ライフサイエンスコーパス: hyperglycemic

1 All patients with prediabetes were hyperglycemic.

2 postoperative day 2, 29.1% of patients were hyperglycemic.

3 owever, this outcome is lower and delayed in hyperglycemics.

4 hich the normal 5.6 mm glucose is changed to hyperglycemic 25.6 mm glucose greatly increase lipid for

5 ompare fluxes through various pathways under hyperglycemic (26 mm) and euglycemic (5 mm) conditions.

6 ere incubated in normoglycemic (NG, 5 mM) or hyperglycemic (30 mM or 50 mM) conditions in the presenc

7 e responses of the animals when submitted to hyperglycemic (40% glucose i.v.) and hypoglycemic (5 U/k

8 ed under clamped euglycemic (4-6 mmol/L) and hyperglycemic (9-11 mmol/L) conditions at baseline and e

9 The anti-hyperglycemic activity was highest (p <= 0.05) in peel a

10 esidual beta-cells: these mice indeed became hyperglycemic after insulin receptor blockade.

11 canonical view that glucagon is primarily a hyperglycemic agent driven by fasting/hypoglycemia and h

12 young type 2 and the target of emerging anti-hyperglycemic agents that function as glucokinase activa

13 This effect was also observed in hyperglycemic Akita mice and in diabetic patients.

14 Subsequently, fa/fa rats became both hyperglycemic and albuminuric.

15 Using the hyperglycemic and euglycemic clamp, we demonstrated impa

16 Also, these mice became progressively hyperglycemic and failed to secrete insulin, although pa

17 treatment with atorvastatin made the animals hyperglycemic and glucose intolerant in comparison with

18 After 16 weeks of the HFD, S2HET mice were hyperglycemic and glucose intolerant, but adiposity and

19 nt with previous reports, GPR120 KO mice are hyperglycemic and glucose intolerant; however, our KO mi

20 ctable in the adult rodent pancreas, even in hyperglycemic and hyperlipidemic models or 1.5-year-old

21 During CGM, average percent time in hyperglycemic and hypoglycemic range was larger in RYGBP

22 tions can result as patients experience both hyperglycemic and hypoglycemic states.

23 s are exacerbated in murine strains that are hyperglycemic and insulin resistant.

24 ATP-to-Pi ratio was reduced in both hyperglycemic and ketotic rats in comparison with contro

25 , but mildly insulin-resistant, KK mice; and hyperglycemic and markedly insulin-resistant KKAy mice w

26 that are infected with KSHV (TIVE-KSHV) into hyperglycemic and normal nude mice.

27 in diabetic mice and in cultured cells under hyperglycemic and proinflammatory conditions.

28 ting vascular repair, are dysfunctional in a hyperglycemic and/or hypercholesterolemic environment.

29 ls that allowed comparison of the effects of hyperglycemic and/or insulin-resistant metabolic stress

30 es of 12.5 mmol/L or greater (>/=225 mg/dL) (hyperglycemic) and/or a glucose level less than 3.9 mmol

31 ation, and resistance artery constriction in hyperglycemic animals on high-fat diet.

32 ycemia-induced renal injury ENaC activity in hyperglycemic animals was elevated in SS but not SS(Nox4

33 ted BAs reduce circulating glucose levels in hyperglycemic animals.

34 knockout mice were compared with age-matched hyperglycemic ApoE(-/-) littermates.

35 Lack of TSP-1 prevented lesion formation in hyperglycemic ApoE(-/-) mice, mimicking the atheroprotec

36 ointimal thickness in aortic root lesions of hyperglycemic ApoE(-/-) mice; also, smooth muscle cell (

37 demonstrated that burn-injured adults remain hyperglycemic, are insulin resistant, and express defect

38 s for the Ins2(Akita) mutation, which become hyperglycemic at approximately 4 weeks old, were studied

39 ltransferase overexpressing mice were mildly hyperglycemic at baseline and, similar to mice treated w

