbA1c at completion of follow-up.

201 The primary endpoint was change in mean HbA1c from baseline to week 30 and the confirmatory seco

202 The primary endpoint was the change in mean HbA1c from baseline to week 30, and the confirmatory sec

203 ons (P = 0.013), which was reflected in mean HbA1c values in black persons being 0.4 percentage point

204 ean FBG and RBG and each 1% increase in mean HbA1c were associated with mortality increases of 18% (9

205 h (5.72%) vs those without (6.01%) SCT (mean HbA1c difference, -0.29%; 95% CI, -0.35% to -0.23%).

206 rom baseline to 12-month follow-up, the mean HbA1c level changed from 6.65% to 6.34% in the lifestyle

207 The mean HbA1c level was 9.1% in black persons and 8.3% in white

208 , 1.09 (95% CI: 1.03, 1.14) for updated mean HbA1c, 1.13 (95% CI: 1.08, 1.19) for updated time-weight

209 , 1.55 (95% CI: 1.42, 1.71) for updated mean HbA1c, 1.58 (95% CI: 1.44, 1.72) for updated time-weight

210 : 1.08, 1.19) for updated time-weighted mean HbA1c, and 1.19 (95% CI: 1.14, 1.26) for the latest upda

211 : 1.44, 1.72) for updated time-weighted mean HbA1c, and 1.64 (95% CI: 1.51, 1.79) for the latest upda

212 nce in change in central-laboratory-measured HbA1c level from baseline to 24 weeks.

213 nt, international normalized ratio measured, HbA1c measurement, speech language pathology consultatio

214 was 0.38 (0.04-0.5) U/kg per day, and median HbA1c was 6.6% (5.9%-8.1%).

215 al survey using data from the China National HbA1c Surveillance System (CNHSS), including 222,773 Chi

216 Novo Nordisk China (for the China National HbA1c Surveillance System [CNHSS]) and Merck Sharp & Doh

217 utcomes only among patients with near normal HbA1c values at baseline.

218 MAGE and AUCpp but not HbA1c were independently associated with the altered epi

219 se race only partially explains the observed HbA1c differences between black persons and white person

220 logy would affect the diagnostic accuracy of HbA1c.

221 modest effects on the diagnostic accuracy of HbA1c.

222 application for electrochemical detection of HbA1c in human blood samples.

223 sociated with greater postpartum increase of HbA1c (beta = 0.08%; P = 0.03) and 2-hour OGTT glucose c

224 Levels of HbA1c and FPG were similar between the evolocumab and pl

225 s, participants with SCT had lower levels of HbA1c at any given concentration of fasting or 2-hour gl

226 Levels of HbA1c track epidemiologically with diabetic complication

227 We therefore expanded the number of HbA1c-associated loci and tested the effect of genetic r

228 enalapril was consistent across the range of HbA1c in the trial.

229 the dental office by chairside recordings of HbA1c levels.

230 center/organ procurement organization use of HbA1c shows that donor HbA1c levels between 3.5 and 6.2

231 od glucose after glucose overload (2h-OGTT), HbA1c, triglyceride (TG) levels and HOMA-IR and positive

232 d a nearly identical DR probability based on HbA1c and SBP.

233 h professionals leads to a greater effect on HbA1c, weight, and LDL cholesterol.

234 of sacubitril/valsartan versus enalapril on HbA1c and time to first-time initiation of insulin or or

235 d regarding the influence the program had on HbA1c.

236 diabetes risk in patients with prediabetes (HbA1c 5.7-6.4% [39-46 mmol/mol] or FPG 5.6-6.9 mmol/L) a

237 Preoperative HbA1c levels were examined as a continuous and categoric

238 Patients with a preoperative HbA1c of more than 6.5% had lower thresholds for postope

239 By contrast, a preoperative HbA1c of more than 6.5% was associated with decreased 30

240 As preoperative HbA1c increased, the frequency of 48-hour postoperative

241 d readmissions with the closest preoperative HbA1c within 90 days and the highest postoperative gluco

242 eased readmission, but elevated preoperative HbA1c was not.

243 A higher preoperative HbA1c was associated with increased postoperative glucos

244 To examine the use of preoperative HbA1c and early postoperative glucose levels for predict

245 operations with measurements of preoperative HbA1c levels and postoperative glucose levels.

246 coronary artery disease, C-reactive protein, HbA1c, height, obesity, smoking status, triglycerides, t

247 t circumference, blood pressure, heart rate, HbA1c, blood glucose, LDL-to-HDL cholesterol ratio, C-re

248 doses of dapagliflozin significantly reduced HbA1c compared with placebo (mean difference from baseli

249 inical observation of a GABAA-R PAM reducing HbA1c levels in diabetic patients.