40 HED pigs were hyperglycemic at time 0, and blood glucose did not retur

41 Islet transplantation was performed in hyperglycemic B-cell-deficient(muMT) mice, in a purely a

42 lycemic and insulin-sensitive C57BL/6J mice; hyperglycemic, but mildly insulin-resistant, KK mice; an

43 in a purely alloimmune setting (BALB/c into hyperglycemic C57BL/6), in a purely autoimmune setting (

44 A subgroup (n=70) received a 2-h hyperglycemic clamp (+125 mg/dL), and first- and second-

45 an oral glucose tolerance test and two-step hyperglycemic clamp (100 and 300 mg/dL) followed by intr

46 normal-weight AA versus C peers during a 2-h hyperglycemic clamp (12.5 mmol/L) on two occasions: 1) i

47 dogs underwent a hyperinsulinemic (4x basal) hyperglycemic clamp (arterial blood glucose 146 +/- 2 mg

48 tration curve during the first 12 min of the hyperglycemic clamp (DeltaC-pep[AUC]0-12) was inversely

49 euglycemia followed by a 60-min +5.5 mmol/L hyperglycemic clamp (HG).

50 We studied healthy individuals using a hyperglycemic clamp and GLP-1 infusion.

51 beta-Cell function was determined with the hyperglycemic clamp and morphometric analysis of pancrea

52 -cell function was measured with a nine-step hyperglycemic clamp before and 48 h and 14 days after th

53 Insulin sensitivity during hyperglycemic clamp declined by ~30% and ~55% (both P <

54 e reabsorption was measured with the stepped hyperglycemic clamp in 15 subjects with type 2 diabetes

55 glucose infusion rate/insulin (mg/kg/min) by hyperglycemic clamp in 50 adolescents with T1D (age 16.1

56 by applying mathematical modeling during the hyperglycemic clamp in 60 normal glucose tolerance (NGT)

57 sma C-peptide concentration curve during the hyperglycemic clamp increased by 22 +/- 4 and 23 +/- 4%

58 he first (10-80 min) and second (90-160 min) hyperglycemic clamp steps increased by 3.8-fold and 1.9-

59 ), respectively, during the first and second hyperglycemic clamp steps.

60 meostasis by hyperinsulinemic-euglycemic and hyperglycemic clamp studies and energy expenditure by in

61 ealthy subjects (HS) was conducted using the hyperglycemic clamp technique together with duodenal nut

62 ciation measuring insulin sensitivity by the hyperglycemic clamp technique.

63 Insulin sensitivity was assessed using the hyperglycemic clamp technique.

64 A subsample of 81 adolescents underwent the hyperglycemic clamp technique.

65 Insulin sensitivity during the hyperglycemic clamp was not affected by empagliflozin in

66 AM, n = 5; CHADN, n = 6), a hyperinsulinemic-hyperglycemic clamp was used to assess whether CHADN cou

67 A hyperinsulinemic-euglycemic and a hyperglycemic clamp were performed in 110 youths to quan

68 e diet [P-HFF]) underwent a hyperinsulinemic-hyperglycemic clamp with intraportal glucose infusion.

69 ndirect calorimetry), insulin secretion (2-h hyperglycemic clamp), and body composition (dual-energy

70 r change in plasma glucose levels during the hyperglycemic clamp, individuals with T1DM had significa

71 as the ratio of the OGTT-betaCGS to the 2-h hyperglycemic clamp-betaCGS.

72 hyperinsulinemic-euglycemic clamp and a 2-h hyperglycemic clamp.

73 se-induced insulin secretion both in vivo in hyperglycemic clamps and ex vivo in isolated islets from

74 nd demonstrated higher insulin levels during hyperglycemic clamps compared to saline controls.

75 Hyperglycemic clamps conducted at baseline, after 12 mon

76 Hyperglycemic clamps confirmed an increase in insulin se

77 ensitivity and secretion were assessed using hyperglycemic clamps in adults and frequently sampled in

78 on GLP-1-stimulated insulin secretion during hyperglycemic clamps in nondiabetic Caucasian individual

79 Hyperglycemic clamps were also performed in a rat model

80 Hyperglycemic clamps were performed in 14 severely obese

81 a randomized order involving 2-h euglycemic-hyperglycemic clamps with coadministration of: 1) SU (gl

82 ut (Cx36(-/-)) mouse phenotype and performed hyperglycemic clamps with rapid sampling of insulin in C

83 ges, glucose tolerance tests, euglycemic and hyperglycemic clamps, as well as isolated islet and peri

84 on during glucose tolerance tests as well as hyperglycemic clamps.

85 animals to succumb to acute pancreatitis and hyperglycemic coma.

86 tatin is a potent insulin secretagogue under hyperglycemic condition, and obestatin's effect on insul

87 We found that under hyperglycemic condition, obestatin augments GSIS in rat

88 In hyperglycemic conditions (e.g., uncontrolled diabetes or

89 Hyperglycemic conditions also attenuated mTORC1 signalin

90 studied by exposing proximal tubule cells to hyperglycemic conditions and monitoring endothelial cell

91 aling in retinal Muller cells cultured under hyperglycemic conditions and the role of beta-adrenergic

92 them against oxidative stress induced under hyperglycemic conditions at a much lower concentration t

93 s (n = 49) were studied under euglycemic and hyperglycemic conditions at baseline and after PUA lower

94 In Muller cells, hyperglycemic conditions attenuated global rates of prot

95 show that human keratinocytes cultured under hyperglycemic conditions display increased levels of O-G

96 ly understood, and we sought to determine if hyperglycemic conditions enhanced EPC adhesion.

97 In R28 retinal cells in culture, hyperglycemic conditions enhanced REDD1 protein expressi

98 Hyperglycemic conditions for up to 3 days reduced cell n

99 ardiac tissue, we tested the hypothesis that hyperglycemic conditions impair CSC function.

100 mia in the retina of diabetic rodents and by hyperglycemic conditions in Muller cells concomitant wit

101 glucose reduces platelet activation whereas hyperglycemic conditions increase platelet activation.

102 trast, in REDD1-deficient R28 cells, neither hyperglycemic conditions nor the absence of insulin in c

103 largely attributed to the adverse effects of hyperglycemic conditions on normal endothelial cell (EC)

104 rates that exposure of brain microvessels to hyperglycemic conditions or advanced glycation end produ

105 Human aortic endothelial cells exposed to hyperglycemic conditions showed increased expression of

106 tions of "normal" and "disturbed flow" under hyperglycemic conditions suggesting that elevated glucos

107 ed human aortic endothelial cells (HAECs) to hyperglycemic conditions under both "normal" and "distur

108 on prevented oxidative stress in response to hyperglycemic conditions, and this protective effect req

109 lycation end products (AGE), generated under hyperglycemic conditions, can specifically interact with

110 In pathological hyperglycemic conditions, EMP-mediated miR-126-induced E

111 treated mice and cells in culture exposed to hyperglycemic conditions, expression of 4E-BP1 and its i

112 gene expression induced by inflammatory and hyperglycemic conditions, reduced migration and prolifer

113 Under hyperglycemic conditions, sirolimus impaired human aorti

114 d Muller cells cultured in normoglycemia and hyperglycemic conditions, to investigate the effects of

115 th large and small vessels are influenced by hyperglycemic conditions, which increase susceptibility

116 Under hyperglycemic conditions, ZEB1 lost its ability to bind

117 to restore beta cell mass and function under hyperglycemic conditions.

118 and its release from human MCs is reduced in hyperglycemic conditions.

119 1) receptor activation under both normo- and hyperglycemic conditions.

120 rization and limited insulin secretion under hyperglycemic conditions.

121 cose, particularly with prolonged culture in hyperglycemic conditions.

122 n in renal tubular cells and podocytes under hyperglycemic conditions.

123 ylation and prolonged expression of Egr-1 in hyperglycemic conditions.

124 on in the chick embryo was studied under two hyperglycemic conditions.