250 off medications) in 26%, complete remission (HbA1c <6% off medications) in 11%, and "cure" (continuou

251 at baseline, P < 0.001), diabetes remission (HbA1c <6.5% off medications) in 26%, complete remission

252 seline parameters versus CSII, respectively, HbA1c (6.4% cf 8.2%), median HYPOscore (0 cf 1085), mean

253 The mean (SD) HbA1c at follow-up was 63.0 (15.5) mmol/mol in the inter

254 MHS) registry of 8.35 (2.63) and a mean (SD) HbA1c level of 6.66 (0.73)% [49 mmol/mol].

255 ol, forced expiratory volume, grip strength, HbA1c, longevity, obesity, self-rated health, smoking st

256 Thirty-nine patients with uncontrolled T2D (HbA1c >7.5%) and 24 age- and sex-matched healthy control

257 ths in patients with T2D to achieve a target HbA1c of </=7.0%.

258 dysfunction in patients with T2D with target HbA1c levels.

259 Intensive glycemic control (IGC) targeting HbA1c fails to show an unequivocal reduction of macrovas

260 onses during oral glucose tolerance testing, HbA1c, beta-cell function, and insulin resistance in hea

261 etic variants associated with HbA1c and that HbA1c variants implicated in erythrocytic biology would

262 These findings suggest that HbA1c may systematically underestimate past glycemia in

263 The HbA1c difference by SCT was greater at higher fasting (P

264 mong 1,933 diabetic patients included in the HbA1c analysis, 46% had HbA1c <7.0%, 36% between 7.0% an

265 ical glycemic markers fasting glucose or the HbA1c, and vice versa.

266 Patients who improved their HbA1c by >/=1.0% had a significantly higher relative imp

267 r basic knowledge in DR and memorizing their HbA1c level showed a higher propensity for SDM (OR = 1.1

268 ere separated into groups according to their HbA1c levels (5 groups: HbA1c < 5.0, 5.0-5.4, 5.5-5.9, >

269 Since GA, compared to HbA1c, is more sensitive to short term changes in glycem

270 inear range of 0.3 to 2000muM in response to HbA1c at +0.2V.

271 m showed excellent selectivity (100%) toward HbA1c at distinctive test lines when challenged with HbA

272 During the first year of follow-up, HbA1c concentrations decreased by 0.16% (SD 1.40) in the

273 (95% CI: 1.14, 1.26) for the latest updated HbA1c.

274 (95% CI: 1.51, 1.79) for the latest updated HbA1c.

275 ong participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs

276 s suggest that prediabetes definitions using HbA1c were more specific and provided modest improvement

277 s suggest that prediabetes definitions using HbA1c were more specific and provided modest improvement

278 ening for the G6PD genotype along with using HbA1c to diagnose T2D in populations of African ancestry

279 The primary outcome was HbA1c reduction at 24 weeks.

280 Secondary outcomes were HbA1c, LDL cholesterol, estimated glomerular filtration

281 While HbA1c, mean glucose and median percent time hypoglycemic

282 ing the risk of hypoglycaemia in adults with HbA1c below 7.5% (58 mmol/mol).

283 Individuals were assessed with HbA1c, Edmonton Hypoglycemia Score (HYPOscore), continuo

284 entify more genetic variants associated with HbA1c and that HbA1c variants implicated in erythrocytic

285 2 erythrocytic variants were associated with HbA1c at genome-wide significance.

286 d 60 common genetic variants associated with HbA1c.

287 data, we did not identify associations with HbA1c (0.03%, -0.01 to 0.08), fasting insulin (0.00%, -0

288 er studies in large multiethnic cohorts with HbA1c, glycemic, and erythrocytic traits are required to

289 els of dG-gx-dC and dG-gx-dA correlated with HbA1c with statistical significance.

290 event over 9.6 years among participants with HbA1c 6.8% or higher, or both HbA1c less than 6.8% and S

291 73%, p=0.038) By contrast, participants with HbA1c less than 6.8% and baseline SF-36 general health s

292 glucose monitoring and compared by race with HbA1c, glycated albumin, and fructosamine values.

293 T2D to remain undiagnosed when screened with HbA1c.

294 (GEE) to examine the association of SCT with HbA1c levels, controlling for fasting or 2-hour glucose

295 d hemoglobin (HbA1c) </=7% and subjects with HbA1c >/=8%.

296 , 95% CI: 1.72% to 3.78%), and in those with HbA1c <6.5% at baseline (3.08%, 95% CI: 2.47% to 3.69%).

297 with baseline HbA1c >/=7.5% than those with HbA1c <7.5% (interaction p = 0.07).

298 o be used as an alternative or together with HbA1c as a surrogate marker indicator for glycemic contr

299 ng fasting plasma glucose (for areas without HbA1c testing).

300 Supermarket loss was associated with worse HbA1c trajectories for those with good, moderate, and po