125 e, and thapsigargin-induced cell death under hyperglycemic conditions.

126 defects observed during late gestation under hyperglycemic conditions.

127 ith previously published data obtained under hyperglycemic conditions.

128 lycation end products (AGEs) generated under hyperglycemic conditions.

129 ls, surgery, and physical trauma can lead to hyperglycemic conditions.

130 ered and aberrant functions of bone cells in hyperglycemic conditions.

131 se pulmonary microvascular ECs in vivo under hyperglycemic conditions.

132 arly regulated by a shift from euglycemic to hyperglycemic conditions.

133 ute decline was in the number of deaths from hyperglycemic crisis (-2.7; 95% CI, -2.4 to -3.0).

134 nterval [CI], -76.2 to -59.3) and death from hyperglycemic crisis (-64.4%; 95% CI, -68.0 to -60.9), f

135 f acute myocardial infarction and death from hyperglycemic crisis (2.7 and 0.1 fewer cases per 10,000

136 yocardial infarction, stroke, and death from hyperglycemic crisis between 1990 and 2010, with age sta

137 ially affected in surviving and nonsurviving hyperglycemic critically ill animals in relation to mito

138 In both liver and kidney of hyperglycemic critically ill rabbits, we observed signs

139 Hyperglycemic culture conditions rendered pericytes more

140 Here, we exposed MPCCs to hypo-, normo- and hyperglycemic culture media for ~3 weeks.

141 imidazolidin-2-ylidene) alpha-amino acids in hyperglycemic diabetes patients.

142 blood monocytes derived from three different hyperglycemic diabetic mouse models: streptozotocin-trea

143 eal fibrosis induced by sodium hypochlorite, hyperglycemic dialysis solutions, or TGF-beta1.

144 Diabetes, a chronic hyperglycemic disorder, is a public health concern in In

145 ovide evidence that the influx of glucose in hyperglycemic dividing RMCs initiates intermediate gluco

146 Conversely, hyperglycemic DM patients did not have an increased risk

147 nd is as effective as VNS in suppressing the hyperglycemic effect of endotoxin exposure.

148 Furthermore, the hyperglycemic effect of galanin is also blunted in G(o)2

149 etite, while GLP-1 would protect against the hyperglycemic effect of glucagon.

150 role of starch-phenolic quality towards anti-hyperglycemic effect of RR.

151 d flavonoids and displayed a noticeable anti-hyperglycemic effect.

152 ronic intravenous injections of EDPs induced hyperglycemic effects associated with glucose uptake red

153 t DM199 administration results in acute anti-hyperglycemic effects in several preclinical models, and

154 We hypothesized that oxygen modifies hyperglycemic effects on ROS formation, resulting in dec

155 n via its anti-hypertriglyceridemic and anti-hyperglycemic effects.

156 The ability of paroxetine to improve hyperglycemic endothelial cell injury was unique among s

157 Hyperglycemic enhancement of necroptosis depends upon gl

158 sponsive to the elevated endogenous Ach in a hyperglycemic environment.

159 therapy are far from ideal resulting in hypo/hyperglycemic episodes associated with fatal complicatio

160 Increased prefrontal glutamate during acute hyperglycemic episodes could explain our previous findin

161 A history of three or more severe hyperglycemic episodes was associated with reduced aniso

162 Exposure to chronic hyperglycemia, severe hyperglycemic episodes, and severe hypoglycemia, as defi

163 Hyperglycemic-euglycemic clamp studies and glucose toler

164 The number of investigator-reported hyperglycemic events was 16 (10%) in the liraglutide gro

165 For the rate of serious hyperglycemic events, there was no significant associati

166 al often results in the largest postprandial hyperglycemic excursion in people with type 2 diabetes.

167 To the extent that hyperglycemic excursions are important in atherogenesis,

168 5-anhydroglucitol (1,5-AG) is a biomarker of hyperglycemic excursions associated with diabetic compli

169 omarker 1,5-anhydroglucitol (1,5-AG) reflect hyperglycemic excursions over the prior 1-2 weeks.

170 Within the T1D group, hyperglycemic exposure was associated with decreased GMV

171 t women with diabetes, a marker of long-term hyperglycemic exposure, predicts macrosomia in their new

172 We examined mice rendered hyperglycemic following low-dose streptozotocin prior to

173 nd there was a trend toward reduction in the hyperglycemic group.

174 carbonyl metabolites were found to change in hyperglycemic HAECs.

175 could participate in the redox signaling in hyperglycemic heart and contribute to the pathophysiolog

176 ubcellular free Zn(2+) redistribution in the hyperglycemic heart, resulting from altered ZIP7 and ZnT

177 Hyperglycemic (HG) and hyperinsulinemic-euglycemic (HI)

178 Purified T cells from chronically hyperglycemic (HG) mice produced higher levels of Th1, T

179 ll receptor repertoires compared to those of hyperglycemic (Hglc) mice.

180 the recruitment of genes from the Crustacean Hyperglycemic Hormone (CHH) and arthropod Ion Transport

181 lated largely by ecdysteroids and crustacean hyperglycemic hormone (CHH) neuropeptide family includin

182 cgamma receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice.

183 ically insulin-resistant patients with T2DM, hyperglycemic-hyperinsulinemia did not increase ER stres

184 In obese, hyperglycemic, hyperinsulinemic female Lepr(db/db) mice,

185 During a postprandial hyperglycemic-hyperinsulinemic clamp after SGLT2-I treat

186 A hyperglycemic-hyperinsulinemic clamp was established in

187 n fat biopsies obtained before and after 8-h hyperglycemic-hyperinsulinemic clamping in 13 normal sub

188 and ATBF on three different occasions during hyperglycemic-hyperinsulinemic clamps with concomitant i

189 Here, the beta-cell-deficient obese hyperglycemic/hyperinsulinemic KS db/db mouse model was

190 At gestational day (GD) 12.5, GDM produced a hyperglycemic, hyperleptinemic maternal state, whereas M

191 In hyperglycemic-hyperlipidemic kidneys, the accumulation o

192 er-capture microdissection in euglycemic and hyperglycemic HypoE mice.

193 Proportion of patient-days classified as hyperglycemic, hypoglycemic, and at-goal (all measuremen

194 -10 demonstrated greatest rewiring, while in hyperglycemics, IL-1beta, IL-6, INF-gamma, and IL-17 exh

195 iated cells to replace beta-cell function in hyperglycemic immunodeficient mice.

196 dult organ donors and transplanted them into hyperglycemic, immunodeficient mice, beta cell replicati

197 xpression differed between normoglycemic and hyperglycemic individuals, siRNA of tetraspanin 33 (TSPA

198 y regulates the sensitivity of the kidney to hyperglycemic-induced renal pathology and that alteratio

199 as a protector of endothelial cells against hyperglycemic injury and raises the potential of repurpo

200 retinopathy fails to halt after cessation of hyperglycemic insult, and a vicious cycle of mitochondri

201 Cancer cells exposed to hyperglycemic insults acquire permanent aggressive trait

202 erence in the expression of TLR4 between the hyperglycemic ischemia and LPS groups or between the hyp

203 In the hyperglycemic ischemia group, TLR4-positive cells were f

204 decrease in HMGB1 immunostaining at 3h after hyperglycemic ischemia that gradually returned to contro

205 he pathogenesis of seizures that result from hyperglycemic ischemia.

206 R4 protein levels in the CA3 region 3h after hyperglycemic ischemia.

207 flow (CBF) in three groups of juvenile rats (hyperglycemic, ketotic, and normal control).

208 Subcutaneous administration of 34 to hyperglycemic Kuo Kondo rats carrying the Ay-yellow obes

209 Here we show that exposure to hyperglycemic levels of glucose enhances necroptosis in

210 after induction of hyperglycemia compared to hyperglycemic littermate controls, although this dysfunc

211 tor-beta1 levels were significantly lower in hyperglycemic MBL-null compared to WT mice, suggesting d

212 d relaxation compared to normoglycemic WT or hyperglycemic MBL-null mice.

213 ents during systole and diastole compared to hyperglycemic MBL-null mice.

214 difying agents, anti-hypertensives, and anti-hyperglycemic medications.

215 rat mesangial cells stimulated to divide in hyperglycemic medium initiate intracellular hyaluronan s

216 t a G0/G1 interphase stimulated to divide in hyperglycemic medium initiate intracellular hyaluronan s

217 66(Shc) is the key effector driving vascular hyperglycemic memory in diabetes.

218 during diabetes, to highlight the effects of hyperglycemic memory on stem cells, and to define ways o

219 al molecular mechanism for the phenomenon of hyperglycemic memory.

220 We tested this using embryos of pregnant hyperglycemic mice and mouse embryonic stem cells (ESC).

221 g blood glucose levels in diet induced obese hyperglycemic mice at 300 and 600 mg/kg, respectively.

222 D2, carrying GAD 206-220 peptide, induced in hyperglycemic mice immune modulation that was able to co

223 ited thrombus formation in normoglycemic and hyperglycemic mice in vivo.

224 icantly higher levels of KSHV lytic genes in hyperglycemic mice than in normal mice.

225 e to a similar magnitude as that observed in hyperglycemic mice with diabetes.

226 In hyperglycemic mice, alpha-dicarbonyl glucose metabolites

227 ntly lowered fasting blood glucose in obese, hyperglycemic mice.

228 reatic beta-cells in streptozotocin-rendered hyperglycemic mice.

229 nists also promoted beta-cell replication in hyperglycemic mice.

230 e analyzed on renal damage in hyperlipidemic-hyperglycemic mice.

231 iabetes in NOD mice and controls diabetes in hyperglycemic mice.

232 peptide that amplifies GIP-mediated GSIS in hyperglycemic mice.

233 The same mechanism might occur in hyperglycemic mice.

234 se glucose, failed to increase activation in hyperglycemic mice.

235 mcitabine in hypoglycemic mice compared with hyperglycemic mice.

236 The hyperglycemic milieu also alters the epigenetic machiner

237 8-OHdG and mtDNA damage despite the adverse hyperglycemic milieu.

238 rmeability by vasoinhibins under diabetic or hyperglycemic-mimicking conditions, but that (ii) vasoin

239 elieve these mice from oxidative stress in a hyperglycemic model.

240 In contrast, hyperglycemic MPCCs displayed significant hepatic lipid

241 ges significantly ameliorated hyperlipidemic-hyperglycemic nephropathy.

242 The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet

243 To test this, we treated hyperglycemic NOD mice with F(ab')(2) fragments of anti-

244 oral insulin or proinsulin does not protect hyperglycemic NOD mice, but the combination with proinsu

245 Increased Sirt6 abundance is found in the hyperglycemic NOD mice, which might increase DNA damage

246 uconeogenesis pathway genes are found in the hyperglycemic NOD mice.

247 normoglycemia and reverse diabetes in newly hyperglycemic NOD mice.

248 n a purely autoimmune setting (NOD.SCID into hyperglycemic NOD), and in a mixed allo-/autoimmune sett

249 mixed allo-/autoimmune setting (BALB/c into hyperglycemic NOD).

250 ere transplanted into streptozotocin-induced hyperglycemic NOD-scid IL2Rgamma(null) mice.

251 cemic ischemia and LPS groups or between the hyperglycemic non-ischemia and control groups.

252 ty of pancreas autoreactive T cells in newly hyperglycemic non-obese diabetic (NOD) mice, protecting

253 on of nucleolar organizing regions (NORs) in hyperglycemic nonobese diabetic (NOD) and old normoglyce

254 in tolerance to islet autoantigens, and that hyperglycemic nonobese diabetic (NOD) mice and T1D patie

255 infusion) but not in two others (Gly) during hyperglycemic-normoinsulinemia.

256 and oxidative metabolism were compared under hyperglycemic normoxic conditions; 51% of the energy cam

257 se, and 53.1% of women and 41.0% of men were hyperglycemic or diabetic.

258 hypoglycemia was not observed in either the hyperglycemic or normal rats.

259 However, hyperglycemic oxidative stress derived from NADPH oxidas

260 The proportion of hyperglycemic patients decreased by 39%, from 6.6 per 10

261 ance testing, whereas SC recipients remained hyperglycemic postglucose challenge.

262 be considered as a dietary source with anti-hyperglycemic potential.

263 Treatment reversed the hyperglycemic progression with a corresponding reduction

264 as better preserved in normoglycemic than in hyperglycemic rabbits, which correlated with improved mi

265 , percentage of CGM values in euglycemic and hyperglycemic ranges, and mean amplitude of glycemic exc

266 We transplanted hyperglycemic rats intraportally with 2500 ferucarbotran

267 We determined that 56.7% of the hyperglycemic rats, but none of the normoglycemic rats,

268 ed rats, compared with mildly and moderately hyperglycemic rats.

269 Ac modification as a potential mechanism for hyperglycemic-regulated gene expression in the beta cell

270 These findings support a critical role for hyperglycemic repression of miR-24 in VWF-induced pathol

271 Moreover, this hyperglycemic response is reproduced by selective activa

272 ia and glucose intolerance by increasing the hyperglycemic response to glucagon and other factors tha

273 tes hepatic gluconeogenesis by enhancing the hyperglycemic response to glucagon and other factors tha

274 In contrast, glucagon signaling and the hyperglycemic response to glucagon were severely impaire

275 od samples, discriminating among healthy and hyperglycemic samples, with good sensitivity (- 0.27micr

276 with normal-appearing retinal morphology in hyperglycemic Sirt3(-/-) or Sirt5(-/-) mice.

277 These data suggest that hyperglycemic spikes high enough to activate persistent

278 of NOD mice at the prediabetic age and early hyperglycemic stage with beta-cell-Ag, along with zymosa

279 een shown to contribute significantly to the hyperglycemic state of patients with diabetes.

280 by the enzymatic oxidation of glucose in the hyperglycemic state promotes the reduction of HS-HA, whi

281 y for diabetic ketoacidosis and hyperosmolar hyperglycemic state resulted in improvements in hospital

282 ch may be related to reduced attention and a hyperglycemic state.

283 with diabetic ketoacidosis and hyperosmolar hyperglycemic state.

284 anage diabetic ketoacidosis and hyperosmolar hyperglycemic state.

285 lated and unmethylated under HG ambience and hyperglycemic states associated with increased MIOX expr

286 rstand the fate of ICCs in hyperinsulinemic, hyperglycemic states characterized by rapid GE, we studi

287 er myocardial infarction (MI), especially in hyperglycemic states, via association with CHIP ubiquiti

288 dification has been observed in diabetic and hyperglycemic states.

289 t rat kidney mesangial cells dividing during hyperglycemic stress abnormally synthesize hyaluronan (H

290 r necrosis factor-alpha, when cultured under hyperglycemic stress, which was inhibited by heparin.

291 Most current treatments ameliorate the hyperglycemic symptom of the disease but are not effecti

292 or conventional therapy aimed at preventing hyperglycemic symptoms.

293 agnosed, the administration of specific anti-hyperglycemic therapy is mandatory to reach a tight glyc

294 In hyperglycemics, there was a doubling at 1 mo but no furt

295 While MK2(-/-)-STZ mice remained hyperglycemic, they showed improved IR and none of the c

296 t role of TSP-1 in diabetic atherosclerosis, hyperglycemic TSP-1(-/-)/ApoE(-/-) double knockout mice

297 However, mice remained hyperglycemic, which was associated with up-regulation o

298 Mice deficient for Hnf1alpha are hyperglycemic, with their pancreatic beta-cells being de

299 increased elastin and collagen deposition in hyperglycemic WT hearts compared to MBL-null hearts.

300 Hyperglycemic WT mice demonstrated dilated cardiomyopath